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164,100 | 3822422-1 | 24,250,031 | noncomm/PMC003xxxxxx/PMC3822422.xml | Role of F18 fluorodeoxyglucose positron-emission tomography/computed tomography in the management of Askin's tumor | A 35-year-old male patient was diagnosed with a PNET of the left chest wall for which he was treated with 15 cycles of chemotherapy. As there was progressive swelling in the left chest wall over 5 months, he was referred for restaging with FDG PET/CT. Increased FDG uptake (maximum standardized uptake value [SUVmax 6.7]) was noted in multiple soft-tissue masses arising from the left chest wall [Figure –]. The largest (measuring 17.4 cm × 9.9 cm) in the lower half of the left hemithorax showed photopenic regions suggestive of necrosis. Erosion of the left 10th and 11th ribs was also noted, along with satellite mass lesions. Since, the scan was suggestive of residual disease, the patient was further treated with five more cycles of chemotherapy in view of the residual disease. Two months after the last cycle of chemotherapy, a follow-up PET/CT showed increase in size of the lesions with extrathoracic and intra-abdominal extensions [Figure –]. However, there was no change in the FDG avidity (SUVmax 6.6) indicating metabolically stable disease. The patient expired 3 months later. | [[35.0, 'year']] | M | {'18245531': 1, '19593561': 1, '19728261': 1, '16855439': 1, '16715954': 1, '17117068': 1, '21193890': 1, '9732497': 1, '18048826': 1, '9669395': 1, '16340719': 1, '20049330': 2, '222426': 1, '18997052': 1, '24250031': 2} | {'3822422-2': 2, '2797374-1': 1} |
164,101 | 3822422-2 | 24,250,031 | noncomm/PMC003xxxxxx/PMC3822422.xml | Role of F18 fluorodeoxyglucose positron-emission tomography/computed tomography in the management of Askin's tumor | A 14-year-old boy presented with a history of pain in the right chest for 2 months. Fine-needle aspiration from the lesion was consistent with PNET and he was referred for F-18 FDG PET/CT for initial staging of the disease. Intense FDG uptake (SUVmax 12.6) was seen in a circumscribed heterogeneously enhancing soft-tissue mass (measuring 13.0 cm × 11.7 cm × 8.0 cm) in the right hemithorax, arising from the chest wall [Figure –]. Areas of photopenia were seen within the mass, suggestive of necrosis. The adjacent posterior part of the 6th rib was directly infiltrated by the lesion. Tracer uptake was also seen in the metaphyseal region of the right humerus and left 2nd rib with mild sclerotic changes (not shown), suggestive of metastases. The patient did not respond to chemotherapy and expired after 9 months. | [[14.0, 'year']] | M | {'18245531': 1, '19593561': 1, '19728261': 1, '16855439': 1, '16715954': 1, '17117068': 1, '21193890': 1, '9732497': 1, '18048826': 1, '9669395': 1, '16340719': 1, '20049330': 2, '222426': 1, '18997052': 1, '24250031': 2} | {'3822422-1': 2, '2797374-1': 1} |
164,102 | 3823385-1 | 24,228,217 | noncomm/PMC003xxxxxx/PMC3823385.xml | Superior Gluteal Artery Pseudoaneurysm Presenting as a Gluteal Mass: Case Report and Review of Literature | A 38-year old female presented to the surgical clinic with pain and swelling in the left gluteal region. The swelling had gradually increased in size over 4 months. The pain was radiating to the left lower limb and associated with numbness. The patient had been involved in a road traffic accident two years earlier and had suffered a left acetabular fracture, which had been treated conservatively.\nPhysical examination revealed a large tender swelling in the left gluteal area simulating an abscess. However, pulsation was observed over the swelling that raised the suspicion of a vascular lesion. Therefore, contrast enhanced computed tomography (CT) was done before trying any intervention. The scan demonstrated a large pseudoaneurysm originating from the left superior gluteal artery measuring 6.4 × 5.8 × 3.4 cm with a small intra-pelvic component and large extra-pelvic component in the gluteal area []. This lesion appeared as a contrast-filled structure in direct communication with the superior gluteal artery. Its two components were communicating in the region of greater sciatic notch.\nMagnetic resonance imaging (MRI) was also performed for better assessment of this vascular swelling and any surrounding hematoma. The aneurysm demonstrated mixed signal intensities; with rounded central signal-void area representing the patent lumen, and a peripheral thick rim of high signal intensity on T1-weighted and low signal intensity on T2-weighted images denoting a thrombus/hematoma []. In addition, the signal void lumen showed some flow artifacts.\nThe patient was referred for endovascular treatment.Digital subtraction angiography (DSA) and transcatheter embolization were done in the same session. The aneurysm was approached by puncturing the right femoral artery and occluded by placing four coils and gelfoam in the feeding vessels [].\nRepeated CT angiography after 1 week confirmed exclusion of the aneurysm with only a residual hematoma in the area [Figure and ]. Patient had an uneventful recovery with the pain disappearing and gluteal swelling gradually regressing in size over several months. Follow-up MRI few months post-embolization showed significant reduction in the size of the hematoma []. | [[38.0, 'year']] | F | {'17939491': 1, '16120928': 1, '18952466': 1, '19917559': 1, '21489927': 1, '28275573': 1, '30374381': 1, '20201182': 1, '33212307': 1, '27239635': 1, '28197249': 2, '17410354': 1, '17267470': 1, '25015326': 1, '21890561': 1, '30787957': 2, '19540714': 1, '24228217': 2} | {'5295570-1': 1, '6375272-1': 1} |
164,103 | 3823386-1 | 24,228,215 | noncomm/PMC003xxxxxx/PMC3823386.xml | Truncus Arteriosus with Persistent Left Superior Vena Cava: Cardiac Computed Tomography Findings in an Unrepaired Adult Patient | A 24-year-old male patient with unrepaired TA presented to the adult congenital cardiology clinic for surgical operation and his history revealed that he had been diagnosed with a complex cyanotic congenital heart disease at the age of 4 years, when he had cyanosis while crying. He had been hospitalized many times for recurrent lung infections. He was placed on a heart-lung transplantation waiting list. Meanwhile, he was started on bosentan therapy as he had developed cardiovascular symptoms. Unfortunately, no appropriate donor could be found during the waiting time. A subsequent cardiac catheterization revealed pulmonary hypertension, for which iloprost had been added to the bosentan therapy.\nOn physical examination, he was normal, except for being cyanotic and his blood pressure was 120/70 mmHg, heart rate was 72 beats/min and respiratory rate was 20/min. Chest X-ray showed increased pulmonary vascularity with an enlarged cardiac silhouette. Echocardiogram was consistent with a TA Type 1, VSD, truncal valvular insufficiency, and Eisenmenger physiology. An electrocardiographic (ECG)-gated cardiac computed tomography (CT) was ordered to characterize the complex cardiac anatomy more in detail.\nECG-gated multidetector CT (MDCT) (Somatom Definition, 128-slice Dual Source CT, Siemens Medical Systems, Erlangen, Germany) was performed. Contrast material of 75 ml (Ultravist 370 mg/mL, Schering, Berlin, Germany) was given through the left antecubital vein at a rate of 5 mm/s. Afterward, 50-cc bolus of intravenous saline solution was given at a rate of 5 cc/s. The region of interest was located relative to the ascending aorta 1 cm distal to the tracheal bifurcation. The scan was automatically started 2 s after the threshold level reached 130 Hounsfield unit. Contrast administration was controlled using bolus tracking. ECG-gated MDCT was performed according to the following protocol: gantry rotation time, 330 ms; temporal resolution, 83 ms; slice acquisition, 64 mm × 0.6 mm; pitch, 0.38 adapted to the heart rate; tube voltage, 120 kV; tube current, 380 mAs per rotation. The scanning duration was approximately 8.2 s, depending on the cardiac dimensions and the pitch and took place during a single breath hold in the craniocaudal direction. The estimated effective radiation dose was 5.5 mSv.\nIn addition to traditional axial images, three-dimensional (3D) volume rendering (VR) images, multiplanar reconstructions (MPR), curved multiplanar reformation and thin-slab maximum intensity projection techniques were employed to evaluate truncus and the additional anomalies.\nMDCT clearly delineated the complex cardiac anatomy in this case with TA [Figure –]. PLSVC drained into great cardiac vein. The coronary sinus was larger than normal and measured 25 mm. The right coronary artery branched from the non-coronary sinus on the left side of the truncus [] while the left coronary artery originated from the non-coronary sinus on the right side of the truncus []. A 2.5 cm VSD was detected on interventricular septum []. The truncal valve was trileaflet. The left inferior pulmonary vein drained into the right side of the left atrium (LA) and a pulmonary vein drained into the left side of the atrium was observed []. Such a pulmonary vein has never been reported in previous cases with TA. | [[24.0, 'year']] | M | {'2856609': 1, '18716119': 1, '20307275': 2, '910720': 1, '14557509': 1, '985630': 1, '27262857': 1, '8897617': 1, '8047491': 1, '26262994': 1, '18141293': 1, '10440171': 1, '24228215': 2} | {'2846925-1': 1} |
164,104 | 3823388-1 | 24,228,214 | noncomm/PMC003xxxxxx/PMC3823388.xml | Radiographically Occult Latent Radiogenic Osteosarcoma Uncovered on Tc-99m Methylene-diphosphonate Bone Scintigraphy | A 70-year-old male presented with mild left hip pain and was found to have an elevated serum alkaline phosphatase (ALK) level of 770 units/L. Unfortunately, due to a language barrier, a complete medical history could not be obtained. In light of the patient's elevated ALK level, the patient was referred for a whole-body Tc-99m MDP bone scan. The planar whole body images [] of the Tc-99m MDP bone scan demonstrated intense diffuse uptake extending from the left femoral head to the proximal shaft of the femur. Initially, we felt this type of appearance could be compatible with early Paget's disease given the markedly elevated ALK, despite the absence of apparent structural deformities.\nTo confirm the initial diagnosis, the patient was sent directly for an X-ray []. However, the pattern of multifocal sclerosis (cotton wool appearance) that would be expected of Paget's disease was not present.[] Instead, the radiograph demonstrated three previously unreported fixation screws, used to repair a femoral neck fracture (later discovered to have occurred 1 year ago). Surrounding the screws were poorly defined osteopenic, potentially lytic lesions in the femoral neck and femoral head []. Correlation of the Tc-99m MDP bone scan with the X-ray changed the initial diagnosis from suspected Paget's disease to a differential of malignancy/metastasis, reparative phase of osteonecrosis, osteomyelitis, or reactive osteolysis to the fixation screws. Though simple loosening of the fixation screws could have explained the patient's mild hip pain, the activity demonstrated by the bone scan was much too diffuse and intense to support this diagnosis.[]\nTo evaluate for metastatic disease, a computed tomography scan of the chest, abdomen, and pelvis was ordered the following day. Evaluation of the scan of the left hip was limited due to streak artifact from the screws; however, it was still possible to appreciate some mixed lytic/sclerotic changes in the native bone [Figure and ]. Even though these changes raised the suspicion of osseous malignancy or metastasis, they were not pathognomonic, as hardware loosening, osteopenia, and degenerative changes could have a similar appearance.[] However these findings in combination with the bone scan findings, provided enough suspicion of a pathology sinister enough to refer the patient for surgical hardware revision with potential biopsy.[]\nSurgical exploration of the left hip revealed a grossly abnormal appearance of the left proximal femur with areas of hemorrhagic bone surrounding lytic lesions. The fixation screws were removed and curettage of the suspicious lesion was performed. Histologic study of the biopsy [] demonstrated sarcomatous, spindle shaped cells with adjacent tumor osteoid production; represented by eosinophilic, amorphous, fibrillary deposits between individual or small aggregates of tumor cells. These histological findings were diagnostic of osteosarcoma.[]\nIn context, the presence of osteosarcoma was highly unlikely as there have been no case reports of primary osteosarcomas occurring in a site of a fracture that was surgically repaired 1 year prior. Additionally, the distal femur would be a far more likely site for a primary osteogenic sarcoma to occur.[] However, upon further interrogation of the patient's past medical history, it was discovered that the patient had prostate cancer 11 years ago. Given the standard of care at that time, one could surmise that he was treated with 60-70 Gy of targeted external beam radiation to the prostate.[] The dose that he received and the time frame since receiving his radiation would be compatible with radiogenic osteosarcoma as there is a latency period of about 10 years.[] The repaired stress fracture 1 year prior was potentially pathologic from the malignancy, but was most likely missed due to the slightly atypical radiographic appearance on the plain film X-ray performed in the surgeon's office. | [[70.0, 'year']] | M | {'22541962': 1, '7607259': 1, '16627266': 1, '12640151': 1, '19038601': 1, '12235348': 1, '11007511': 1, '10640974': 1, '11061690': 1, '24228214': 2} | {} |
164,105 | 3824736-1 | 23,605,476 | noncomm/PMC003xxxxxx/PMC3824736.xml | Proximal aortic stent migration | A 21-year-old man underwent stent implantation (8Z45CP stent on 18 mm BiB-balloon, Numed, Hopkinton, NY) for a recurrent aortic obstruction, after previous repair of an aortic interruption type A. At the age of two weeks after birth an end-to-side anastomosis of the descending aorta onto the distal arch (left subclavian artery) was performed. Diagnosis of restenosis was based upon upper limb hypertension, a diastolic run-off with echo-Doppler, and an invasive systolic gradient of 36 mmHg (Fig. ). Stenting was followed by post-dilatation with a 20 mm high pressure balloon. The peak systolic gradient decreased from 15 to 0 mmHg and the diameter increased from 11 to 17 mm (Fig. ). One year later, transthoracic echocardiography (TTE) suggested a more proximal position of the stent, which was confirmed with a CT scan (Figs. and ). Systolic gradients were measured during diagnostic catheterisation (Fig. ) and with angiography the position of the stent was further visualised. The case was discussed within our team and with external experts. Two treatment options were considered. One option was fixation of the stent with one or two distal stents including redilatation of the narrowed segment. The second option was surgical removal of the stent with reconstruction of the aortic arch. Although the votes were divided, surgical intervention was our preferred approach. At surgery the stenotic part of the aorta was resected and the stent removed. In the ascending aorta an unexpected ulceration due to an eroding effect of the proximal stent end was found. This potentially lethal lesion was included in the resection as well. Aortic arch reconstruction was performed with interposition of a 24 mm vascular graft between the ascending and descending aorta, with replantation of the subclavian artery in the prosthesis. Surgery was successful and postoperative recovery was uncomplicated (Fig. ). Four years after surgery no further complications occurred and the patient was normotensive without medication. The anatomical situation assessed with CT was excellent (Fig. ). | [[21.0, 'year']] | M | {'18695443': 1, '20862238': 1, '16181033': 1, '11691533': 1, '10827387': 1, '21948021': 2, '10525517': 1, '17630670': 1, '23605476': 2} | {'3189313-1': 1} |
164,106 | 3825154-1 | 23,771,403 | noncomm/PMC003xxxxxx/PMC3825154.xml | Persistent primitive olfactory artery connected with middle cerebral artery: case report | A 78-year-old woman presented with headache. CT–angiography revealed a right PPOA. The vessel originated from the right distal A1, ran along the right olfactory tract toward the olfactory bulb, and made an abrupt posterior turn, ultimately becoming the distal MCA. In this patient, I identified the normal A1 and a short anterior communicating artery (Fig. ). Her headache was relieved with medication. | [[78.0, 'year']] | F | {'9689332': 1, '3703117': 1, '22540402': 1, '21901376': 1, '24271941': 1, '18597962': 1, '21061008': 1, '5584541': 1, '19779285': 1, '26494407': 1, '23771403': 2} | {} |
164,107 | 3825521-1 | 24,273,619 | noncomm/PMC003xxxxxx/PMC3825521.xml | Me, Myself and My Brain Implant: Deep Brain Stimulation Raises Questions of Personal Authenticity and Alienation | Patient 1, a 38-year-old female journalist married with one child, had PD (caused by a mutation in the parkin gene) for 30 years […] with motor fluctuations and severe dyskinesias. Before stimulation, in spite of her motor handicap, she was dynamic: ‘Combating the disease gave meaning to my life. I hope that stimulation will allow me to get on with my life and my projects. ‘Six months after the operation, the patient was not satisfied in spite of a 75% improvement of her motor handicap and the withdrawal of her antiparkinson medication. She complained that the stimulator was not well programmed and she wanted to be able to adjust it herself at home. After 18 months of stimulation, she was no longer able to work, had a loss of inspiration and a taste for her work and for life in general. ‘Now I feel like a machine, I’ve lost my passion. I don’t recognize myself anymore. ‘Her family no longer interested her, she was easily exhausted, and had a loss of vitality (in the absence of a depressive syndrome), which led her to interrupt all professional activity. In short, a loss of vitality and a goal in life occurred despite major improvement of her motor symptoms by STN stimulation. ([]: 1812).\nA short analysis of this case reveals that four elements of felt-alienation and the loss of authenticity are at work in the patient’s experience:\nFirst, after successful treatment, the patient feels alienated from her work and indulges in leisure activities instead. This will be surprising to the reader given that she proclaimed that one of her main aims in undergoing the treatment was enhancing her ability to work. However, although her motor disability has improved remarkably, she nevertheless experiences her formerly much-beloved work as alienating after surgery.\nSecond, she experiences alienation from herself because she has lost a goal in life. It seems that this is the case because she no longer has anything to fight for and this has resulted in a loss of energy. She even goes so far as to say,‘I don’t recognize myself anymore’ – presumably because she used to be goal-oriented and energetic, but now has lost her drive, which she identified with. This corresponds with what Schüpbach et al. [] suggest:Fighting PD was a driving force for many patients that was frustrated in 12 (41%) after surgery […] causing disorientation. As expressed by another patient: ‘Before stimulation, I wanted to be like everybody else, I didn’t want to be considered only as sick. I fought for that every day! Now I find myself less impassioned, I regret the period where I did battle. Now it’s the warrior’s repose, I no longer have something to struggle against, my life is empty. I get up every day, but have no goal, no horizon.’ ([]: 1814).\nThird, the patient feels alienated because she feels heteronomous – ‘like a machine’, as she puts it. The case report does not give any details, but this may be due to the fact that a mechanical device is implanted in her brain. Phenomenologically speaking, it could be that the patient perceives the device as an alien technology that, as it were, remote-controls her feelings, behavior and thoughts (cf. []: 169 ff.). Another patient reports feeling ‘like an electronic doll’ ([]: 1815). As Schüpbach et al. put it: ‘The altered body image may result from difficulty in accepting psychologically the implanted material, as previously described in patients with pacemakers and implantable cardioverter defibrillators.’\nWhat is interesting here, however, is that the self-description of some patients of being remote-controlled by an electronic device runs contrary to the patients’ actual gain in autonomy, because their motor abilities usually improve remarkably under treatment. In a certain sense, patients become more autonomous after successful surgery because they have a better command of their body. But in another, Aristotelian sense, a feeling of heteronomy arises: if a person is not entirely ‘self-moved’, but is or feels moved by a force outside her control, she might feel heteronomous. In this case study, the feeling of heteronomy goes hand in hand with the patient feeling alienated from life.\nFourth, this case raises another key issue involving authenticity and alienation: the split between mind and body. The authors of the study even chose this phenomenon to be the report’s subtitle: ‘A distressed mind in a repaired body’. They reveal that some patients experience feelings of alienation from their improved health condition. As the authors also report about other patients, some of them do not yet dare to trust their bodies and are aware of the fact that their disease will come back at some point (‘negative anticipation’). ‘In spite of successful surgery, 8 patients (28%) felt mentally unable to resume a more normal life style. Although with STN stimulation they could, they did not dare to perform activities that had been impossible with PD before surgery. Past experience led to a negative anticipation that was objectively unjustified after surgery. ‘My body is cured, but my mind is still sick,’ said one patient ([]: 1814). This is exemplified by Patient 1: although she describes herself as physically healed, her psychological condition cannot catch up to this new bodily state. This results in a feeling of alienation because the patient experiences her body as being in a state different than the one of her mind.\nTo sum up these findings, this first case study shows a patient who, under treatment, has lost her felt-authenticity and eventually feels alienated from herself in several respects. After treatment, not only does her work-life seem alienating, but also she feels alienated from life-goals she identified with, as well as from her new, improved body (cf. []: 1814). In the following case study, however, the patient experiences an opposite result. | [[38.0, 'year']] | F | {'34925637': 1, '21255750': 1, '10763472': 1, '15291417': 1, '31011471': 1, '30853878': 1, '26240430': 1, '25597042': 1, '18466265': 1, '17533932': 1, '30098651': 1, '24273622': 1, '19724092': 1, '26740906': 1, '24587963': 1, '30774052': 1, '25183320': 1, '34471390': 1, '32189235': 1, '32268846': 1, '28320773': 1, '34531923': 1, '21475717': 1, '30595661': 1, '16801642': 1, '34790274': 1, '17909988': 1, '20866019': 1, '19072907': 1, '24273618': 1, '29937948': 1, '10753488': 1, '34721724': 1, '32954260': 1, '27618110': 1, '33764258': 1, '19177805': 1, '34574440': 1, '19527264': 1, '20179289': 1, '15291423': 1, '16092400': 1, '29163010': 1, '28426824': 1, '19241141': 1, '28620655': 1, '25352789': 1, '15824249': 1, '24273619': 2} | {'3825521-2': 2, '3825521-3': 2} |
164,108 | 3825521-2 | 24,273,619 | noncomm/PMC003xxxxxx/PMC3825521.xml | Me, Myself and My Brain Implant: Deep Brain Stimulation Raises Questions of Personal Authenticity and Alienation | ‘Patient 2, a 48-year-old male accountant, worked half-time for 7 years because of PD […]. Before the operation, his wife assisted him in all tasks of daily living, assumed all domestic and financial responsibilities, spent hours with him, and helped him to conceal his disease from his entourage. After 18 months of stimulation, his motor condition was much improved […]. The patient regained confidence in himself and aspired to more autonomy: ‘I want to recover my social standing and establish new relationships outside my couple. During all these years of illness, I was asleep. Now I am stimulated, stimulated to lead a different life.’ Confronted with the radical change in her husband’s behavior, his wife became depressed: ‘Ever since the operation, I feel lost. Before, when he was sick, we were a perfect couple. Now, he wants to live the life of a young man, go out, meet new people, all of that is intolerable! I would rather he be like he was before, always nice and docile!’ The patient persisted in his desire for change: ‘All these years I allowed myself to be carried like a child, because I didn’t have the means to fight. That period is over, I want to get back the position I left open. I am going to take my life in hand, my life before PD.’ In short, a grave marital conflict was caused by the newly regained autonomy of the patient and his wife’s loss of status as caregiver. ([]: 1812)\nThis story differs considerably from the first one. This patient says that under treatment he now feels like himself, whereas before he felt alienated, i.e. not himself. In this case, what is gained from the treatment is authenticity, qua implicit self-ascription at least. The patient claims that in all the years of illness he was ‘asleep’. This can be interpreted as him saying that he was not aware of himself, i.e. not in a self-conscious mode and, therefore, in this sense not really ‘himself’. From a philosophical point of view, this could mean that he did not possess any self-reflective capacities and could not lead his life autonomously.\nAs he puts it after successful surgery: ‘I want to regain my life, my life before PD’. In stating this, he refers to the life before his illness that was really his, his real life, he being conscious of himself and ‘master of his own destiny’, as one could say. During the years of illness, however, according to his own retrospective assessment, he feels he was not himself, i.e. inauthentic, alienated, and not fully conscious. His life was not really his own, existing as someone else’s heteronomous object of care. This is at least how he describes his time of illness in hindsight.\nWith respect to authenticity and alienation, at least three points about his case are important.\nFirst, the patient’s self-ascription of authenticity is interesting. It seems that, after surgery, the patient distinguishes two modi in his life. On the one hand, there is ‘mode one’, the mode he experienced when he was healthy before Parkinson’s disease struck him. This mode he experiences retrospectively as his ‘authentic mode’. On the other hand, there is ‘mode two’, the mode he experienced when he became sick. He says in hindsight that this mode is one in which he was not authentic, but ‘asleep’ and thus alienated. Finally, once he is successfully treated via DBS and switches back to ‘mode one’, he begins to feel authentic again.\nThe second remarkable point is that this contradicts what Patient 1 had reported. Adapting the model from above, she experienced ‘mode two’, i.e. the mode of being diseased, as her most authentic mode. When she was sick, she had something to strive for: to overcome her disease and to lead a meaningful life despite her handicaps. The daily struggle gave her life meaning. When she returns to ‘mode one’ as the mode of health, however, she describes herself as feeling alienated, because she has lost her goal in life. It seems she no longer experiences herself as authentic once she is healthy.\nOn a theoretical level, this points towards the fact that the ascriptions of authenticity and alienation depend on subjective factors. It seems there is no general, trans-individually valid correlation between being healthy and feeling authentic, and being sick and feeling alienated. On the one hand, an existentialist or phenomenological notion of authenticity, which emphasizes mortality, fits for Patient 1: a person is ‘authentic’ (eigentlich) only when she is confronted with her vulnerability and thereby her mortality through her disease (cf. []: 152) and struggles for survival. On the other hand, however, the opposite holds for Patient 2: he defines himself essentially as a healthy person and does not accept the diseased person he used to be as himself. Furthermore, the fact that there is no unifying account of the subjective experience of DBS has implications with respect to how we understand DBS treatment. Whereas the treatment for one person can be authenticity-generating, for another, it has an alienating effect.\nThird, it is worth noting that Patient 2 correlates authenticity, i.e. living his own life, with autonomy. For Patient 2, in order to be himself, he must be autonomous like an adult person, not dependent and heteronomous like a child. He wants to return to the autonomous social- and work-life he led before the disease – and the treatment makes this possible.\nThis, of course, stands in sharp contrast to the second- and third-person perspective of his wife. According to her, her husband is alienated from himself in ‘mode two’, the healthy state. She complains he wants to ‘live the life of a young man’, i.e. a life that is not only inappropriate to him in her eyes, but actually is the life of someone else and not his. Additionally, now that she as the caregiver is no longer needed and wanted, she has lost all meaning in her life. She wants to get divorced, because she feels alienated from her relationship with a person who she no longer views as her husband.\nThe third case presented by Schüpbach et al. [] reveals yet another feature of authenticity and alienation. | [[48.0, 'year']] | M | {'34925637': 1, '21255750': 1, '10763472': 1, '15291417': 1, '31011471': 1, '30853878': 1, '26240430': 1, '25597042': 1, '18466265': 1, '17533932': 1, '30098651': 1, '24273622': 1, '19724092': 1, '26740906': 1, '24587963': 1, '30774052': 1, '25183320': 1, '34471390': 1, '32189235': 1, '32268846': 1, '28320773': 1, '34531923': 1, '21475717': 1, '30595661': 1, '16801642': 1, '34790274': 1, '17909988': 1, '20866019': 1, '19072907': 1, '24273618': 1, '29937948': 1, '10753488': 1, '34721724': 1, '32954260': 1, '27618110': 1, '33764258': 1, '19177805': 1, '34574440': 1, '19527264': 1, '20179289': 1, '15291423': 1, '16092400': 1, '29163010': 1, '28426824': 1, '19241141': 1, '28620655': 1, '25352789': 1, '15824249': 1, '24273619': 2} | {'3825521-1': 2, '3825521-3': 2} |
164,109 | 3825521-3 | 24,273,619 | noncomm/PMC003xxxxxx/PMC3825521.xml | Me, Myself and My Brain Implant: Deep Brain Stimulation Raises Questions of Personal Authenticity and Alienation | Patient 3, a 45-year-old female executive, married with 3 children, had levodopa-responsive PD for 6 years […] with severe motor complications. Before the operation, she was ashamed to be sick and concealed her disease from her colleagues and employer. She invested herself in her work, assumed more and more responsibilities, and had great hopes that the operation would help her to progress in her career: ‘If I’m not operated in the coming months, the beast is going to sleep. As long as I have my work, I still exist; the day I can no longer go to work, it will be as if the curtain came down on my life. ‘Six months after the operation, she had no trace of a motor handicap […]. She put off going back to work, however, because she felt anxious, had lumbar pain, dizziness, difficulty walking, but had no neurologic substrate. […]. An episode of severe depression was treated successfully. Eighteen months after the operation, she had tried several times without success to go back to work:’ I don’t have the same ability to concentrate as before. I have a lot of work and prefer to spend my time doing other things. ‘She requested unjustified sick leaves, preferred to go out, buy things on the Internet. She threatened to divorce, although there had been no marital conflict before the operation. She announced her disease to her entourage, was active in associations, and wanted to ‘be recognized as sick.’ In short, a loss of professional status after the operation occurred, in spite of spectacular motor improvement, which was the cause of a marital crisis.\nHere, at first glance, the picture is very similar to the first case: now that the patient’s condition has improved, she experiences leisure as authenticity, whereas she experiences work as alienating. The cured patient prefers to spend her time doing other things outside her employment, spending money on the internet and joining social activities. However, in contrast to the first case study, it is interesting to see that now that the patient’s body condition is improved drastically, she somehow paradoxically wants her disease acknowledged.\nBefore the treatment, she had attempted to hide her disease from her family, employer, and colleagues. Now that she is better than before, it seems that she, to a certain extent, actually denies being better and does not want to recognize her own improvement. The fact that she demands attention for and recognition of her diseased state, even when she is ‘healthier’ than before, suggests that she identifies her diseased state as her authentic state. Similarly to Patient 1, the bodily self-image of Patient 3 seems to be dissociated from her mind. Her mind is still that of a sick person, although it has gained the strength to now recognize and even publicly proclaim her disease, whereas her body improved already – a fact that does not seem to have made it through to her consciousness. Her battle-cry is: ‘I want to be recognized as sick’, now that her symptoms are much better than before surgery.\nAll in all, to me the case of Patient 3 reads like a story of emancipation, revelation, or even revolt. It even sounds as if she regarded her personal, retrospective coming out as a Parkinson’s patient as a political mission, probably also willing to fight for the rights of other people in her situation.\nIf we use the notions of alienation and authenticity, we can shed light on Patient 3’s experience. We could interpret the patient’s situation before treatment as alienating: she used to live a life under permanent pressure, being an ambitious working mother who has PD, and who, on the top of that, felt the need to conceal her ailment. DBS helps this patient reach a state authenticity, insofar as she is now able to be sincere, honest, and self-confident with respect to herself. In hindsight, the patient truthfully recognizes her own past condition and pays herself due respect for all she has undergone and has nevertheless achieved. Paradoxically, this happens at the very moment she experiences a substantial relief of most of her preeminent PD symptoms. Her newly gained self-confidence makes her demand full recognition for her achievements from others as well. In this vein, due to the treatment, she has gained the strength to be truthful and open with the people in her life, making her disease public instead of shamefully trying to hide it. Now that her bodily symptoms have remarkably improved, it seems that the time is ripe for her to reap some ‘reward’ and compensation for all the hardships she underwent during her disease.\nTo sum up: interpreted this way, what is important in this third case study is that the patient escapes from felt-alienation through treatment and achieves a state of authenticity as a result. Here, authenticity means liberation and emancipation.\nSo far, I have offered an interpretation of these three case studies within the philosophical framework of authenticity and alienation; however, as I mentioned above, my interpretation differs from the conclusions that the authors of the study draw. In the following section, I want to turn my attention to their conclusions and to what, from my vantage point, is unsatisfying in their account. | [[45.0, 'year']] | F | {'34925637': 1, '21255750': 1, '10763472': 1, '15291417': 1, '31011471': 1, '30853878': 1, '26240430': 1, '25597042': 1, '18466265': 1, '17533932': 1, '30098651': 1, '24273622': 1, '19724092': 1, '26740906': 1, '24587963': 1, '30774052': 1, '25183320': 1, '34471390': 1, '32189235': 1, '32268846': 1, '28320773': 1, '34531923': 1, '21475717': 1, '30595661': 1, '16801642': 1, '34790274': 1, '17909988': 1, '20866019': 1, '19072907': 1, '24273618': 1, '29937948': 1, '10753488': 1, '34721724': 1, '32954260': 1, '27618110': 1, '33764258': 1, '19177805': 1, '34574440': 1, '19527264': 1, '20179289': 1, '15291423': 1, '16092400': 1, '29163010': 1, '28426824': 1, '19241141': 1, '28620655': 1, '25352789': 1, '15824249': 1, '24273619': 2} | {'3825521-1': 2, '3825521-2': 2} |
164,110 | 3825539-1 | 24,273,612 | noncomm/PMC003xxxxxx/PMC3825539.xml | Septic pulmonary embolism originated from subcutaneous abscess after living donor liver transplantation: a pitfall of postoperative management | A 49-year-old male underwent LDLT because of primary sclerosing cholangitis. Preoperative performance score was 1 and the model for end-stage liver disease score was 24.8. The patient had a history of total colectomy because of ulcerative colitis. The donor was the patient’s wife, and the blood types were identical. A right hemiliver graft was used. Graft size was 750 g and the ratio of graft volume/standard liver volume of the recipient was 52.1 %. The cold and warm ischemic time was 111 and 56 min, respectively. Duct-to-duct anastomosis was adopted for biliary reconstruction because postoperative management of strictures is easy to perform by endoscopic methods. Splenectomy was also performed because of preoperative thrombocytopenia resulting from splenomegaly. Expected amount of bleeding was 29,876 ml. He was treated with tacrolimus, mycophenolate mofetil, and steroids as immunosuppressants. The whole-blood trough level of tacrolimus was adjusted to 10–12 ng/ml during the first postoperative week, and was tapered thereafter. The mycophenolate mofetil doses ranged from 500 to 1,000 mg/day. Methylprednisolone (700 mg) was administered twice intraoperatively, tapered gradually thereafter, and discontinued on postoperative day (POD) 35. The patient was discharged on POD 40.\nHe was re-admitted on POD 48 because of severe acute cellular rejection. After three courses of steroid pulse therapy using methylprednisolone (each comprising 500 mg per session for 3 days; total dose of 4.5 g of methylprednisolone) were performed, the liver dysfunction gradually improved (Fig. ); however, continuous peripheral intravenous drip infusion therapy via the left forearm was necessary for 20 days because of appetite loss. The patient was discharged on POD 83; however, he visited our hospital on POD 87 complaining of pyrexia accompanying pain in the left forearm. Laboratory results showed a peripheral white blood cell count of 4,000/mm3 with 22.0 % stab cells, C-reactive protein (CRP) levels of 10.3 mg/dl and albumin level of 2.4 g/dl. Liver function tests, including alanine aminotransferase (ALT) measurements, were almost within the normal range (Fig. ). Rubefaction accompanying the subcutaneous abscess was present at a wound on the left forearm formed by intravenous drip therapy during the last hospital stay (Fig. ). Although respiratory symptoms were not present and performance status was zero, chest computed tomography (CT) revealed five pieces of cavitary or wedge-shaped nodules in the periphery of the bilateral lung (Fig. ). The lung nodules ranged from 0.8−2 cm in diameter, and were indistinct on a chest X-ray. β-d glucan levels were <6.0 pg/ml, Aspergillus antigens were not detected and mycobacterial culture of sputum was negative. The smear from the incisional drainage of the skin, blood and sputum revealed the presence of Gram-positive coccus; empiric broad-spectrum intravenous antibiotics using vancomycin (2 g/day) were thus started immediately. Lastly, methicillin-sensitive Staphylococcus aureus was cultured both from the blood and the subcutaneous abscess of the left forearm.\nThe pathogenesis was diagnosed as SPE secondary to S. aureus septicemia originating from the subcutaneous abscess of the left forearm. Vancomycin was de-escalated to cefazolin (6 g/day) for 11 days following cefaclor treatment (1.5 g/day) for 4 days with drainage of the subcutaneous abscess. The patient showed a good response to the antibiotic therapy; blood cultures detected no bacteria, the subcutaneous abscess in the left forearm epithelized, and the lung cavitary lesions disappeared by 141 days after LDLT. | [[49.0, 'year']] | M | {'11780550': 1, '18515934': 1, '19917418': 1, '30218430': 1, '18158141': 1, '18158437': 1, '18722742': 1, '18837421': 1, '642559': 1, '2735296': 1, '17112879': 1, '12244005': 1, '15491398': 1, '11428999': 1, '20496132': 1, '19261131': 1, '11274848': 1, '16002930': 1, '15561227': 1, '20831782': 1, '21509424': 1, '24273612': 2} | {} |
164,111 | 3825578-1 | 23,700,192 | noncomm/PMC003xxxxxx/PMC3825578.xml | Starch accumulation in the lungs of two infants following positive ventilation | Case 1: The first infant was a 10-month-old male who died on a cold winter day in a nursery. He was fed milk and cookies at approximately 10:00 a.m. At approximately 11:00 a.m., he was placed together with two other infants in the prone position in the middle of a large baby bed covered with a fitted bed sheet and a blanket that was usually kept in a bedroom. Two school staff were in the living room performing work on a computer until approximately 11:30 a.m. One of the staff members checked on the infant in bed at this time and found him unresponsive. CPR was performed immediately and he was taken to the emergency room in a hospital, but resuscitation was unsuccessful. He suffered from ventricular fibrillation in the ambulance and from cardiac arrest after arriving at the hospital.\nA complete judicial autopsy examination showed an anatomically normal infant. The infant appeared adequately developed and well nourished for his age; he weighed 9,500 g and was 76 cm in length. There was no evidence of trauma. All internal viscera were unremarkable, except for visceral congestion, including pulmonary (lung weight, left/right: 75/90 g) and cerebral edema (brain weight, 930 g), and congestion. | [[10.0, 'month']] | M | {'20292162': 1, '836067': 1, '6372845': 1, '7246501': 1, '14475255': 1, '14224947': 1, '17849249': 1, '4905831': 1, '8859920': 1, '23700192': 2} | {'3825578-2': 2} |
164,112 | 3825578-2 | 23,700,192 | noncomm/PMC003xxxxxx/PMC3825578.xml | Starch accumulation in the lungs of two infants following positive ventilation | Case 2: The second infant was an 8-month-old female who died on an early summer day in a nursery. This infant and nursery had no known direct familial link or relationship to Case 1. She was fed approximately 200 mL of milk at approximately 12:40 p.m. She was put to bed in the supine position with her head turned sideways at approximately 1:35 p.m. and was heard to cry once at 2:45 p.m. The school’s staff were in the same room playing with the infant’s 2-year-old brother until approximately 4:15 p.m. The staff checked on the infant in bed at this time and found her unresponsive. CPR was undertaken immediately, but death was certified after 1.5 h.\nA complete judicial autopsy examination showed an anatomically normal infant. The baby appeared adequately developed and well nourished for her age; she weighed 7,500 g and was 70 cm in length. An autopsy revealed no evidence of trauma. All internal viscera were unremarkable, except for visceral congestion including pulmonary (lung weight, left/right: 60/70 g) and cerebral edema (brain weight: 900 g). | [[8.0, 'month']] | F | {'20292162': 1, '836067': 1, '6372845': 1, '7246501': 1, '14475255': 1, '14224947': 1, '17849249': 1, '4905831': 1, '8859920': 1, '23700192': 2} | {'3825578-1': 2} |
164,113 | 3825672-1 | 24,232,291 | noncomm/PMC003xxxxxx/PMC3825672.xml | A case of bismuth intoxication with irreversible renal damage | A 21-year-old woman was admitted to the emergency department 4 hours after taking 20 tablets of CBS in a suicide attempt. Each tablet included 300 mg of CBS, which is equivalent to 120 mg of Bi2O3. There was no alcohol or another intravenous drug usage. In the emergency service, the patient underwent gastric lavage and received intravenous fluid therapy, after which she was admitted to the internal medicine intensive care unit.\nPhysical examination upon admission was unremarkable: blood pressure, 100/60 mm Hg; pulse, 76 beats/minute; respiration rate, 12 breaths/minute; and body temperature, 36.5°C. Laboratory tests were as follows: white blood cell count, 7860/mm3; hemoglobin, 10.8 g/dL; platelet count, 445,000/mm3; serum sodium, 141 mEq/L; potassium, 4.3 mEq/L; chloride, 104 mEq/L; glucose, 108 mg/dL; amylase, 85 U/L; aspartate aminotransferase (AST), 35 U/L; alanine aminotransferase (ALT), 14 U/L; lactate dehydrogenase (LDH), 150 U/L; hepatitis B surface antigen, nonreactive; and anti-hepatitis C virus, nonreactive. Her INR was reported to be normal at 1.1. Thyroid function tests were normal. Chest radiography also showed no abnormalities. Abdominal ultrasonography demonstrated slightly increased echogenicity in the renal parenchyma. Electrocardiography and echocardiography findings were normal. The patient rapidly became oliguric (<500 mL/day) and thereafter was anuric (0 mL/day). Blood creatinine increased to 2.6 mg/dL (blood urine nitrogen [BUN], 8 mg/dL) during the first 24 hours and to 3.1 mg/dL (BUN, 11 mg/dL) the next day. The baseline creatinine value was normal. Nevertheless, levels of LDH, ALT, and AST were elevated at 1,129 U/L, 62 U/L, and 139 U/L, respectively. Her scleraes were anicteric. The abdomen was soft, flat, and without palpable organomegaly. There was no edema. Arterial blood gases showed metabolic acidosis with a pH of 7.28, PaCO2 of 30 mmHg, PaO2 of 80 mmHg, BE of −11 mmol/L, and HCO3 of 14 mmol/L. Blood chemistry and urine sediment showed signs of proximal tubular dysfunction (Fanconi’s syndrome) with hypophosphatemia, hypouricemia, metabolic acidosis, and renal glycosuria despite normal plasma glucose concentration.\nAfter consultation with personnel at Turkey’s National Poison Information Center, we started oral treatment with the chelating agent sodium-2,3-dimercapto-1-propanesulfonate (DMPS), which is related structurally to 2,3-dimercapto-1-propanol (dimercaprol, also known as British anti-Lewisite), using the following regimen: DMPS, 600 mg orally every 8 hours for 14 days. Hemodialysis was performed because of anuria and severe metabolic acidosis. Hemodialysis was conducted daily for the first 4 days and then three times weekly. Arterial blood gases returned to normal. Afterwards, the patient’s urine output progressively increased. Levels of LDH, ALT, and AST also returned to normal. The patient recovered clinically and was discharged after 15 days in hospital. Her serum creatinine and BUN levels upon discharge were 5.2 mg/dL and 20.0 mg/dL, respectively. Eight weeks after discharge, the patient’s renal function (serum creatinine and BUN) test results remained high. The patient is still on hemodialysis approximately 1 year later. | [[21.0, 'year']] | F | {'21781925': 1, '2199292': 1, '11043489': 1, '3053124': 1, '9630041': 1, '29636776': 1, '7566586': 1, '9581027': 1, '16034160': 1, '15947979': 1, '24232291': 2} | {} |
164,114 | 3825694-1 | 24,235,849 | noncomm/PMC003xxxxxx/PMC3825694.xml | MUCI positive cutaneous metastasis with transepidermal elimination from a breast carcinoma | In February 2010, a 48-year-old Argentine woman had undergone tumorectomy in her left breast with diagnosis of an invasive ductal carcinoma with low nuclear and histological differentiation grades; estrogen (ER) and progesterone (PR) receptors were negative and Her2/neu was positive. In September 2011, a mastectomy with immediate breast reconstruction was performed due to local tumor recurrence and the patient received systemic chemotherapy. In March 2012, she consulted because multiple skin nodules had appeared 3 months before. Lung, bone, and hepatic metastases were also detected.\nPhysical examination revealed an erythematous nodule that was 4 cm in diameter, polylobulated, and with ulcerated surface on the chest region. Multiple erythematous painful nodules from 5 mm to 2 cm were distributed on her chest and over the reconstructed breast ().\nA skin biopsy of one of the small lesions revealed skin metastasis from breast carcinoma (ER-PR-Her2/neu+). Histopathologically, tumor cell nests were seen in the dermis. By immunohistochemistry, MUCI expression was studied and a strong reaction was found with a mixed pattern at the plasma membrane and in the cytoplasm (). Some epidermal cells at the Malpighi stratum also showed cytoplasmic positive staining. Tumor cells in the papillary dermis appeared to penetrate through the epidermis, suggesting transepidermal elimination. The epidermis showed no signals of ulceration (), and in some malignant cells, a MUCI moderate reaction was found. | [[48.0, 'year']] | F | {'11547902': 1, '11391575': 1, '3662570': 1, '1892326': 1, '19625949': 1, '20190910': 1, '1592525': 1, '14620915': 1, '2431118': 1, '19922483': 1, '12754289': 1, '18311448': 1, '12630642': 1, '6365800': 1, '20804570': 1, '8682949': 1, '8335743': 1, '2045853': 1, '9301149': 1, '6190927': 1, '19615029': 1, '24235849': 2} | {} |
164,115 | 3825927-1 | 24,055,918 | noncomm/PMC003xxxxxx/PMC3825927.xml | An unusual presentation of EATL type 1: Emergency surgery due to life-threatening gastrointestinal bleeding | A 76-years-old male admitted to emergency service with sudden and severe gastrointestinal bleeding and hypovolemic shock. There were massive hematochezia and hematemesis. There is no history of celiac disease in his/family history. Systolic arterial blood pressure was 60 mmHg, diastolic was unmeasurable. The patient was monitored and resuscitation were started immediately. Crystalloids and erythrocyte suspensions were given intravenously. After the initial resuscitation hemodynamic stability was provided and then the patient transferred to Intensive Care Unit (ICU). The hemoglobin value increased from 4 mg/100 mL to 8 mg/100 mL. Emergency upper and lower gastrointestinal endoscopy revealed no lesion or active bleeding. There was blood clots in the colon and stomach. A short time later, second severe bleeding was observed in ICU. Despite the resuscitation and transfusions, the patient re-entered the hypovolemic shock. We decided to emergency laparatomy in doubt.\nIn exploration there was an adhesion between the transverse mesocolon and the jejunum just after the ligament of Trietz. We divided the adhesion. There was a perforated lesion that had been bleeding, on antimesenteric surface of jejunum (). Perforated area was attached to adjecent intestine so that there was no blood in peritoneal cavity. We resected the lesion with margins of a few centimeters of healthy jejunum in both sides. End-to-end anastomosis was performed.\nIn histopathological examination, macroscopically, there were traces of bleeding and almost complete necrosis. Microscopically, intestinal mucosa showed extensive ulceration and necrosis. Extensive necrosis made the diagnosis very hard. But the following findings led us to the diagnosis of EATL type 1. The muscularis propria had abundant atypical lymphoid infiltrate in diffuse pattern (a). Neoplastic lymphocytes were medium to large sized cells with irregular nuclear contours and hyperchromatic nuclei. Some large cells with vesicular nuclei had prominent nucleoli (c). The jejunal mucosa adjacent to the tumor showed effacement of normal villous architecture (villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis, pyloric metaplasia) (a and b). Immunohistochemically, atypical lymphoid cells positive for CD3 (b) and CD30 (d). They were immunonegative for CD56, CD4, CD8, CD20, ALK1. The background population was composed of reactive B and T lymphocytes. The intraepithelial lymphocytes in the adjacent mucosa were positive for CD3 and negative for CD4 and CD8.\nThe patient was discharged after surgical healing and referred to hematology clinic in eighth day postoperatively. The patient received combined chemotherapy regimen composed of bleomycin, doxorubicin, cyclophosphamide, vincristine, and prednisone. Since then he has been followed up by 18F-fluorodeoxyglucose positron emission tomography. The patient is alive in twenty-fourth month after diagnosis, there were no findings suggesting recurrence or metastasis. He continues to strict gluten-free diet. | [[76.0, 'year']] | M | {'26265987': 1, '9817252': 1, '21566094': 1, '20801285': 1, '8132301': 1, '17484883': 1, '15591504': 1, '17470479': 1, '21171509': 1, '8583077': 1, '10673521': 1, '34377617': 2, '18618372': 1, '15643667': 1, '20206108': 1, '21686880': 1, '8899409': 1, '10611170': 1, '34720538': 2, '15825131': 1, '3094712': 1, '29062389': 2, '24055918': 2} | {'8517785-1': 1, '8349507-1': 1, '5636209-1': 1} |
164,116 | 3825949-1 | 24,236,260 | noncomm/PMC003xxxxxx/PMC3825949.xml | Grisel Syndrome: Pathophysiological Evidence from Magnetic Resonance Imaging Findings | A 9-year-old male child was referred for evaluation of torticollis, and his recent medical history was significant for an episode of acute lymphadenitis on the neck 20 days ago, which was treated with intravenous antibiotics (ceftriaxone; Ceftriaxone, 2 g per day) and antiphlogistic therapy (diclofenac; Difexin, 45 mg per day) for 9 days. Otherwise, the parents reported no history of trauma or pre-existing health condition. He presented with torticollis of sudden onset 20 days after acute lymphadenitis of the neck.\nPhysical examination revealed limited cervical range of motion. His head was rotated to the right and tilted to the left. Nuchal spasm was present on the left side. No neurological impairment was observed.\nContrast CT of the neck was performed with side-to-side neck rotation, which revealed a significant rotary subluxation of C1 on C2 and an increased anterior atlantodental interval (), consistent with a Fielding type 2 rotatory subluxation. Contrast MRI of the neck revealed no neural involvement but demonstrated enhancement of the occipital condyle, C1 superior articular process, C1/C2 facet joint and atlantoaxial interval, indicating inflammation of those structures (, ). A Philadelphia neck brace was applied initially, and the patient was treated with halter traction for 14 days and antiphlogistic (morniflumate; Morniflu, 350 mg per day) therapy for 7 days. The torticollis resolved after three weeks, and the patient had complete return of cervical ranges of motion. Follow-up with dynamic CT and MRI scans taken 21 days from onset of the torticollis revealed complete resolution of the inflammation. He was discharged home with the Philadelphia neck brace and had no lasting limitation or deficits. | [[9.0, 'year']] | M | {'31258633': 1, '20390289': 1, '33922701': 1, '15978678': 1, '3688763': 1, '30656135': 1, '32904901': 2, '33274097': 2, '28758092': 2, '2645074': 1, '27340580': 2, '15487635': 1, '6707036': 1, '11791252': 1, '18143937': 1, '24236260': 2} | {'4909899-1': 1, '7676959-1': 1, '7676959-2': 1, '7462130-1': 1, '5532360-1': 1} |
164,117 | 3825950-1 | 24,236,261 | noncomm/PMC003xxxxxx/PMC3825950.xml | Anterior Cervical Osteophytes Causing Dysphagia and Paradoxical Vocal Cord Motion Leading to Dyspnea and Dysphonia | A 62-year-old male patient visited our hospital with dyspnea and mild dysphagia that began approximately 4 months prior to the visit as the main symptoms. Gentle exercise, such as steps, caused difficulty of inspiration 1 month ago, but it had become worse around the time of his visit, he appeared at rest and accompanied by dysphonia. Dysphagia emerged as foreign body sensation and intermittent aspiration during a solid meal, but he did not have history of weight loss or aspiration pneumonia. Various physicians, from a pulmonologist to an otorhinolaryngologist, failed to make an accurate diagnosis and the symptoms of the patient continued to progressively deteriorate.\nThe patient did not have any particular past internal or surgical medical history other than being a smoker for the last 20 years. The patient had clear consciousness without cognitive dysfunction at the time of his visit to our hospital. In physical examination, stridor was auscultated during inhalation. There was no abnormality of the tongue and no atrophy of the body muscles. The sensory tests displayed normal findings, and normal muscular strength was observed in all muscles of the upper and lower limbs on both sides in the manual muscular strength tests along with normal findings in the deep tendon reflex tests. Fibrillation was not observed in neurological examinations, and masticatory function and gag reflex were normal without observation of particular findings, such as dysarthria in linguistic assessments. Brain magnetic resonance imaging (MRI) for intracranial pathology did not show any abnormalities. There were no abnormal findings in the electrodiagnostic studies that were screened for neuromuscular diseases such as progressive bulbar paralysis. In addition, all the enzymes related to muscular diseases, such as creatine kinase, lactate dehydrogenase, and so on, were in the normal range of the laboratory test. Pulmonary function test was performed to find the cause of dyspnea, but normal pulmonary function was observed without abnormal findings, such as obstructive or restrictive pulmonary patterns. A VFSS showed that osteophytes were severely protruding at the anterior portion of the 5th to 7th cervical spine and translocated the lower pharynx and the upper esophagus anterosuperiorly. In the oral phase, there was no abnormality except for premature bolus loss. In the pharyngeal phase, although laryngeal elevation and epiglottic closures were normal and aspiration was not observed, a lowering of food took a circuitous route around the osteophytes and the pharyngeal transit time of the solid food was delayed by 1.4 seconds. X-ray and computerized tomography (CT) scan of the cervical vertebrae were performed to verify these anterior cervical osteophytes and revealed that the formation of large osteophytes was caused by overgrowth of cortical bones of the 5th to 7th cervical vertebrae. Osteophyte in the 5th cervical spine was the most prominent and protruded 8 mm outside of the vertebral body. C-spine MRI showed anterior herniation of the intervertebral disc accompanied with a ruptured anterior longitudinal ligament, with fluid collection in the retropharyngeal space. A T2-weighted image showed high signal intensity with irregular enhancement caused by retropharyngeal irritation and inflammatory changes due to the large cervical osteophytes (). Anatomical deformities or mass-like lesions on the oropharynx and laryngopharynx were not observed in the larynx endoscopic examination. However, the paradoxical vocal cord motion, adducted vocal cords during the time of inhalation, was observed.\nBecause we did not find any possible etiology of these symptoms other than the anterior cervical osteophytes and the patient displayed a tendency of gradually aggravating dyspnea with severe anxiety and sleep disturbances, we decided to perform surgical treatments. Surgery was conducted through the anterior approach method. Removal of the anterior osteophytes and 5th to 6th cervical herniated disc were performed and interbody fixation with a bone graft was executed.\nDysphagia disappeared immediately due to relief of mechanical pressure on the larynx, but dyspnea and paradoxical vocal cord motion still remained. Accordingly, for correcting the abnormal vocal cords motion, the patient performed the breathing exercises, such as relaxation technique and diaphragmatic breathing method. Finally, the respiratory difficulties and dysphonia were gradually improved after 3 months of continuous self-treatments. | [[62.0, 'year']] | M | {'21484285': 1, '7420148': 1, '31799480': 1, '22434681': 1, '18513179': 1, '1812251': 1, '7606974': 1, '33824560': 1, '27924209': 2, '28119739': 2, '19816305': 1, '28801330': 1, '9706891': 1, '15468371': 1, '24236261': 2} | {'5133240-1': 1, '5227134-1': 1} |
164,118 | 3825951-1 | 24,236,262 | noncomm/PMC003xxxxxx/PMC3825951.xml | Intractable Abdominal Pain in a Patient With Spinal Cord Injury: A Case Report | A 37-year-old male patient was admitted to the department of rehabilitation medicine at our hospital with a major complaint for severe abdominal pains. He was affected by flaccid paraplegia in July 2011 due to a SCI at the T10 level in a traffic accident which led to compression fracture of vertebral body T10 with dislocation. After a long hospitalization in the intensive care unit, he developed a stage IV sacral pressure ulcer (length 10 cm, width 10 cm, depth 5 cm) which was steadily worsened due to fecal incontinences despite the intensive dressings three times a day. Plastic surgeons, therefore, recommended a colostomy to provide a clean environment for healing the pressure ulcer. He also suffered from intermittent abdominal pain 1 month after the injury. The pain was mainly localized in the periumbilical area and did not appear in a radiating pattern. The initial pain scale was 60 mm on visual analog scale (VAS). Physical examination demonstrated no tenderness or distension to palpation of the abdomen. Peripheral blood tests showed elevated erythrocyte sedimentation rates with 69 mm/hr and C-reactive protein was elevated to 3.77 mg/dL. His past medical history included antibiotics therapy for acute cholecystitis a month ago. Computerized tomography (CT) on abdomen showed mild nonspecific gallbladder wall thickening (). Chronic cholecystitis was diagnosed and the patient was referred to the general surgery department for a colostomy and cholecystectomy. Laparoscopic cholecystectomy and sigmoid colon loop colostomy were performed on November 2011, but the abdominal pain around umbilicus persisted and became even more severe. The pain intensity scored 80 mm on VAS. The pain was not associated with food intakes or defecations. No other possible causes of visceral pain such as constipation, paralytic ileus or abdominal distension were identified. Laboratory findings on the peripheral blood tests were nonspecific and follow-up CT images of abdomen showed no abnormalities. The pain was not aggravated by positions, activities, movement and not associated with somatic tenderness, thus, we can rule out the possibility of musculoskeletal origin, such as mechanical instability, muscle spasm, overused syndromes. A magnetic resonance imaging scan of the thoracolumbar spine revealed no evidence for compression of the nerve root in the foramen by bone or disc that are correlated with the location of the pain. The nature of pain was either burning, pricking, electric shock-like, painful cold, tingling or an itching pain, which would fit the diagnostic criteria for neuropathic pain based on the Douleur Neuropathique 4 (DN4) questionnaire [] and had a correlation with the dermatomal pattern within the level of injury. Thus, we concluded the pain as neuropathic at 5 months after the injury and exercised a medication according to guidelines []. We administrated amitriptyline 10 mg twice a day, pregabalin 150 mg four times a day, and oxycodone 5 mg twice a day, after which the pain slightly subsided from 80 to 65 mm on VAS. However, he still suffered from insomnia and could not tolerate rehabilitation programs. He was then referred to the department of anesthesiology for intrathecal injections, with 12 mL of 0.4% lidocaine and 3 mL of 10 mg/mL triamcinolone. The pain level was reduced from 80 to 40 mm on VAS. The effect was not long-term and intrathecal lidocaine injection was scheduled more frequently, once a week for 3 consecutive weeks, keeping the oral medications. A repeated injection resulted in a remarkable decrease in pain level up to 30 mm on VAS for at least 2 months. | [[37.0, 'year']] | M | {'2241311': 1, '22457863': 1, '15851891': 1, '22430511': 1, '19002150': 1, '11094007': 1, '2389723': 1, '19909700': 1, '17621311': 1, '16116488': 1, '24236262': 2} | {} |
164,119 | 3825952-1 | 24,236,263 | noncomm/PMC003xxxxxx/PMC3825952.xml | Thoracic Infectious Spondylitis After Surgical Treatments of Herniated Lumbar Intervertebral Disc | A 32-year-old Mongolian male developed lower back pains after a traffic accident and was diagnosed to have traumatic L3-4 and L4-5 herniation of intervertebral disc via magnetic resonance imaging (MRI) at a Mongolian orthopedic clinic. The patient had no past medical history of high blood pressure, diabetes, tuberculosis or hepatitis, and he was not a smoker. After a week, he had an operation on total laminectomy and discectomy at L3-4, L4-5 levels and posterior interbody fusions at L3-5 (). The patient had a fever 3 weeks after the surgery, and also developed bilateral lower extremities and external anal sphincter muscle weakness.\nTo investigate the causes of fever and neurological deficits, a lumbosacral MRI follow-up was performed but no definite abnormalities were found. Seven weeks after surgery, the patient was transferred to the department of neurosurgery at our medical institution for further evaluations and treatments. When performed a whole spine MRI, the T2 and T3 vertebral body destruction and compressive myelopathy were detected (, ). Anterior and posterior epidural mass formations caused the compressive myelopathy at T2 to T4 levels. In addition, the epidural mass was extended to bilateral T3-T4 neural foramen, thus, forming the paravertebral mass.\nBased on the laboratory studies, white blood cell (WBC) count resulted to 7,020/µL, the erythrocyte sedimentation rate (ESR) is at 54 mm/hr, and the C-reactive protein (CRP) level reached 0.87 mg/dL. The reported values represented increases from the normal ranges.\nUpon physical examinations, voluntary anal contracture was not checked. Therefore, a manual muscle testing in accordance to the Medical Research Council (MRC) scale was performed to the bilateral hip flexors and knee extensor which resulted in the MRC grade II. Bilateral ankle dorsiflexors, big toe extensors, and plantar flexors were checked as MRC grade I. Sensory deficit was noted below bilateral T9 dermatome. In addition, there were also no perianal and deep anal sensations. Both the left knee and ankle jerks were brisk. Babinski sign was bilaterally checked while the ankle clonus was not.\nOpen bone biopsy of thoracic vertebrae, blood culture, and antigen detection assays were performed to determine microorganisms. The specimens were sent for bacterial culture, acid-fast bacilli smear and culture, fungal culture and polymerase chain reaction for Mycobacterium tuberculosis. The results of the tests were all negative. Microscopic histological examinations of thoracic vertebrae biopsy revealed chronic spondylitis. T2 and T3 vertebrae showed hypercellular bone marrow tissues with bone desorptions and high cellularity with focal infiltrations of chronic inflammatory cells including plasma cells in normal marrow. An open biopsy of the soft tissues at the lumbar operative site was also performed which showed foreign body reactions with granulation tissues and fat necrosis.\nFor the treatment of compressive myelopathy, the patient had a decompression laminectomy at T2-T3 level. The patient was also treated by antibiotics. Nafcillin was applied for 11 days followed by cefadroxil for 5 weeks. The patient was then transferred to a rehabilitation medicine department when his neurological and medical conditions were stabilized.\nThe laboratory tests showed improvements after surgery and antibiotics treatments. Results were 5,900/µL, 14 mm/hr, and 0.38mg/dL, for the WBC count, ESR, and CRP level, respectively.\nAfter decompressions of laminectomy and antibiotics treatment, the weaknesses of bilateral lower extremities were improved. Bilateral hip flexor, bilateral knee extensors, and right ankle dorsiflexor were checked for MRC grade IV. Left ankle dorsiflexor, bilateral big toe extensors, and bilateral ankle plantar flexors were checked as grade III. Moreover, the voluntary anal contraction was mildly checked, and the perianal skin sense and deep anal sense were recovered. After positive examinations, the patient was discharged from the hospital with no additional complications. | [[32.0, 'year']] | M | {'22033610': 1, '10415237': 1, '15570436': 1, '30509282': 1, '3875878': 1, '22307558': 1, '24236263': 2} | {} |
164,120 | 3825953-1 | 24,236,264 | noncomm/PMC003xxxxxx/PMC3825953.xml | Application of Percutaneous Cervical Nucleoplasty Using the Navigable Disc Decompression Device in Patient of Cervical Herniated Intervertebral Disc: A Case Report | A 38-year-old female came to complain of neck pain with radiating to the bilateral upper extremities after a traffic accident at April 26, 2009. The rate of her pain was at 7-8/10 by visual analog scale (VAS) and the pain was aggravated by bending backward and relieved only slightly by resting.\nA physical examination revealed a positive Spurling sign in the bilateral upper extremities. She had no sensory deficits but mild motor weaknesses in the right upper extremity. Deep tendon reflexes are normal and symmetrical. MRI images () demonstrated central disc extrusion at C4-C5, making contact with bilateral C5 nerve roots. The patient was diagnosed with a C4-C5 disc extrusion with bilateral C5 roots impingement. Percutaneous cervical nucleoplasty (PCN) with the navigable disc decompression device (L'DISQ) was performed at C4-C5 disc level with CT and fluoroscopic guidance on June 3, 2009. The procedure was performed using a standard midline approach () []. Procedure time required 3 hours. Her pain was reduced to 5/10 by VAS the first postoperative day. After leaving the hospital, she visited hospital again on June 9, 2009 and did not appeal any pains at that time. However, she admitted again due to aggravation of neck pains radiating to the right upper extremities from January 2010. The rate of her pain was at 6-7/10 by VAS. A physical examination revealed a positive Spurling sign in the right upper extremity. She has no motor deficits but only mild paresthesia on right C4 and C5 dermatomes. The patient was diagnosed with a C4-C5 disc extrusion with right C5 roots impingement. PCN using the L'DISQ was performed again at the same level on March 25, 2010 with fluoroscopic guidance (). Tip of the L-DISQ catheter reached the end of the bulging disc, and disc decompression was done successfully. Her pain was reduced to 5/10 and negative Spurling sign was observed the first postoperative day. After the procedure, posterior neck area axial pain was improved to 4/10 at 2 months and 2/10 by VAS at 6 months later without the pains radiating to the right upper extremity. | [[38.0, 'year']] | F | {'22882411': 1, '30761876': 1, '7760784': 1, '14609691': 1, '30653911': 1, '18830638': 1, '2910608': 1, '1485502': 1, '21332936': 1, '11034644': 1, '9137174': 1, '24236264': 2} | {} |
164,121 | 3825954-1 | 24,236,265 | noncomm/PMC003xxxxxx/PMC3825954.xml | Supplementary Motor Area Syndrome and Flexor Synergy of the Lower Extremities | In May 2008, a 60-year-old woman developed paraparesis and was diagnosed with falx meningioma (). On June 23, 2008, she underwent a tumor resection surgery and on July 1, 2008, she was transferred to the department of rehabilitation medicine for rehabilitation of paraparesis.\nOn July 1, 2008, neurologic examination showed grade I spasticity on the Modified Ashworth Scale (MAS) at hip, knee, and ankle joints; a hip flexor (right/left) power of fair grade/fair(-) grade, a hip extensor power of poor grade/trace grade, a knee extensor power of fair(-) grade/poor(+) grade, a knee flexor power of fair grade/fair(-) grade, an ankle dorsiflexor power of zero grade/zero grade, and an ankle plantar flexor power of zero grade/zero grade. On sensory function tests, she was bilaterally normal. Deep tendon reflexes of the knees and ankles were increased bilaterally and Babinski sign was positive bilaterally. Her lower extremity Fugl-Meyer score was 31/30. After receiving gait training for 2 weeks, she could walk with supervision. Although she did not drag her feet when walking, the motor power of her ankle dorsiflexor was still zero grade. On July 15, 2008, a gait analysis was performed and showed a normal pattern (). | [[60.0, 'year']] | F | {'29875717': 1, '11439375': 1, '11361322': 1, '14867993': 1, '11180211': 1, '10912196': 1, '28321186': 1, '12007269': 1, '29541539': 2, '18813154': 1, '1998884': 1, '11844264': 1, '19163477': 1, '24236265': 2} | {'3825954-2': 2, '5840439-1': 1, '5840439-2': 1} |
164,122 | 3825954-2 | 24,236,265 | noncomm/PMC003xxxxxx/PMC3825954.xml | Supplementary Motor Area Syndrome and Flexor Synergy of the Lower Extremities | In March 2008, a 48-year-old woman who developed left hemiparesis was diagnosed with a 2-cm-sized low grade glioma in the right superior frontal gyrus. She underwent tumor resection on June 24, 2008 () and was later transferred to the department of rehabilitation medicine.\nOn July 19, 2008, neurologic examination showed that the degree of spasticity was MAS grade I at hip, knee, and ankle joints. The power of her left upper extremities was fair grade, and her hip girdle, knee, and ankle powers were trace, zero, and zero grades, respectively. She was normal on sensory function tests. The deep tendon reflexes of her left knee and ankle were increased, and Babinski sign was positive.\nAfter receiving rehabilitation treatment for 2 weeks, her motor function was much improved. The power of her left upper extremity was good grade, her hip flexor power fair(+) grade, her extensor power poor grade, her knee flexor power fair(+) grade, her extensor power poor grade, her ankle dorsiflexor power trace grade, her plantar flexor power poor grade, and her lower extremity Fugl-Meyer score 17. Her gait function was much improved, and she was able to walk independently. Though her ankle dorsiflexor was still trace grade, she did not show foot-dragging during the swing phase. On August 2, 2008, a gait analysis was performed, which showed a decreased range of motion at ankle plantarflexion and dorsiflexion. But ankle dorsiflexion was sufficient not to show foot-dragging. Other findings were not significant (). | [[48.0, 'year']] | F | {'29875717': 1, '11439375': 1, '11361322': 1, '14867993': 1, '11180211': 1, '10912196': 1, '28321186': 1, '12007269': 1, '29541539': 2, '18813154': 1, '1998884': 1, '11844264': 1, '19163477': 1, '24236265': 2} | {'3825954-1': 2, '5840439-1': 1, '5840439-2': 1} |
164,123 | 3825955-1 | 24,236,266 | noncomm/PMC003xxxxxx/PMC3825955.xml | Multiple Cranial Neuropathies Without Limb Involvements: Guillain-Barre Syndrome Variant? | A 48-year-old male patient was admitted for bilateral facial palsy, ptosis, diplopia, dysarthria, and dysphagia without limb weaknesses. His prodromal symptoms included watery diarrhea, fever, and myalgia for seven days. He had no remarkably neurological, medical, or family history and had worked in a piano making factory for 20 years. Following the acute treatment at the department of neurology, he was transferred to the department of physical and rehabilitation medicine. Specific CN tests were performed at the time of admission and periodically after his admission.\nRegarding initial neurological symptoms, the patient reported an unpleasant sensation of the tongue with bilateral ptosis. At the same time, his speech became slurred and he experienced difficulty in swallowing and limitations of tongue movements with respect to lateralization and protrusion. He reported loosing bitter and sour taste sensations and was indicated as negative for gag reflex. At the time of admission, his eyes were in an internal strabismus state with complaints of diplopia in vertical gaze (). In addition, he had bilateral symmetrical facial palsy, marked impairments of mastication and deglutition, and together with aphonia and palatal palsy (which both continued until discharge), and weakened hearing. Sternocleidomastoid (SCM) and trapezius muscle strengths were compromised, but his gait was normal and tendon reflexes were well preserved ().\nComprehensively, he showed bilateral CN III, IV, V, VI, VII, VIII, IX, X, XI, and XII involvements, but no cerebellar signs, including ataxia, or other evidences were suggestive of autonomic or sphincter dysfunctions. He was alert without cognitive impairments. Manual muscle test grades of his upper and lower extremities were all normal. He showed no spasticity with respect to elbow, knee, or ankle joints (Modified Ashworth Scale grade zero). Sensation in limbs was intact.\nBrain magnetic resonance images obtained at admission were normal. Nerve conduction studies (NCS), including motor, sensory, and F-wave examination, were performed on all limbs, and needle electromyography, repetitive nerve stimulation (RNS), and blink reflex testing were performed on hospital days of 3, 17, and 59. NCS and RNS findings were normal for all limbs. However, blink reflexes and facial nerve conduction velocity (NCV) were not evoked bilaterally, and at his last facial NCV study conducted 6 weeks after presentation, his left side findings had improved to normal and right side findings remained abnormal. Needle electromyography studies showed acute denervation (positive with fibrillation in the resting state, reduced recruitment, and polyphasic motor unit potentials during the volition state) of bilateral facial (frontalis, orbicularis oculi, orbicularis oris, nasalis) and laryngeal muscles (cricothyroid, thyroarytenoid), masseter, hyoglossus, and SCM muscles. Six weeks after onset, the motor evoked potentials (MEP), brainstem auditory evoked potentials (BAEP), somatosensory evoked potentials (SEP), and NCV and EMG follow-up studies were performed, and the NCV were normal and needle EMG findings remained abnormal. Transcranial magnetic stimulation (TMS) evoked MEPs recorded from the first dorsal interosseous and tibialis anterior muscles using surface gel electrode were normal. For this TMS study, the active electrode was placed over muscle bellies, while the reference electrode was placed over the distal interphalangeal joint of the index finger or the medial malleolus in upper and lower extremities. The motor cortex area was stimulated. BAEP study was performed by using a click sound for stimulation at 90 dB. Interpeak latencies and amplitudes were recorded. Results revealed shallow waves on right sides. SEP studies using the trigeminal nerve stimulation revealed delayed latencies on both sides, and SEP studies using the median nerve stimulation showed normal values with no statistical difference on both sides.\nCSF analysis performed at admission showed elevated IgG (12.04 mg/dL) but a normal albumin level. Serum anti-ganglioside Ab analysis revealed positivity for anti-GQ1b IgG Ab (140 titer units) and negativity for anti-GM1 Ab. All other laboratory findings were normal.\nThree days after the onset, intravenous immunoglobulin (IVIg) was started at 2 g/kg for five consecutive days. During the 11 weeks of inpatient period, many cranial neuropathies recovered slowly. In particular, his hearing difficulty and SCM weaknesses were completely normalized, but on the other hand, the mild diplopia, dysphonia, and dysphagia persisted at discharge. Videofluoroscopic studies were performed at 4 and 9 weeks after presentation and showed liquid aspiration during swallowing at 4 weeks but no aspiration or penetration at 9 weeks (functional dysphagia scale 71 → 53). Despite the mild improvements being observed, an extended transit time of oral phase due to a tongue propelling weakness, and the pharyngeal phase due to reduced pharyngeal peristalsis, the cricopharyngeal function remained ().\nA dysarthria test performed in a speech therapy room at 5 weeks after presentation showed poor tongue movements in all directions (protrusion, retraction, lateralization, and elevation), and these persisted at discharge. Voice and speech patterns were low-pitched with short phrase phonations and hypernasal resonances. | [[48.0, 'year']] | M | {'28217155': 2, '21698648': 1, '17657801': 1, '21336874': 1, '28223738': 2, '30186502': 1, '15372537': 1, '19324375': 1, '9037391': 1, '25712542': 1, '11150289': 1, '32023583': 1, '2946281': 1, '1318358': 1, '24236266': 2} | {'5296210-1': 1, '5314846-1': 1} |
164,124 | 3825956-1 | 24,236,267 | noncomm/PMC003xxxxxx/PMC3825956.xml | Syringomyelia Coexisting With Guillain-Barre Syndrome | A 67-year-old man was hospitalized in our department on August 27, 2010, due to a sudden onset of weakness and numbness of his feet and fingertips. He had no medical history for diabetes mellitus, hypertension, immunization, and other special syndromes except for upper respiratory infection (URI) about 1 week ago. Moreover, he had not experienced any difficulties when performing daily activities, such as walking, self-caring, and house chores. Due to the lack of severity for his URI symptoms which consisted of rhinorrhea, cough, and myalgia, his medications were not consumed. On physical examination, the patient's vital signs were normal. A neurological examination revealed quadriplegia showing fair grade on manual muscle test (MMT) for all limbs, and superficial and deep sensory disturbances for all limbs with absent DTRs. His weakness and numbness were not exactly matched with the dermatome of the limbs. Upper motor neuron signs were not detected in all limbs. In addition, there were no abnormal intracranial findings on his brain computed tomography scans.\nAfter two weeks from his initial presentation, the patient experienced progressive muscle weaknesses, which corresponded to poor grade at upper extremities and grade traces at both lower extremities on MMT. The electrophysiological studies were carried out. The sensory nerve conduction study (NCS) showed relatively normative findings. However, the motor NCS showed decreased amplitude and a partial motor conduction block at the right median nerves and at both the common peroneal and posterior tibial nerves. The motor NCS also showed a prolonged F wave and an absent H-reflex. The needle electromyography showed decreased recruitment and active denervations at the upper and the lower distal muscles. These electrophysiological findings were suggestive of demyelinating polyneuropathy.\nTo make confirmative diagnosis, a cerebrospinal fluid (CSF) study-via a lumbar spinal puncture-was also performed. The CSF findings showed albuminocytological dissociation. The cumulative findings consisted of the patient's history of preceding infection, neurological examination, electrophysiological studies, and the CSF analysis which met the diagnostic criteria for GBS. The patient also experienced urinary dysfunctions during the initiation of voiding phase in addition to the loss of sensation on bladder fullness. Therefore, he required clean intermittent catheterization. The serum prostate specific antigen level showed mild elevations and a transrectal ultrasonography (TRUS) of the prostate was consistent with benign prostate hyperplasia. Urodynamic studies (UDS) showed an abnormal bladder voiding phase indicated by bladder areflexia. Since he didn't have a history of regular medical consumptions except for immunoglobulin of GBS, thus, medications are less likely to be culprits for his urinary symptoms. The urinary dysfunction in GBS has rarely been reported but there exists few cases of GBS coexisting with bladder areflexia. Therefore, we initially assumed that his bladder areflexia was related to GBS. The motor power of all limbs had slightly improved after a course of intravenous immunoglobulin (IVIG) injection for five days (at a dose of 235 mg per day), but the patient was unable to walk independently. On September 28, 2010, he was transferred to a local rehabilitation facility.\nOne month later, the patient appeared again at our department. This time, he was found to have new myelopathic signs through examinations that were evidenced by both hypotonic upper extremities showing fair grade on MMT, urinary dysfunction, and spastic lower extremities of both knee flexors with Modified Ashworth Scale grade 2 at follow-up examinations. Although there were no differences in weakness of upper and lower extremities as compared to previous outcomes, we recommended that the patient be admitted to identify other potential causes. He had been kept for conservative treatments at a local rehabilitation facility for 3 months subsequently while his myelopathic signs had continued.\nHe was hospitalized again in our department on February 11, 2011. He still incurred stiffness in the lower extremities and showed different patterns of urinary dysfunctions which included frequency and urgency with retaining of a large amount of postvoid residual urine. There was bilateral sensory loss of pain and temperature over the dermatomes C5 to T1 with weaknesses of bilateral upper extremities that corresponded to poor on MMT, whereas the deep and superficial perianal sensations were preserved. On neurological examination, he had increased biceps tendon and patellar reflexes. The brain magnetic resonance imaging (MRI) showed no abnormal findings, whereas the MRI scans of the cervical spine revealed a syrinx cavity. This is evident by the hypointense signals in T1-weighted section and the hyperintense signals in T2-weighted section extending between the 5th cervical and the 1st thoracic vertebral segment of the cord (). In addition, mild disc bulging with spinal stenosis at L45/S1 was also found on the whole-spine MRI. The electrophysiological studies showed improvements when compared to the previous study, but still had slow nerve conduction velocities and partial motor conduction blockades. An additional neurological workups consisting of bulbocavernosus (S2-4) reflexes (BCRs), somatosensory evoked potential (SEP) and motor evoked potential were performed. The BCRs were intact while the median nerve SEP showed a sensory pathway defect between both the brachial plexus and the brain stem. These results corresponded to the syrinx extending between the 5th cervical and the 1st thoracic vertebral segments in the cord. To reveal the cause of the urinary dysfunction, voiding cystourethrogram (VCUG), TRUS and UDS were performed. There were no abnormal findings in urine analysis with culture, VCUG and TRUS. The UDS findings were consistent with overactive bladder, but the detrusor external sphincter dyssynergia could not be confidently ruled out. Therefore, based on the imaging studies, the neurological examinations and the findings indicated areflexic bladder, and the patient was diagnosed with syringomyelia.\nIt is hard to know the exact timing of the onset of syringomyelia. By the time he was diagnosed with GBS, he had no suspicious symptoms of syringomyelia. However, we suggested that GBS and syringomyelia coexisted given his history, neurological examination, and imaging studies. As a result, he received steroid therapy. After one month of medical treatment with inpatient rehabilitation, his weakness in all limbs had slightly been getting better and thus, needed minimal assistance with mobility. Yet, his urinary symptoms failed to improve significantly. Currently, the patient has been discharged home and has visited our outdoor patient department periodically. The last date of the follow-up visit was May 25, 2012. There have been no noticeable improvements of overall physical functions but noticeable improvements in his urinary symptoms allowed him to urinate independently. | [[67.0, 'year']] | M | {'20396937': 1, '2194422': 1, '18710806': 1, '30262531': 1, '16676925': 1, '22285113': 1, '16676930': 1, '22794351': 1, '19533016': 1, '15473652': 1, '24236267': 2} | {} |
164,125 | 3825957-1 | 24,236,268 | noncomm/PMC003xxxxxx/PMC3825957.xml | Recurrent Cerebral Infarction Caused by Mobile Aortic Arch Thrombus Refractory to Warfarin Therapy | A 61-year-old male was presented with sudden onset of left upper and lower extremities weakness and aphasia on July 8, 2010. He has a medical history of hypertension and diabetes mellitus and had been taking medication and insulin therapy for three years. Brain MRI revealed newly developed cerebral infarction by occlusion of the right middle cerebral artery (MCA). Chest radiography, echocardiography, and transthoracic echocardiography did not show any abnormalities. Laboratory test for hypercoagulability and lipid profile at admission was normal: low-density lipoprotein 116 mg/dL (reference, 0 to 130 mg/dL), total cholesterol 197 mg/dL (reference, 0 to 200 mg/dL), and homocysteine 7.45 µmol/L (reference, 5.08 to 15.39 µmol/L). However, TEE demonstrated echogenic finger-like thrombi with rocking motion (9.6 and 8 mm) on the top of the aortic arch (just proximal to the subclavian artery) with minimal atherosclerotic wall. Chest CT showed multiple ulcerations with intramural hematoma ().\nWe diagnosed embolic cerebral infarction originating from the aortic arch thrombi. The patient was initially treated with intravenous unfractionated heparin for 5 days. Because the location of the aortic arch thrombus did not allow surgical treatment, the patient was treated with 5 mg warfarin, initially, with an internationalized ratio (INR) between 2 and 3. Three days after onset, a rehabilitation program began at the bedside. Training for passive range of motion exercise, rolling and sitting was conducted at bedside. After transferring to the ward, gait training, strengthening exercises of left side muscles and balance training were performed. At the first discharge, 35 days from onset, he had fair grade of weakness in the left proximal upper and lower extremities and poor+grade in the left distal upper and lower extremities, according to the manual muscle test and grade II spasticity by Modified Ashworth Scale (MAS) in the left upper and lower extremities. He was able to walk indoors independently using a straight cane and plastic ankle-foot orthosis (AFO). The Korean-Modified Barthel Index (K-MBI) was 90 points and the Korean-National Institutes of Health Stroke Scale (K-NIHSS) was 5 points. The prescribed warfarin of 4 mg and INR was 2.5.\nOn November 8, 2010, the patient was admitted again with progressive weakness of the left extremities and dysarthria. He showed poor grade in the left proximal upper extremities and distal lower extremities. He was not able to walk or sit up by himself. Brain MRI revealed new developed anterior cerebral arterial infarction, and MR angiography conveyed obstruction of distal anterior cerebral artery (). He was treated with increased doses of warfarin by up to 5 mg and comprehensive rehabilitation was initiated. At the second discharge, onset after 25 days, it was examined that the left proximal and distal upper extremities were fair grade, the muscles of the left hip and knee were poor+, ankle was poor, and left extremities had spasticity with grade II by MAS. He was able to walk using a straight cane and plastic AFO under minimal assistance. K-MBI was 68 points and K-NISS was 7 points. He was hospitalized again on April 15, 2011 due to weaknesses in the left extremities and dysarthria, while maintaining 5 mg of warfarin with INR at 2. Left upper and proximal lower extremities were poor grade, and ankle dorsiflexor was trace grade. Brain MRI disclosed the recurrence of cerebral infarction of the right MCA territory. He was unable to walk and showed depression symptoms due to stroke recurrence. He and his wife wanted to be discharged after an acute phase treatment, 10 days after onset, and maintain 3 mg of warfarin (INR 3.14) medication at the outpatient clinic. At the third discharge, it was examined that the muscle strength of his left upper and lower extremities was poor grade; he was able to walk 30 m indoor using a quadricane and AFO under moderate assistance. K-MBI was 60 point. On January 2, 2012, he was unfortunately re-admitted to the stroke unit again with progressive weakness of left extremities and aphasia. He was again diagnosed with right MCA infarction. Brain MR angiography revealed occlusion in the M1 area of the right MCA territory. TEE showed one hypermobile aortic arch thrombus of approximately 3 mm in size at the top of the aortic arch, which was more decreased compared with the last study (2 mobile thrombus, 9.6 and 8 mm). He was treated with anticoagulation and comprehensive rehabilitation again. Also, he was prescribed 4 mg of warfarin (INR 2.61) and 100 mg of aspirin for additional thrombus control, along with 40 mg of atorvastatin. At the fourth discharge after rehabilitation therapy, 30 days after onset, the strength of muscles in the upper left extremity were trace grade, the muscles of hip were poor, knees were trace, ankles were trace, and the spasticity in the left upper and lower extremities was grade III by MAS. He needed at least minimal assistance for daily activities, including sitting up and standing up. He was able to walk 10 m with the help of a quadricane and AFO under a moderate degree of assistance. K-MBI was 47 points and K-NIHSS was 8 points. | [[61.0, 'year']] | M | {'2389701': 1, '7305488': 1, '3773130': 1, '3191002': 1, '8606279': 1, '20661342': 1, '21145267': 1, '15337213': 1, '7969297': 1, '9236447': 1, '24236268': 2} | {} |
164,126 | 3825992-1 | 24,236,247 | noncomm/PMC003xxxxxx/PMC3825992.xml | Segmental osteotomy for mobilization of dental implant | The patient, a 38-year-old female, visited the Oral Implantology Unit in conjunction with the Oral Rehabilitation Unit of the Universidad de La Frontera for problems she had detected in the installation of a singular fixed prosthesis in implants that had previously been installed by other professionals.\nThe clinical examination revealed a mesomorphic patient, facially proportionate, with no prior alterations or surgeries at the facial level. A slight vertical excess of the maxilla (approximately 3 mm) was observed, coinciding with a high smile level and greater tooth exposure with the lips at rest.\nThe intraoral examination showed partial edentulism, alterations in occlusal balance, diastemas with poor tooth positions, and the position of two implants in 11 and 21 (3.75 mm×13 mm) with their respective healing abutments. Both implants were found with the emergence in a more anterior position than appropriate, but implant 11 was found with high (3 mm over the ideal) and anterior emergence, suggesting an angulation greater than 30° (). The radiographic study revealed stability of the implants with no signs of peri-implantitis or alterations in the osseointegration ().\nAfter studying some treatment options, it was determined that a segmental osteotomy of implant 11 should be performed for inferior and posterior repositioning, placing it closer to the position and angulation of implant 21. In the study model, the model surgery was conducted that would make it possible to define the inferior repositioning as having to be at least 3 mm and the anterior displacement in the upper sector as having to be 2 mm using the middle area of the implant as the rotation axis that allowed the cervical sector to perform a 2 mm movement posteriorly ().\nThe procedure was performed under local anesthesia with 8 mL of lidocaine with 2% epinephrine, 1:100.000, in the vestibular and palatal sector.\nA 2-mm linear incision was made on the mucogingival border 3 cm long (), a total subperiosteal detachment of the vestibular region was performed, and the implant area was completely exposed from the cervical to the lower edge of the piriform aperture.\nAfter identifying the entire extension of the implant, the horizontal osteotomy was conducted 5 mm above the edge of the implant and vertical osteotomies in the medial and lateral sectors with a 5-mm safety margin (). The osteotomies went from the vestibular cortical to the palatal cortical layer. For this, a 701 drill mounted on a low-speed (20,000 rpm) handpiece was used. The osteotomy was completed with a straight chisel and the block was mobilized, keeping it adhered to the palatal periosteum to ensure the blood supply of the mobilized block.\nLater, a bone block of the mandibular ramus was obtained (), extracted using a conventional technique [] that allowed the insertion of this block into the upper sector of the mobilized block to stabilize the sector, permitting stabilization of the planned 3-mm descent. The remaining autogenous bone was crushed and served to fill the spaces from the osteotomy and defects caused by the procedure (). Given the overall stability of the block, another type of fixation system was unnecessary. The suture was made on a plane with simple 3-0 Vycril stitches. The emergence of the implant that would allow prosthetic rehabilitation was confirmed intraoperatively ().\nAfter 4 months of follow-up, new radiographs were taken, identifying the total repair of the bone tissue and the stability of the installed implant. No complications associated with the procedure were observed. The conventional rehabilitation techniques for implants were then used, with tailor-made casting abutments with a chromium-cobalt machined base, and the angulation and desired form of the abutment were attained to make cemented metal ceramic crowns (); Ketac Cem permanent glass ionomer cement was used for this (3M ESPE Dental Product, St. Paul, MN, USA). | [[38.0, 'year']] | F | {'26023650': 1, '17166700': 1, '15839587': 1, '16161748': 1, '9796158': 1, '16465977': 1, '31983851': 2, '22976653': 1, '15635945': 1, '17227383': 1, '11168254': 1, '12747459': 1, '15635946': 1, '16818018': 1, '7490653': 1, '11168255': 1, '11564115': 1, '24236247': 2} | {'6961453-1': 1} |
164,127 | 3826008-1 | 24,250,209 | noncomm/PMC003xxxxxx/PMC3826008.xml | Paroxetine in the treatment of recurrent brief depressive disorder | Our patient was a 48-year-old lady who was a local politician and who was carrying out her duties satisfactorily for the past several years. About a year and a half prior to her presenting to us, she developed symptoms characterized by low mood, anhedonia, easy fatigability, decreased concentration, hopelessness, and decreased sleep and appetite. These symptoms developed following a minor stressor at work and were clearly disproportionate to the stress. The symptoms had developed abruptly and the patient had never experienced such symptoms earlier. She had been an emotionally strong and confident lady earlier and was herself surprised at her current condition. She also developed prominent suicidal ideations and tried to kill herself by setting herself on fire, but was incidentally found and rescued by her maid. These symptoms continued for 4-5 days and were spontaneously remitted. Similar episodes occurred on almost a monthly basis for the next 18 months, each lasting 3-5 days. The interval varied between 15 and 40 days. They were unrelated to her menstrual cycles. There was no history of mania or psychosis. In the inter-episodic period, the patient was fully functional and carried out all her duties satisfactorily. Initially, the patient did not realize that it was a psychiatric illness, but after several such episodes, she consulted a private psychiatrist who started her on escitalopram (10 mg). It was continued for 4 months with no improvement. She changed psychiatrists and was tried on mirtazapine (15 mg) irregularly for 3 months without improvement. She did not follow-up with one psychiatrist and therefore full doses were not tried. She eventually presented to us during an episode and was off all psychotropics at that time. We made a diagnosis of RBDD as per ICD 10 and started her on paroxetine (10 mg). She scored 24 on Hamilton depression rating scale[] at the time of presentation. Although her symptoms resolved in about 4 days time, the dose was gradually increased to 25 mg/day, but, in the following month, she again had an episode lasting for about 4 days. She scored 20 on Hamilton depression rating scale this time and had somewhat less frequent suicidal ideation. Paroxetine dose was further increased to 50 mg. About 25 days later, the patient again developed depressive symptoms in the form of mild fatigue and some decrease in self-confidence, which lasted for 3-5 days. She now scored only 7 on Hamilton depression rating scale during the episode. There were no ideas of hopelessness, helplessness, worthlessness, or suicidal ideation. However, the lack of confidence still prevented her from carrying out her duties in those 3-5 days, although otherwise she was symptomatically much better. However, with one session of supportive counseling, she managed to get back to work as well. In the subsequent month, although she complained of mild fatigue, there were no other symptoms and she started doing her duties satisfactorily. The patient was continued on the same dose and is on regular follow-up. Thereafter, for the subsequent 9 months, she maintained the full symptomatic improvement. | [[48.0, 'year']] | F | {'7888413': 1, '14399272': 1, '16194772': 1, '9807652': 1, '9546002': 1, '9988366': 1, '18651345': 1, '17293713': 1, '24250209': 2} | {} |
164,128 | 3826009-1 | 24,250,210 | noncomm/PMC003xxxxxx/PMC3826009.xml | Phenytoin induced Stevens-Johnson syndrome exacerbated by cefepime | A 28-year-old female patient with a medical history of left sided pleural effusion was started on anti-tubercular treatment (ATT) [Tablet (tab.) isoniazid, rifampicin, pyrazinamide and ethambutol] at a local hospital for 1 month. Although the patient was non-complaint to therapy, she developed ATT induced hepatitis with aspartate aminotransferase-136 IU/L, and alanine transaminase - 331 IU/L. Following this, ATT was promptly withdrawn. Patient had one episode of generalized tonic clonic seizures (GTCS) 1½ months after the stoppage of ATT medication. She was given a loading dose of phenytoin and was brought to a tertiary care hospital in southern India for further management.\nOn day 1, during the presentation in emergency room, patient developed an episode of seizures and was treated with Tab. phenytoin 300 mg at night. On day 2, patient developed one more episode of GTCS, Tab. Phenytoin 300 mg was continued and pleural effusion was managed with inj. amikacin 500 mg and ethambutol 800 mg. On day 3, patient had a mild fever (39.5°C), itching, and erythematous rash all over her body. Her fever was managed with tab. paracetamol 50 mg, in addition to tab. hydroxyzine 25 mg, calamine lotion and tab. embramine 25 mg for the management of erythematous rashes. Tab. phenytoin was stopped due to rash and tab. levetiracetam 500 mg bid was started.\nOn day 4, patient developed oral ulcers and generalized skin rash that was suspected to be SJS. Tab. paracetamol was stopped and inj. pheniramine maleate 25 mg, inj. hydrocortisone 100 mg were started and oral ulcer was managed with the candid mouth paint and choline salicylate. On day 6, patient's condition remained unchanged. Inj. hydrocortisone 100 mg was replaced with tab. methylprednisolone 6 mg and tab. levetiracetam and tab. embramine 5 mg were also discontinued.\nFrom day 7 to day 19, there were no fresh complaints and rash was improving. Same medications were continued. On day 16 Inj. cefepime 1 g infusion was started for managing urinary tract infection (UTI) caused by multi drug resistance (MDR) Klebsiella/Escherichia coli. On day 20, patient presented with extensive skin peeling all over her body followed by pigmentation and scaling of skin managed with same medicines and was transferred to intensive care unit. Inj. tigecycline 50 mg bid was given for managing MDR Acinetobacter and tab. prednisolone was replaced with inj. methylprednisolone 40 mg.\nOn day 21, inj. cefepime 1 g infusion was stopped. Skin lesions worsened, considering her condition physician planned for tapering of steroids. Possibility of involvement of collagen vascular disease was high hence advised for skin biopsy and antinuclear antibody. On day 22, the patient's condition was unimproved and managed with saline compressor, silver sulphadiazine cream and paraffin gauze dressing. On days 23 and 24, skin lesions persisted and the patient complained of burning sensation over the lesions, chills and rigors, and redness of skin-reduced.\nOn day 25, inj. methylprednisolone 40 mg was changed to 40 mg tablet. Skin lesions and peeling along with desquamation of the skin was present, redness was decreased and lesions on the trunk were dried. On day 28, inj. tigecycline was stopped and inj. polymyxinE 1 million units was started for the treatment of MDR Acinetobacter and MDR Klebsiella. Patient had one episode of fever, skin lesions and peeling were present, redness and new skin eruptions were observed. On day 29, tab. methylprednisolone dose was decreased from 40 mg to 32 mg. Skin lesions showed signs of healing, and no new skin eruptions were observed.\nOn day 30, skin biopsy revealed interface dermatitis with pityriasis versicolor. On day 31, tab. methylprednisolone dose was decreased to 24 mg and to 20 mg on day 34. Patient complained of itching over the face. Facial edema, generalized hyperpigmentation and desquamation were observed. On day 35, Inj. amikacin and tab. ethambutol were stopped, as there was no conclusive evidence of tuberculosis. On day 40, skin peeling was reduced and methylprednisolone dose was decreased to 12 mg. On day 43, polymyxinE was stopped and all other medications were continued. On days 44 and 45, lesions were healed and the dose of methylprednisolone was decreased to 8 mg and to 4 mg on 46th day.\nOn day 48, patient had recurrent UTI and urine culture showed Pseudomonas which was sensitive to cefepime. On day 49, patient was given a test dose of cefepime and was observed for any signs of SJS. When no adverse reactions were observed, a full dose of cefepime 1 g was administered. 2 h later, she developed burning sensation on both upper limb and epigastrium. Patient complained of fever, vomiting (5-6 episodes), generalized weakness, chills and rigors. She was therefore administered inj. pheniramine 1 amp i.v. On day 50, inj. cefepime was stopped. Patient had burning sensation and fever. On day 51, no fresh complaints were observed and patient was better. Hence, she was planned for discharge. | [[28.0, 'year']] | F | {'20525360': 2, '21991171': 1, '18794645': 1, '17620821': 1, '8566720': 1, '18583791': 1, '21572786': 1, '10392983': 1, '16394456': 1, '20729944': 1, '25709351': 1, '12816151': 1, '24250210': 2} | {'2894848-1': 1} |
164,129 | 3826010-1 | 24,250,211 | noncomm/PMC003xxxxxx/PMC3826010.xml | Elevation of blood ciclosporin levels by voriconazole leading to leukoencephalopathy | One 18-year-old 46-kg female patient was admitted on the 70th day postoperative with complaints of dizziness, headaches, and blurred vision for 2 days. Her consciousness was distinct without nausea, vomiting, cough, expectoration, urinary, or fecal incontinence on admission. Her vital signs suggested normal body temperature and normal blood pressure with heart rate (HR) of 98 bpm. Examination of ocular fundus was normal. She did not have pre-existing neurological disorders and had not received significant amounts of psychotropic drugs before. Her medication history revealed that she was receiving “CsA (100 mg, q12h, po)-mycophenolate (1g, q12h, po)-methylprednisolone (8 mg, q12h, po)” antirejection therapy, because she had received allogeneic HSCT for myelodysplastic syndromes (MDS) 70 days before. The patient suffered from coughing accompanying expectoration 14 days ago, and the chest computed tomography (CT) showed pulmonary infections in the superior lobe of right lung. Cefaclor sustained release table had been administrated for one week, however symptoms did not improve. Fungus infection was suspected. Tablet voriconazole (400 mg, q12h, po) on the first day, followed by 200 mg every 12 h orally was added for the prophylaxis of IFI one week later. During this period, other medications, including herbal remedies and vitamins, had not been used; her liver function and renal function tests during the past 2 months were normal. After admission carbamazepine, rotundine, and citicoline sodium were administrated immediately for symptomatic treatment and supportive management; however, her condition continued to deteriorate in the next 2 hours, she dropped into locked jaw and convulsion of limbs, presented with epileptiform seizures, which was gradually improved by 10 mg diazepam (once) and 7 days of phenobarbital (0.1 g, bid, im) afterwards.\nA standard fluorescence polarization immunoassay (FPIA) was used to detect the trough blood concentration of CsA before the next administration. Historical trough whole blood concentration of CsA (reference range 150-300 ng/ml) was collected within the past month (average 230 ng/ml) before the combination with voriconazole. On the second day of admission, the blood concentration of CsA was 378 ng/ml. On the same day other examinations such as blood counts, cerebrospinal fluid, and serum chemistries are shown in . Blood smear showed plenty of leukocytes which were well distributed, and the immunochemical assay for cytomegalovirus (CMV) showed negative result on the third day of admission, the chest CT showed inflammation in anterior segment of superior lobe and median lobe in the right lung on the same day. Magnetic resonance imaging (MRI) of head showed leukoencephalopathy in bilateral occipital and left frontal lobe on the 4th day of admission.\nAccording to the clinical symptoms, laboratory examinations, and imaging examinations, the interaction between CsA and voriconazole was suspected. The concentration of CsA had risen slowly to 378 ng/ml during the past 7 days of co-administration with voriconazole. So voriconazole was suspended, and alprostadil, clopidogrel, and atorvastatin were administered from the second day of hospital stay to improve microcirculation and decrease hyperlipemia. From the third day of hospital stay, cefoperazone sodium and sulbactam sodium for injection were added to control the inflammation in the right lung. Her condition improved gradually. Because of the phenobarbital's induction of enzymes, the blood concentration of CsA dropped to 57 ng/ml on the 8th day of hospital stay; therefore, phenobarbital was suspended after 7 days’ medication under the circumstances of improved neurologic signs. On the 9th day of admission, the CT in chest showed amelioration in superior lobe of right lung comparing to anterior results besides miliary tuberosity in bilateral lungs, probable fungus infection, and the 1-3-β-D polyglucosan elevated to 89.57 pg/ml on the 10th day of admission. Voriconazole treatment was administered again to control fungus infection in bilateral lungs. To prevent drug toxicity, the dose of CsA was adjusted to 3/4 compared to the initial dose. Satisfactory steady-state blood concentration of CsA was achieved (250 ng/ml around). She was discharged 12 days later. The trough concentration of CsA and the important co-administered drugs (including enzyme inhibitors or enzyme inductors) during different time periods are shown in\n. | [[18.0, 'year']] | F | {'18492124': 1, '23084335': 1, '20633034': 1, '8879634': 1, '20497762': 1, '18023106': 1, '10202600': 1, '20653361': 1, '23061764': 1, '34335446': 1, '6385799': 1, '20653678': 1, '19270729': 1, '11722596': 1, '24250211': 2} | {} |
164,130 | 3826069-1 | 26,038,440 | noncomm/PMC003xxxxxx/PMC3826069.xml | The expanding spectrum of human infections caused by Kocuria species: a case report and literature review | A 57-year-old man, a previously known case of diabetic nephropathy with end-stage renal disease undergoing continuous ambulatory peritoneal dialysis (CAPD) for the last four years, was admitted to a tertiary-care hospital in Puducherry, with complaints of abdominal pain, pedal edema and loose stool for three days. Upon initial physical examination, he was not febrile and had a normal-appearing catheter exit site. However, the peritoneal dialysate fluid was turbid. Subsequently, he became febrile, and a peripheral blood examination showed a total cell count of white blood cells 8700 cells/cu mm, neutrophils 84%, lymphocytes 12% and eosinophils 4%. The hemoglobin concentration was 9.0 g/dL, and the blood urea and creatinine levels were 161 mg/dL and 8.4 mg/dL, respectively. Random blood sugar was 170 mg/dL, total protein 5.9 mg/dL, serum albumin 1.8 mg/dL and globulin 4.1 mg/dL; the C-reactive protein level was raised to 10 mg/dL.\nThe peritoneal dialysis fluid (7 mL) inoculated into a BacT-alert FA bottle showed growth within 12 h (BacT-alert 240; bioMérieux, France). Direct microscopy of the sample showed gram-positive cocci in pairs and clusters. We performed all culturing procedures according to the 2005 update of the International Society for Peritoneal Dialysis recommendations and guidelines using specimens collected prior to antibiotic treatment. Subcultures of the peritoneal fluid were performed using sheep blood agar, MacConkey agar and chocolate agar; the plates were incubated at 35 °C for 48 h. After incubation, sheep blood agar yielded the pure luxuriant growth of pale-pink non-hemolytic colonies that were 1–2 mm size (). Subculture on nutrient agar yielded smooth, small, pale-cream to pale-pink colonies (). Gram staining of the culture revealed the cells to be gram-positive cocci in pairs or clusters (). The organism was preliminarily identified as Kocuria based on phenotypic test results, such as positive reactions for catalase, oxidase, nitrate reduction and growth in 5% NaCl and motility test negativity.\nSubsequent additional tests, such as bacitracin susceptibility, lysozyme sensitivity at 200 μg, resistance to furazolidone and lysostaphin, helped to discriminate micrococci from Staphylococci. The culture (designated as PKS1409) was later identified with a 97% probability as Kocuria rosea using a Vitek-2 system (bioMérieux) of 64 tests; the ID-GPC card panel tested positive only for α-glucosidase, leucine arylamidase, α-galactosidase, alanine arylamidase and tyrosine arylamidase. To verify the culture results, a second sample from the peritoneal fluid was evaluated, which also grew the same organism. The second isolate obtained from the second peritoneal dialysate fluid taken after 3 days showed a colony morphology, growth characteristics, biochemical test results and antibiogram identical to that of first isolate. However, an examination of the removed CAPD catheter and subsequent blood culture results showed no growth. Additionally, repeat blood samples collected from the patient who was already on antibiotics showed no growth.\nWe performed 16S rRNA gene sequencing, as previously described and compared the sequence results using the basic local alignment search tool with the EzTaxon database. The 16S rRNA gene amplified using a polymerase chain reaction Mastermix (Fermentas, Thermo Scientific, MA, USA) with the conserved primers PKRF (5′-ATC CTG GCT CAG AGC GAA CG-3′) and PKRR (5′-CCC TAC GGC TAC CTT GTT ACG-3′) generated a nearly complete sequence of the 16S rRNA gene (∼1365 bp) (Veriti-PCR; Applied Biosystems Inc., CA, USA). The polymerase chain reaction product was purified (Hi-Media, Mumbai, India) and sequenced using ABI technology (Eurofins, Bangalore, India). The basic local alignment search tool nucleotide sequence analysis revealed a high degree of homology (99.78%) with K. rosea (GenBank accession number JN084143); and the second closest match was K. polaris, with 99.56% homology (accession number AJ278868). This isolate was precisely identified and confirmed as K. rosea by a phylogenetic analysis of the 16S rRNA gene sequences by EzTaxon, a web-based tool used for the identification, using 16S rRNA gene sequences. Similar results were obtained when we constructed a neighbor-joining phylogenetic tree with the 16S rRNA gene sequences of all Kocuria species using MEGA v5.1 program ().\nSusceptibility testing through a modified Kirby-Bauer disc-diffusion technique and minimum inhibitory concentration (MIC) by microbroth dilution method was performed according to the Clinical and Laboratory Standards Institute guidelines for Staphylococcus. The disc-diffusion method revealed that PKS1409 was susceptible to ampicillin, cefotaxime, ciprofloxacin, cloxacillin, gentamicin, erythromycin, amikacin, imipenem, linezolid, teicoplanin and vancomycin, but showed intermediate resistance to ceftazidime. The MIC values for co-trimoxazole (10 mg/L), tetracycline (2 mg/L) and ceftazidime (2 mg/L) were relatively high when compared to other antimicrobials, such as benzylpenicillin (0.06 mg/L), clindamycin (0.5 mg/L) and levofloxacin (0.5 mg/L). The MIC value was less than 0.5 mg/L MIC for all the other antibiotics tested, including ciprofloxacin, erythromycin, gentamicin, linezolid, rifampicin, vancomycin and quinupristin–dalfopristin. The disc-diffusion results correlated well with the MIC values for all the common antibiotics evaluated. Biofilm production was assessed by the microtitre plate assay, and PKS1409 did not produce a biofilm. Biofilm production was further checked by growing the bacterium under a different set of conditions with different media, namely, brain–heart infusion, nutrient and Luria-Bertani broth, for different incubation time intervals of 6, 12 and 24 h. American Type Culture Collection reference strain Staphylococcus epidermidis 35984 was used as a positive control. All the experimental conditions reconfirmed that PKS1409 was not able to produce biofilm.\nA chest X-ray of the patient was normal, and an abdominal ultrasound showed findings suggestive of chronic renal failure. The intraperitoneal administration of amikacin and cefazolin was started for the empirical treatment of CAPD peritonitis. In addition, intravenous injections of vancomycin (1 g) and amikacin were given for 5 days. Improvement of the patient was visible after the initiation of antibiotic treatment, with fever subsiding and a decrease in the C-reactive protein level. Two methods of susceptibility testing showed that PKS1409 was susceptible to vancomycin. The patient responded well to the vancomycin treatment and did not develop any other complications. The patient was symptomless after 14 days of antibiotic therapy and catheter removal and was discharged.\nThe nearly complete sequence of the 16S rRNA gene of the Kocuria rosea isolate from this study has been deposited in GenBank under accession number HQ830206. | [[57.0, 'year']] | M | {'18395377': 1, '21935583': 1, '20218989': 1, '27630804': 1, '28348760': 2, '28914802': 1, '12791862': 1, '23096480': 1, '2345296': 1, '7547287': 1, '12908418': 1, '18408034': 1, '29300305': 1, '21282394': 1, '9038293': 1, '16029488': 2, '29063496': 1, '33634670': 1, '20884772': 1, '22259211': 1, '28102479': 1, '15615593': 2, '19692561': 1, '20423506': 2, '15634954': 1, '12892116': 1, '16924917': 1, '33100541': 1, '32587199': 2, '34584818': 2, '11594599': 1, '12656171': 1, '1401003': 1, '24657860': 1, '27391488': 1, '22806295': 1, '33189010': 1, '17591894': 1, '26653310': 1, '23518651': 1, '21864336': 2, '27190805': 1, '29211248': 1, '19519547': 1, '30443312': 2, '31134025': 1, '17911292': 1, '11773142': 1, '18614658': 1, '15796137': 1, '16597925': 1, '34104924': 1, '19621623': 1, '15750130': 1, '30460590': 1, '21282396': 1, '12054223': 1, '6381527': 1, '31324234': 1, '16272536': 1, '28397739': 2, '26038440': 2} | {'5330228-1': 1, '5330228-2': 1, '5414425-1': 1, '1181815-1': 1, '6232278-1': 1, '545057-1': 1, '8458495-1': 1, '2875226-1': 1, '3184040-1': 1, '7574134-1': 1} |
164,131 | 3826602-1 | 24,260,733 | noncomm/PMC003xxxxxx/PMC3826602.xml | A case of levocetirizine-induced fixed drug eruption and cross-reaction with piperazine derivatives | A-73-year-old female patient visited our clinic with multiple round well-demarcated dark pigmented lesions with desquamation. She took medications because of common cold eighteen days ago. Medications were bepotastine besilate (Talion®; Mitsubishi Tanabe Pharma, Japan), levocetirizine (Xyzal®; UCB Korea Co., Ltd, Korea), acetaminophen, pseudoephedrine 60 mg / triprolidine 2.5 mg (Actifed®; Samil Pharm. Co., Ltd, Korea), dihydrocodeine bitartrate 5 mg / di-methylephedrine hydrochloride 17.5 mg / chlorpheniramine maleate 1.5 mg / guaifenesin 50 mg (Codening®; Chong Kun Dang Pharmaceutical Corp., Korea) and aluminium hydroxide 200 mg / magnesium carbonate 120 mg (Antad®; Hanbul Pharm Co., Ltd, Korea). After taking these medications, the patient experienced generalized itching and multiple erythematous macules with several bullae formation in about two h. These cutaneous lesions were spontaneously resolved after stopping taking medications and changed to pigmented lesion with desquamation. The patient had already experienced similar adverse reactions twice after taking bepotastine besilate, levocetirizine, acetaminophen, Actifed®, Codening®, Antad®, dexibuprofen and roxithromycin one and a half years ago. Multiple cutaneous erythema and bullae occurred and were resolved after two weeks with localized pigmentation.\nThe patient was a house wife and had diabetes mellitus and penicillin induced acute hypersensitivity. She denied alcohol intake and smoking.\nIn laboratory findings, complete blood cell counts were as follows; white blood cell 8,600/mm3 (neutrophil 76.6%, lymphocyte 15.7%, monocyte 8.8%, eosinophil 4.5%, basophil 0.6%), hemoglobin 11.9 g/dL, platelet 207,000/µL. C-reactive protein was 1.0 mg/dL. Hepatic enzymes, blood urea nitrogen and serum creatinine were within normal ranges. Patch test was done with suspected drugs such as bepotastine besilate, levocetirizine, acetaminophen, Codening®, codein, Actifed® and Antad® at both normal skin and pigmented skin. Petroleum (Vaseline®) was used to make appropriate concentration to test and control. All drugs were made to 10% concentration except codein 5% and additional Actifed® 1% concentration []. After 48 h, patch was removed and readings were performed 48 h after initial patch applying. At the normal skin site where levocetirizine had been applied, erythema was presented (). At the pigmented skin site where levocetirizine had been applied, infiltration and vesicle were presented (). We additionally performed patch test for other antihistamines including levocetirizine (5% and 10% of Pet.), cetirizine (10% of Pet.), hydroxyzine (10% of Pet.), ebastine (10% of Pet.), loratadine (10% of Pet.) and fexofenadine (10% of Pet.). Erythema was observed at patch test sites of cetirizine and hydroxyzine which were piperazine derivatives (). But the patch tests of ebastine, fexofenadine and loratadine which were piperidine derivatives showed negative response (). The open oral challenge test with fexofenadine was done. The patients took 120 mg fexofenadine a day for 3 days as the open oral challenge test, and there was no adverse reaction.\nThe patient was diagnosed as levocetirizine-induced fixed drug eruption which was confirmed by patch test. She has cross-reactions with other piperazine derivatives such as cetirizine and hydroxyzine. We recommended that the patients avoid taking these antihistamines. Fexofenadine could be an alternative drug without adverse reaction to patient. | [[73.0, 'year']] | F | {'9066941': 1, '34212158': 1, '19552754': 1, '12072003': 1, '27803886': 2, '26090114': 1, '17614812': 1, '16135160': 1, '15548781': 1, '30050965': 2, '11846746': 1, '15230812': 1, '12514519': 1, '15785059': 1, '27440959': 2, '19563995': 1, '30078879': 1, '17017922': 1, '22092850': 1, '19474709': 1, '28761848': 1, '16689192': 1, '8349874': 1, '28765820': 1, '24260733': 2} | {'6036876-1': 1, '5088262-1': 1, '4936078-1': 1} |
164,132 | 3826609-1 | 24,260,734 | noncomm/PMC003xxxxxx/PMC3826609.xml | Recurrent intradialytic heparin induced anaphylaxis: workup and management | A 70-year-old Chinese female with hypertensive kidney disease was deemed to require dialysis. She had no known allergies and never received angiotensin converting enzyme (ACE) inhibitors. Dialysis was commenced through a permanent catheter with 500 U of unfractionated heparin/hr for intradialytic anticoagulation. She tolerated 3 hemodialysis sessions per-week in the initial 2 weeks. The following week she developed hypotension and dyspnea at the start of a dialysis session. First use syndrome was the postulated cause and she was discharged after observation and treatment with intravenous hydrocortisone and antihistamines. However, she mounted a more severe reaction within minutes of starting the subsequent dialysis session two days later, with flushing, hypotension and rhonchi, requiring admission to the high dependency unit. A serum tryptase level by fluorescent enzyme immunoassay done immediately after the reaction was elevated at 43.1 µg/L (ref <11.4 µg/L). Heparin was thought to be the common inciting agent and the cause for her recurrent anaphylaxis. Furthermore, although no subsequent dialysis sessions with heparin were carried out, she developed urticaria on the following day. As heparin was used in the central catheter lock solution, it was postulated that systemic extension of heparin from within the tubing was responsible for this particular reaction. She was subsequently able to tolerate heparin-free dialysis, lending support to our hypothesis that heparin was indeed the culprit. In addition, citrate substituted heparin as catheter lock solution, and no further reactions were observed. Other variables, including the dialysis membrane and sterilant, were not modified. Further evaluation to confirm the suspected heparin allergy and determine safe alternatives for subsequent hemodialysis was indicated.\nSkin prick tests were done with unfractionated heparin (5,000 U/mL), and its possible alternatives: dalteparin (2,500 U/mL), enoxaparin (20 mg/0.2 mL), tinzaparin (3,500 IU/0.35 mL) and fraxiparin (2,850 IU/0.35 mL) (). Histamine (0.1 mg/mL) and 0.9% normal saline solution were used as positive and negative controls. The prick test was positive for heparin but negative for the rest. This was further substantiated by a positive intradermal test with heparin at 1:10 dilution of the above concentration (negative at 1:1,000 and 1:100). Intradermal tests were negative for dalteparin at similar dilutions (1:1,000, 1:100 and 1:10). This was followed by subcutaneous and intravenous challenges with dalteparin at incremental concentrations as described in , reaching up to 1,250 U of intravenous dalteparin. She has tolerated hemodialysis with dalteparin for the past 2 years. | [[70.0, 'year']] | F | {'22830297': 1, '12097752': 1, '15663568': 1, '15025697': 1, '23617635': 1, '26714689': 1, '8725623': 1, '16409199': 1, '18598335': 1, '20609865': 1, '27831511': 1, '11174034': 1, '10427508': 1, '10916114': 1, '17073874': 1, '8072263': 1, '24260734': 2} | {} |
164,133 | 3827494-1 | 24,244,214 | noncomm/PMC003xxxxxx/PMC3827494.xml | Parotid sialolithiasis in a two-year-old boy | A 2-year-old male patient was referred from a local clinic complaining of painful swelling in the right parotid area and low grade fever. He had no past medical history except for the treatment of his right parotitis at the local clinic 2 weeks before. At that time, he had suffered from painful swelling in the same right parotid area for 5 days, which was relieved the next day after the oral antibiotic was switched.\nOn admission, extraoral examination revealed a broad area of swelling in the right parotid area with indurated overlying skin that was warm and tender to the touch. Intraorally, a solid mobile formation was revealed near the right parotid duct opening on palpation, possibly the calculus, as well as pus discharge at the duct opening on pressing.\nA CT scan of the neck was performed, which showed an asymmetric enlargement and heterogenous enhancement in the right parotid gland () and two oval sialoliths located near the orifice of the right Stensen's duct (), suggesting acute suppurative parotitis with duct sialolithiasis.\nOn laboratory test, leukocytosis (white blood cells, 17,200/µL) and elevated C-reactive protein (1.54 mg/dL) were observed. The amylase (42 U/L) level was within the normal range and the IgG/IgM antibodies of mumps virus were negative. The total serum calcium (10.3 mg/dL) level was within the normal range and the Mantoux test was negative.\nAbdominal sonography showed no calculus in the regions of the gall bladder, kidneys, pancreas and other parts of the abdomen.\nMedical treatment was initiated immediately with analgesic-anti-inflammatory drugs and intravenous antibiotics. The pus was drained daily by means of dilating and milking the duct orifice with a lacrimal probe.\nOn the third day of hospitalization, the swelling and fever began to subside. As the calculi were located near the duct orifice, and the patient continued to complain of colicky pain, we planned their surgical removal by an intraoral approach. A simple sialolithotomy was performed with no invasive incision, because the calculi were just beneath the duct orifice that had become enlarged due to the drainage of pus. Appropriate pressure on the duct orifice was on its own satisfactory to retrieve the calculi and purulent discharge.\nThe calculi had irregular borders and a yellowish color. The fusiform-shaped one measured about 6 mm×2 mm in size and the rather ovoid-shaped one measured around 3 mm×3 mm (). Culture of the drained pus grew α-hemolytic streptococci, while the blood culture was sterile.\nThe patient was kept on parenteral antibiotics for 4 days and switched to an oral alternative when discharged from the hospital. On one week follow-up, the swelling was almost normalized without any further problems and the patient was prescribed 3 additional days of oral antibiotics. | [[2.0, 'year']] | M | {'30894988': 1, '8634200': 1, '33489575': 2, '2114453': 1, '17336398': 1, '2254602': 1, '20204313': 1, '10435141': 1, '10477789': 1, '16105693': 1, '21960397': 1, '10334226': 1, '8741203': 1, '5645112': 1, '11058627': 1, '15573365': 1, '10602786': 1, '10102595': 1, '7729992': 1, '24244214': 2} | {'7813980-1': 1} |
164,134 | 3827495-1 | 24,244,215 | noncomm/PMC003xxxxxx/PMC3827495.xml | Cystic fibrosis of pancreas and nephrotic syndrome: a rare association | A nine-year-old male patient diagnosed with CF, lung disease, and pancreatic insufficiency had been monitored for three years. A gradual increase in the ratio of decline in the urine and complaints of swelling of the face and both ankles had begun two years previous. Physical examination revealed the following: temperature, 36.8℃; pulse, 92/min; blood pressure, 109/71 mmHg (95th percentile); edemas in both lower extremities and the sacral region; and more prominent edemas around the face. Other system examinations were normal. Liver function tests, viral hepatitis panel results, alpha-1 antitrypsin levels, and abdominal ultrasonography were normal but sweat test was 98 mmol/L (chloride concentration).\nAt that time he was detected hypoalbuminemia and proteinuria on a random urine sample. Complement factors 3 and 4 were normal, antinuclear antibody was negative, serum urea was 11 mg/dL, triglyceride was 175 mg/dL, total cholesterol was 230 mg/dL, creatinine was 0.6 mg/dL, and albumin was 0.5 g/dL in diagnosis time and 24-hour urine collection revealed nephrotic range proteinuria (>960 mg/m2/day).\nThe patient began steroid therapy following NS diagnosis. At follow-up, the patient was found to have steroid-resistant NS, and a renal biopsy was performed under light microscopy and immunofluorescence microscopy. The renal biopsy showed mesangial proliferation without AA. Partial remission was achieved using low-dose steroids (15 mg/day prednisolone, for a period 1 year) and cyclosporine A therapy (3 mg/kg/day; for a period 4 months). Serum albumin and total protein levels in serum were 3.2 g/dL, 5.5 g/dL after treatment, respectively. Renal biopsy was the second time in the last 6 months. Serum Amyloid A protein was negative. At the moment, our patient has treated with 0.5 mg/kg/every other day prednisone and his proteinuria (30 g/day) has continued. The patient is still in partial remission.\nThe patient's radiological imaging showed destruction around the peripheral airways, and bronchiectasis was detected. Pulmonary function tests provided the following values: forced expiratory volume in 1 second (FEV1) 78% and forced vital capacity (FVC) 85%; FEV1/FVC values were low. The patient was treated with recombinant human DNase, followed by treatment with inhaled bronchodilators and pulmonary rehabilitation. | [[9.0, 'year']] | M | {'11420273': 1, '19406970': 1, '4024933': 1, '17547751': 2, '12606185': 1, '12357328': 1, '9260572': 1, '18839205': 1, '31767021': 1, '18475229': 1, '19403164': 1, '1776895': 1, '16290154': 1, '16554808': 1, '11792901': 1, '24244215': 2} | {'3827495-2': 2, '1896172-1': 1} |
164,135 | 3827495-2 | 24,244,215 | noncomm/PMC003xxxxxx/PMC3827495.xml | Cystic fibrosis of pancreas and nephrotic syndrome: a rare association | A two-year-old male patient was referred to Dicle University Department of Pediatric Pulmonology Unit. In history, he had diagnosed as CF due to chronic diarrhea, while he was two months of age. During follow-up, no pulmonary involvement was observed; however, eight months prior to this study a decrease in urine volume was detected, as well as, edemas in the patient's face and bilateral lower extremities.\nThe patient's medical history included an upper respiratory tract infection two weeks prior. Physical examination revealed the following: temperature, 36.8℃; pulse, 84/min; blood pressure, 94/50 mmHg (50th percentile); and edemas in the patient's face and bilateral lower extremities. Other system examinations were normal.\nLaboratory examinations results revealed the following in diagnosis time; sweat test was repeated 122 mmol/L, liver function tests and complement factors 3 and 4 were normal, antinuclear antibody was negative, albumin was 0.6 mg/dL, total cholesterol was 220 mg/dL, urea was 16 mg/dL, and creatinine was 0.4 mg/dL. Twenty-four-hour urine collection was found nephrotic proteinuria (>960 mg/m2/day) and the patient was diagnosed with NS and started oral corticosteroids 2 mg/kg/day, 6-week therapy and achieved remission. The patient was regarded as minimal change disease. The patient is still in remission and being followed for NS. | [[2.0, 'year']] | M | {'11420273': 1, '19406970': 1, '4024933': 1, '17547751': 2, '12606185': 1, '12357328': 1, '9260572': 1, '18839205': 1, '31767021': 1, '18475229': 1, '19403164': 1, '1776895': 1, '16290154': 1, '16554808': 1, '11792901': 1, '24244215': 2} | {'3827495-1': 2, '1896172-1': 1} |
164,136 | 3827516-1 | 24,249,896 | noncomm/PMC003xxxxxx/PMC3827516.xml | Purely Cutaneous Rosai-Dorfman Disease with Immunohistochemistry | A 65-year-old white male presented with a singular, 0.8 cm, and slowly growing mass on the right back for evaluation. Grossly, the lesion was a firm, dome-shaped nodule that was brownish-red in color. There was minimal erythema on the underlying skin. There was no history of trauma. The patient reported no associated systemic symptoms, such as fever, weight loss, or malaise. Lymphadenopathy was not appreciated on physical examination. Past medical history of this patient, includes hypertension, steatosis, and over 20 subcutaneous nodules scattered over the forearms, trunk, and neck, which have been surgically excised and diagnosed as lipomas after histopathologic examination. Previous radiologic studies with magnetic resonance imaging demonstrated multiple solitary mobile subcutaneous nodules of fatty tissue measuring a few centimeters in diameter. All pertinent laboratory results including complete blood count with differential and erythrocyte sedimentation rate were unremarkable.\nHistologic evaluation shows the dermis occupied by a sheet of confluent histiocytes with scattered neutrophils, lymphocytes, and plasma cells interspersed []. The histiocytes have indistinct cell borders, abundant eosinophilic cytoplasm, low nuclear to cytoplasmic ratio, round vesicular nuclei, and prominent nucleoli. Within some of the histiocytes were intact lymphocytes, plasma cells, and neutrophils that were engulfed by the histiocytes, a process called emperipolesis []. The histiocytes are positive for S-100 [] and CD (cluster of differentiation) 68 [], and negative for CD1a. The lesion did not penetrate the epidermis or the subcutaneous fat. The lesion was completely resected and follow-up reveals no recurrence or new nodules, and no signs of systemic involvement. | [[65.0, 'year']] | M | {'17325475': 1, '19840336': 1, '26588339': 1, '16394460': 1, '21431448': 1, '19688167': 1, '16433797': 1, '33287799': 2, '21920257': 1, '21838087': 1, '22264933': 1, '22356918': 1, '22470214': 2, '19335436': 1, '12121554': 1, '19668942': 1, '1498408': 1, '18410979': 1, '18837709': 1, '21564180': 1, '20877523': 1, '17988346': 1, '15583585': 1, '2180012': 1, '19542928': 1, '18929211': 1, '24249896': 2} | {'3312662-1': 1, '7720066-1': 1} |
164,137 | 3827519-1 | 24,249,899 | noncomm/PMC003xxxxxx/PMC3827519.xml | Giant Inflammatory Linear Verrucous Epidermal Nevus: Successfully Treated with Full Thickness Excision and Skin Grafting | A 17 year old female presented with a linear pruritic lesion extending from lateral border of right foot to right gluteal region []. The parents noticed that lesion in the second month of life, which continued to grow up to puberty. Since last 2 years it was stable. Pruritus was intense leading to recurrent secondary infection. There were no other systemic abnormalities. None of the family members had similar type of lesion. She was prescribed oral, topical and intralesional steroid, isotretinoin and methotrexate in past, without any improvement. The routine investigations including tests for HIV were within normal limits.\nHistopathology showed hyperkeratosis with alternate parakeratosis and orthokeratosis and hypergranulosis beneath the orthokeratotic area. There was mild spongiosis with psoriasiform epidermal hyperplasia and mild to moderate perivascular lymphocytic infiltrate in superficial dermis [].\nA diagnosis of ILVEN was made on the basis of intense pruritus, histopathological findings and lack of response to antipsoriatic treatments. Considering the marriageable age, posteriorly placed lesion and malignant potential, she had underwent full thickness excision followed by split thickness skin grafting. The postoperative period was uneventful. She was followed up for one year without any recurrence or significant scarring []. The cosmetic result was acceptable and the patient was satisfied. | [[17.0, 'year']] | F | {'6852314': 1, '3906609': 1, '11562033': 1, '1723870': 1, '629580': 1, '16549730': 1, '8075448': 1, '3033033': 1, '26120188': 1, '3740101': 1, '16191860': 1, '24249899': 2} | {} |
164,138 | 3827520-1 | 24,249,900 | noncomm/PMC003xxxxxx/PMC3827520.xml | Idiopathic Calcinosis Cutis of the Vulva | The patient was a 42-year-old female with two children. On physical examination, there were firm, non-tender, pedunculated nodules measuring approximately 1 cm × 6 cm alongside both vulva without any skin ulceration. It had slowly grown in size during the last 5 years and then remained static. The laboratory investigations revealed within normal serum calcium levels of 9.5 mmol/dL, magnesium levels of 2.4 mg/dL and phosphorus levels of 2.9 mmol/dL. Complete hemogram showed following results; Hb 13.5 g/dL, WBC 5.2 10 3/mL, PLT 270 10 3/mL, and sedimentation rate 25 mm. Blood sugar, uric acid, electrolyte, and liver function and kidney function tests, and routine urine examination were normal. Anti- nuclear cytoplasmic antibodies, serum C3, C4, and CH50 levels, and rheumatoid arthritis test were within normal limits. C-reactive protien (CRP) and antistreptolysine O (ASO) levels were 0.6 mg/dL and 221, respectively. Parathormone level was 63.7 pg/mL. The enyzme linked isosorbent assay (ELISA) tests for anti-human immune deficiency viruse (HIV), anti-hepatit C virıse (HCV), and hepatit B surface antigen (HBSAG) were negative.\nIt caused discomfort during intercourse as the solid nodular masses mobile. The masses were excised under general anesthesia and there was no recurrence at 1-year follow-up [Figures and ]. Skin biopsy specimen demonstrated dermal calcification with a diagnosis of idiopathic calcification [Figures and ]. Any special staining except H and E, was not applied. | [[42.0, 'year']] | F | {'19882024': 1, '30679229': 1, '30537979': 2, '12170541': 1, '26712983': 2, '10546909': 1, '33299246': 1, '12594118': 1, '14725667': 1, '15235189': 1, '21540566': 1, '22837567': 2, '15902514': 1, '21112670': 1, '8942931': 1, '9403246': 1, '15274707': 1, '15283797': 1, '15280829': 1, '24249900': 2} | {'4683491-1': 1, '6290501-1': 1, '3401848-1': 1} |
164,139 | 3827522-1 | 24,249,902 | noncomm/PMC003xxxxxx/PMC3827522.xml | Giant Congenital Melanocytic Nevus with Developmental Dysplasia of Bilateral Hip: A Rare Association | A 7-month-old male child presented to us with a large, pigmented flat lesion of irregular shape and colour, covering almost 70% of the trunk. The lesion was present since birth and has been following a proportional growth with the growth of the child. The mother also gave a history of noticing asymmetry of girth of the thighs since birth. The child has been otherwise healthy and there was no history of trauma or any neurological symptoms. He was delivered through a full term normal vaginal delivery without any obstetric complications. His physical, mental, and social milestones were appropriately achieved without any signs of developmental delay till the present date. The mother denied noticing any changes suggestive of malignant transformation like sudden accelerated growth, ulceration, bleeding, and induration in the nevus. There was no family history of similar presentations.\nOn cutaneous examination, the child had a large, irregular, well-defined, unevenly pigmented, flat melanocytic nevus with diffuse bluish-brown to black color, encircling the entire trunk. The maximum diameter was measured to be 33 cm, extending from the upper back to the left thigh, posteriorly. It had a smooth surface, with localized hypertrichosis over the left thigh. There were a total of 20 satellite lesions distributed over the arms, forearms, upper trunk, thighs, and legs, beyond the border of the main nevi. The child also had a swelling, measuring about 6 cm in diameter, on the lateral side of left lumbar area covered by the GCMN [].\nThe swelling was well defined, soft and non-tender, mobile, without any surface changes. Systemic examination was unremarkable. Palpation of spines revealed no abnormalities. The child had asymmetry of thighs’ girth, with the mid-thigh circumference of the right thigh measuring 4 cm more in contrast with the left thigh. Systemic examination was unremarkable. Mucosa, hair, nail, palms, and soles were normal. Ophthalmologic and neurological examinations revealed no abnormalities. On investigation, complete hemogram, biochemical parameters, and urine complete examination were all within normal limits. X-ray of hip showed developmental dysplasia of bilateral hip. Ultrasound examination of both hips demonstrated non-ossified femoral cartilage [].\nBrain and spinal magnetic resonance imaging was performed to detect neurocutaneous melanocytosis, which revealed a normal study. An excision biopsy from the nevus showed nests of rounded melanocytes in the papillary dermis extending deep into the reticular dermis confirming the diagnosis of CMN. Biopsy was performed from the mass over the left lumbar area, which revealed mature adipocytes, suggestive of lipoma []. | [[7.0, 'month']] | M | {'27057033': 1, '21664206': 1, '8629825': 1, '34513374': 2, '4037819': 1, '55278': 1, '29933750': 2, '26955112': 1, '20541682': 1, '20877115': 1, '20161871': 1, '8349853': 1, '1185098': 1, '15692463': 1, '32055515': 2, '20888464': 1, '15078366': 1, '24249902': 2} | {'8405355-1': 1, '6015456-1': 1, '7001409-1': 1} |
164,140 | 3827523-1 | 24,249,903 | noncomm/PMC003xxxxxx/PMC3827523.xml | A Curious Case of Sweating Blood | A 12-year-old girl visited us with a history of bleeding from the intact skin over the forehead, scalp, cheek, nose, and trunk [Figures and ] for the last 2 years. The bleeding occurred in episodes, once or twice a day, sometimes more frequently, especially on waking up in the morning. No preceding history of stress or anxiety and no preceding episode of tingling sensation were found. Each episode started with mild watery secretion over the forehead or other body parts, followed immediately with bright-red colored secretion. Each episode lasted for about 10-15 min, and the patient remained perfectly alright during the post-episode period until the next episode. There was no history of bleeding from any other site. No history of ingestion of any anticoagulants, dyes, or other drugs was obtained from her. She did not have any history of major medical or surgical illness in the past. No family member had similar complaints. Menstrual cycles were regular and normal.\nHer general physical examination and systemic examinations did not reveal any abnormality. The skin over the forehead was normal. There was no local tenderness. Blood or red colored secretion could not be extruded on manipulation. On gross examination, the secretion was bright-red in color, less viscous than blood, and it was not frank blood. On collection of the secretion and examination of its smeared preparation under a microscope, plenty of erythrocytes were observed; the sample was benzidine test positive [] and alkaptonuria negative. Her routine hemogram, blood counts, platelet count, bleeding time (2 min), clotting time (3 min 30 sec), active partial thrombin time (25 sec; normal range 24-32 sec), prothrombin time, liver function tests, and renal function tests were within normal limits. Peripheral smear of the secretion showed multiple red blood cells (RBCs) along with numerous gram-positive cocci and bacilli []. Urine and stool examination did not reveal erythrocytes or any abnormalities.\nPsychiatric analysis revealed Intelligent Quotient (I.Q.) between 60 and 70 and a loss of insight. Histopathological examination revealed no abnormalities in blood vessels and intact walls. Hair follicles, sweat glands, and sebaceous glands are normal. Direct immunofluorescence study ruled out vasculitis.\nThe patient was given atropine transdermal patch over the involved sites and she noticed gradual improvement in both the severity and frequency of the episodes. Gradually, after 1 month, the patient stopped getting similar episodes. We followed the patient for 2 months after stopping the atropine treatment. During this period, she did not have any more episode. | [[12.0, 'year']] | F | {'25657464': 2, '27051537': 2, '7650970': 1, '15182582': 1, '18360116': 1, '8982961': 1, '20161867': 2, '20666570': 1, '10590858': 1, '13935682': 1, '24249903': 2} | {'2810702-1': 1, '4808663-1': 1, '4314924-1': 1} |
164,141 | 3827524-1 | 24,249,904 | noncomm/PMC003xxxxxx/PMC3827524.xml | Familial Multiple Basal Cell Carcinoma (Gorlin's Syndrome): A Case Report of a Father and Son | A 70-year-old male presented with multiple black colored papules and plaques of various sizes present over the left infraorbital region and behind both retroauricular ear pinnae. This slowly progressed to form ulcerative lesions since last 1 year. On examination, the lesion over cheek was 4 × 3 cm in size with rolled on margins and hemorrhagic crust at the center []. Similar lesion of 2 × 1 cm size with mild oozing was also present behind the ear pinnae []. Apart from this, the patient also had multiple blackish hyperpigmented plaques of varying sizes ranging from 0.5 cm × 0.5 cm to 1 × 1 cm over forehead, scalp, abdomen, and axillae. Along with these he also had multiple palmoplantar pits [Figures and ]. Skeletal examination revealed bony deformities such as kyphoscoliosis, short neck, pectus carinatum, and sprengel deformity [Figures and ]. On investigating his X-ray skull revealed multiple osteolytic changes in the mandible secondary to odontogenic cyst, anterior wedge compression of D12, L1, L2 vertebral bodies with the presence of anterior osteophyte bodies in L1 and L2 vertebra []. Electencephalogram study was within their normal limits. CT brain did not reveal any abnormality. Diagnosis of basal cell carcinoma (BCC) was confirmed by histopathology []. On the basis of above-said clinical, histopathological, and radiological findings, diagnosis of Gorlin syndrome was made. Further ulcerative BCC lesions were treated with wide excision followed by full thickness graft sutured with 5-0 prolene.\nHis only unmarried 28 year-old son was also examined for features of Gorlin syndrome and was found to have multiple palmar pits and bony deformities, that is, kyphoscoliosis, short neck, sprengel deformity, and pectus carinatum since birth. But there was no evidence of any basal cell carcinoma at time of examination. | [[70.0, 'year']] | M | {'26604574': 1, '20061742': 1, '13851319': 1, '6491017': 1, '8326488': 1, '20068110': 1, '8315076': 1, '19032739': 1, '17649773': 1, '9096761': 1, '30967739': 2, '24249904': 2} | {'6421933-1': 1} |
164,142 | 3827528-1 | 24,249,908 | noncomm/PMC003xxxxxx/PMC3827528.xml | Asymptomatic Peri-orifical Papular Lesions in a Child | A six-year-old boy presented with a one month history of asymptomatic raised lesions around the mouth, eyes and chin. There was no history of contact allergens. The remainder of his medical history was unremarkable. Cutaneous examination revealed multiple tiny flesh-colored as well as erythematous papules, some of which were shiny and distributed around the mouth, nose, eyes and chin [] with a tendency to become confluent at a few places. Results of the examination of the rest of the skin and mucous membranes were completely normal. Chest roentgenogram was normal. Findings of the skin biopsy specimen taken from a flesh colored papule above the chin is shown in Figures and . The complete blood cell count and blood chemistry panel were within normal limits. Erythrocyte sedimentation rate was 25 mm at the end of one hour. Mantoux test for tuberculosis was negative. | [[6.0, 'year']] | M | {'24249908': 2} | {} |
164,143 | 3827529-1 | 24,249,909 | noncomm/PMC003xxxxxx/PMC3827529.xml | Pseudoepitheliomatous Keratotic and Micaceous Balanitis: A Rare Condition Successfully Treated with Topical 5-Fluorouracil | A 50-year-old circumcised male presented with asymptomatic growth on glans penis of 6 months duration.\nPatient had undergone circumcision for phimosis 8 months back. Two months later, patient noticed an asymptomatic scaly lesion over the glans penis, which slowly increased in size and became dry, rough, and elevated.\nThere was no history of trauma, localized dermatoses, or systemic diseases. There was no history of exposure to risk of sexually transmitted diseases (STD) and no symptoms and signs of STD. There was no significant illness in the partner.\nClinical examination revealed a well-defined dry, rough, hard elevated, mica-like scaly, and verrucous and hyperkeratotic plaques, measuring 4 × 3 cm over glans penis, around urethral meatus [Figures and ].\nThe shaft of the penis, scrotum, and inguinal area was normal. There was no regional lymphadenopathy.\nHis blood Venereal Disease Research Laboratory Test and HIV were negative. Hematological, biochemical, and radiological examination did not reveal any abnormality.\nHistopathological examination revealed skin with epidermis displaying massive hyperkeratosis, parakeratosis, and pronounced epithelial hyperplasia without cellular atypia. The dermis showed mild lymphocytic infiltrate [Figures -].\nThe scaly material had dissolved completely in 10% KOH [potassium hydroxide] overnight [].\nThe patient was treated with topical 5-fluorouracil cream application once daily for 3 weeks and the whole lesion regressed completely without any recurrence for a period of 10 months follow-up [Figures and ]. | [[50.0, 'year']] | M | {'7259225': 1, '22092361': 1, '8659009': 1, '20169317': 1, '20456408': 1, '30684817': 1, '3343410': 1, '20885051': 1, '14466728': 1, '20826996': 1, '26557598': 1, '24249909': 2} | {} |
164,144 | 3827530-1 | 24,249,910 | noncomm/PMC003xxxxxx/PMC3827530.xml | Zosteriform Palisaded Encapsulated Neuroma: An Unusual Presentation | A 30-year-old female patient presented to us with asymptomatic skin lesions on the face of 4 years duration. These lesions began as pinhead sized elevations and gradually grew in size to the present state. On examination, lesions were multiple, discrete, mostly multi-lobulated, flesh colored, soft to firm, papules, and nodules arranged in a curvilinear fashion on the face [] starting from tip of the nose and gradually deviating to the left along the nose, left eyebrow, and forehead region along the distribution of the ophthalmic division of the trigeminal nerve. There was no accompanying history of hearing defect or other neurological disorders. None of the family members were affected. On thorough cutaneous examination, there was no café au lait macules, axillary freckling or plexiform neurofibromas. Hair nails and mucous membranes were normal. On ophthalmological examination no signs of neurofibromatosis were detected. No other clinical sign suggestive of systemic neurofibromatosis was noted. Routine blood investigations, chest X-ray, ultrasonography of the whole abdomen were normal. Skin biopsy specimen showed a tan granular surface of the base and histopathological examination revealed a normal epidermis. In the dermis, there was a partially encapsulated, well-circumscribed nodule [] composed of fascicles of small spindle cells with wavy nuclei interlaced with small slits and clefts []. There was no nuclear pleiomorphism or mitoses. The tumor cells were positive for S-100 protein []. These findings and the clinical presentation were consistent with a diagnosis of PEN. We had sent the patient to the plastic surgery out patient departmentfor excision of the lesion. | [[30.0, 'year']] | F | {'8030761': 1, '1730169': 1, '11466253': 1, '4639250': 1, '27630799': 2, '8468415': 1, '26090480': 1, '26955159': 1, '8884829': 1, '19840332': 1, '9185909': 1, '31543539': 2, '1587489': 1, '29201976': 2, '1705947': 1, '15696992': 1, '24249910': 2} | {'5702437-1': 1, '5016044-1': 1, '6749752-1': 1} |
164,145 | 3827531-1 | 24,249,911 | noncomm/PMC003xxxxxx/PMC3827531.xml | Psoriatic Arthritis with Acral Lentiginous Melanoma: Role for Methotrexate? | A 50-year-old male with psoriatic arthritis since 20 years on methotrexate, since 12 years on and off with a cumulative dose of 1080 mg, developed an asymptomatic black lesion over his right sole near the instep since 2 years which was gradually increasing in size over last 6 months. No h/o bleeding or ulceration of the lesion. He was a known hypertensive and diabetic. On examination, patient had pallor and right inguinal lymph nodes were enlarged and firm in consistency.\nExamination of right sole revealed a hyperpigmented plaque of 3 × 5 cm with surface and border irregularities []. There was no scaling, ulceration, bleeding or induration. Multiple hyperpigmented macules were present over both soles varying in size from 0.3 × 0.3 cm to 1 × 1 cm. There were also multiple discrete and confluent erythematous papules and plaques over thighs, forearm, arms and trunk. Scalp showed scaly plaques. There was subungual hyperkeratosis in all nails. Oral mucosa revealed a black pigmentation.\nExamination of musculoskeletal system revealed swan neck deformity of left lateral 3 fingers and right 4 fingers and Boutennaire deformity of left index finger, proximal dislocation of middle toes bilaterally. There was swelling and deformity of both knee joints. With all these findings, we made a provisional diagnosis of psoriasis with mutilating type of psoriatic arthropathy with acral lentiginous melanoma.\nInvestigations showed an ESR of 130, rheumatoid factor was negative, but C-reactive protein was positive. SGOT was slightly elevated and cytology from the knee joint aspiration was sterile and predominantly composed of neutrophils. Excision biopsy of the blackish plaque revealed epidermis with junctional activity and nests of cells of melanoma cells containing melanin in dermis consistent with malignant melanoma Clark level-III with no involvement of the circumferential deep margin [Figures and ]. Another biopsy from the smaller hyperpigmented macule on the sole was unremarkable. Lymph node biopsy from right inguinal lymph node showed only reactive hyperplasia.\nLesion was completely excised with a margin of 2 cm and chemotherapy with Inj. Dacarbazine 300 mg infusion for 4 days every month was given for 6 months. Lesions completely subsided [] and there were no signs of relapse or metastases till date. | [[50.0, 'year']] | M | {'21057746': 1, '20678147': 1, '20810498': 1, '19280165': 1, '10342628': 1, '19344980': 1, '18951733': 1, '1054764': 1, '24249911': 2} | {} |
164,146 | 3827532-1 | 24,249,912 | noncomm/PMC003xxxxxx/PMC3827532.xml | Bullous Systemic Lupus Erythematosus | A 39-year-old lady, a homemaker and mother of three, presented with largely asymptomatic vesicobullous lesions (2 months duration), involving head and neck, upper limbs, and trunk over both photo-exposed and unexposed areas. The blisters would rupture over 2-3 days; yielding clear (sometimes hemorrhagic) fluid; heal over 2-3 weeks; leaving behind pigmentation and occasional scarring. Concurrent painful oral ulcers were reported; though, other mucosae were uninvolved. A 6-month history suggestive of Raynaud's phenomenon; arthralgias involving small joints of hands and feet; photosensitivity; and intermittent episodes of mild to moderate fever was present. The patient reported three previous, spontaneous abortions, (5months gestation) the last one being 6 years back.\nOn examination, there were multiple, tense, clear as well as hemorrhagic, vesicles and bullae, arising over an erythematous base and predominantly involving upper body []. Bulla spread sign and Nikolsky sign were positive. In addition, superficial erosions, areas of postinflammatory hyperpigmentation, and small superficial scars were noted. Superficial erosions were also noted over the buccal mucosa, hard palate, and lips. Her systemic examination was essentially normal.\nA provisional diagnosis of BSLE was considered and she was thoroughly investigated. She had a significant anemia (8.8 gm/dL) with evidence of iron deficiency on peripheral smear and iron studies. Other biochemical investigations were essentially normal, with no evidence of renal derangement. Extensive serological workup revealed antinuclear antibody positivity of 1:640 (using hep-2 cells); positive anti-dsDNA, anti-Ro, and anti-La antibodies; low levels of C3 and C4 with a normal CH50 component; negative antiphospholipid antibody, rheumatoid factor, and C-reactive protein. Russell's viper venom test revealed no lupus like anticoagulant. X-rays of chest and involved joints were normal.\nA lesional biopsy revealed subepidermal split with neutrophilic infiltrate in the papillary dermis []. Direct immunofluorescence (both perilesional and distant-covered skin) revealed IgM and C3 deposition along the basement membrane zone (BMZ) as well as perivascular location. Due to resource constraints, indirect immunofluorescence or salt-split skin could not be performed. Based on clinical, histopathological, and serological evidence, a diagnosis of BSLE was confirmed.\nWith a normal glucose 6-Phosphate dehydrogenase (G6PD) activity, we planned to start her on dapsone; however, her low hemoglobin prevented this. She was started on prednisolone (1 mg/kg/day as a single morning dose); hydroxychloroquine (200 mg twice a day); along with complete sunprotection and topical care. Hematinics were also initiated. There was only partial improvement with new lesions developing even after 4 weeks; wherein, she was started on dapsone. She responded quite favorably with no new lesions and satisfactory healing of pre-existing ones []. Over the next 6 months, steroids were completely withdrawn, and dapsone and hydroxychloroquine continued for further 1 year. The patient has remained in remission without any systemic manifestations as well, over the last 1 year. | [[39.0, 'year']] | F | {'3279084': 1, '11105368': 1, '7662571': 1, '11274208': 1, '15234014': 1, '8423389': 1, '29267441': 2, '26090480': 1, '7530271': 1, '8320353': 1, '10328198': 1, '25276277': 1, '24249912': 2} | {'5726672-1': 1} |
164,147 | 3827533-1 | 24,249,913 | noncomm/PMC003xxxxxx/PMC3827533.xml | A Strange Ulcer | A 13-year-old girl presented with a 3 cm deep necrotic wound on her lower back []. One week before observation, she had begun to complain of flu-like symptoms and achiness. Three days before observation, she was falling in and out of consciousness. When her condition worsened, she was rushed to the emergency room. A lumbar puncture was performed, meningococcal meningitis was diagnosed and she was transferred to the Infectious Disease Ward of our hospital to start antibiotic therapy.\nHer medical history was unremarkable. She was otherwise healthy and had never suffered from allergies.\nPatch tests performed with 1%, 5%, and 10% PVP-I in Vaseline resulted negative. Circulating IgE levels were within normal limits.\nThe cutaneous lesion was treated with topical antibiotics (mupirocin cream) and clostridiopeptidase A ointment. At the third week follow-up, the lesions had healed with minimal reliquates. | [[13.0, 'year']] | F | {'17845191': 1, '15701122': 1, '12934425': 1, '20523874': 2, '24249913': 2} | {'2875742-1': 1} |
164,148 | 3829088-1 | 24,493,991 | noncomm/PMC003xxxxxx/PMC3829088.xml | Complicated Varicella Infection at 8-year-old Boy with Pulmonary Agenesis | The case presents a boy, aged 8 years, hospitalized with the clinical picture of complicated chickenpox. From history of disease: Disease begun 8 days before admission, manifested with fever and characteristic varicella rash. Two days before admission to hospital he complained on pain under right rib arch and intensive cough, otogenic secretion also was noted. In previous history he has been often treated for obstructive bronchitis. After admission he became tachydispnoic, with high fever, tachycardia, hypotensive, with positive auscultatory finding on the lung indicating pneumonia. Extremely high values of nonspecific parameters of inflammation: SE 108/ I hour, CRP 301 mg/l, L 18.5 10 9/L, fibrinogen 7.9 indicated bacterial infection. In other laboratory findings it was registered elevation of AST 196, ALT 297, with signs of hypoxemia. Patient was treated by combined antimicrobial treatment (initially vancomycin and imipenem, as well as antiviral treatment with acyclovir together with other supportive treatment. Due to extensive empyema in right hemithorax thoracocenthesis was performed and about 600 ml of purulent fluid was evacuated. Etiology of bacterial infection was not confirmed. Disease was complicated by further progression of MODS, treated by multidisciplinary approach in Intensive care unit. Disease had a favorable outcome without sequels, but congenital agenesis of right lower lobe and transposition of brachiocephalic trunk were discovered. | [[8.0, 'year']] | M | {'15578404': 1, '18166616': 1, '18419410': 1, '18171285': 1, '16261302': 1, '17046469': 1, '8183171': 1, '24493991': 2} | {} |
164,149 | 3829092-1 | 24,493,990 | noncomm/PMC003xxxxxx/PMC3829092.xml | Varicella Pneumonia in a 39-year-old Female in Third Trimester Twin Pregnancy | A 39 years old female smoker, in a high grade twin pregnancy, referred to Clinic for infectious diseases with five days history of illness. In a first two days she had a high temperature, up to 38.8oC, and later she noticed „vesicular“ rash, distributed mostly on head and torso. She visited general practicioner and specialist for infectious diseases, with suggestion to take symptomatic therapy. Before the admission in hospital her condition get worse, with fatigue, exhaustion, and shortness of breath. The patient did not have a history of chickenpox during childhood but her son developed chickenpox 10 days earlier. There was no past history of diabetes, cardiac or pulmonary disease.\nAt admittance the patient was febrile (39.2°C), tachypnoic (respiratory rate 30 breaths/min), tachycardic (cardiac pulse 110/min), pale and sweaty. She had typical chickenpox vesicles with some pustules over the face, neck, torso and abodmen. Peripheral lymphonodes were enlarged in neck area. Some vesicles were presented in oral mucosa. Pulmonary examination revealed billateral inspiratory crackles over the lung bases. Arterial blood gases indicated respiratory failure (oxygen saturation 83%). Blood tests show high C-reactive protein (CRP), normal leukocytes and differential blood count, with low platelets. In a first three days patient was febrile up to 39.3OC, tachydispnoic and ortopnoic, with bullosus rash over the trunk. Initially we started with intravenous therapy with acyclovir, cefepime and cloxacillin. Fourth day of hospital stay we noticed detoriation in patient’s condition, with intensive chest pain, bloody cough and intermittent disorientation and dominant tachypnea (over 40/min). Chest X-ray revealed infiltrative shadows in basal parts of lung. CT confirmed billateral infiltration with signs of alveolo-interstitial syndrome, with massive inflammatory changes. Antimicrobial therapy was changed to vancomycin and rifampicin, corticosteroids are associated (hydrocortison), with cardiotonic, diuretic, albumin infusions, pantoprasole, heparin and continuous oxygenation on facial mask. Significant improvement was noticed after five days of this therapy. Blood tests show normal CRP, platelets and WBC. Control chest X-ray revealed siginificant regression of infiltrative changes. Gynecologist indicated arteficial abruption of pregnancy. After 19 days of intesive care in our clinic, patient was transferred to Clinic for gynecology and obstretition where artefitial abrubtion has been completed.\nOn follow-up after 14 days patient was in good condition, with normal chest x-ray and blood tests. | [[39.0, 'year']] | F | {'15342855': 1, '17577346': 1, '2237118': 1, '11865393': 1, '8533407': 1, '22385673': 1, '10191458': 1, '24493990': 2} | {} |
164,150 | 3829216-1 | 24,250,841 | noncomm/PMC003xxxxxx/PMC3829216.xml | Chronic meningitis as the first presentation of sarcoidosis: an uncommon finding | A 40 year old woman was presented to Shariati hospital (TUMS), with headache, nausea, and episodic amnesia. The episodes lasted less than five minutes, and resolved after vomiting.\nThe patient complained of no fever, focal weakness, or sensory symptoms; but she mentioned episodic dyspnea for more than 5 years, leading to cardiac and respiratory evaluations, which failed to show any specific etiology.\nShe had a history of admission to other hospital, about 9 months earlier, due to headache, blurring of vision and diplopia. At that time she was diagnosed as cerebral venous sinus thrombosis and had been treated with anticoagulants.\nExamination disclosed blurred optic disc margins and slight neck rigidity. Brain MRI showed diffuse leptomeningeal enhancement, with scattered white matter changes ().\nCerebrospinal Fluid (CSF) examination showed lymphocytosis (WBC:37,70% lymphocyte), elevated protein (277mg/dl) and low glucose (13mg/dl); but cytological examination, stains for bacteria, mycobacteria, and fungi, VDRL, Wright, and PCR for TB, all were negative in the CSF.\nCSF exam was repeated three more times, each time with complete laboratory evaluation (including cytological examination), with similar results.\nRoutine hematology and biochemistry tests, liver function tests, thyroid function tests, PPD (purified protein derivative), HIV antibody, C-ANCA, P-ANCA, C3, C4, CH50, anticardiolipin and antiphospholipid antibodies, were normal/negative, as well as tumor markers in search of malignancy. Chest roentgenography, HRCT of thorax, and the result of bronchoscopy with BAL (BronchoAlveolar Lavage) were unrevealing.Serum ACE level was normal, but CSF ACE was raised (24; NL < 5).\nThe patient was treated with IV methyl prednisolone and continued on prednisolone with the impression of probable neurosarcoidosis.\nTwo weeks later, she developed another episode of dyspnea. She was re-evaluated by pulmonary specialist, and because of an abnormality in the base of her lung, an open biopsy was performed. The pathology report was consistent with Sarcoidosis. Dyspnea was ascribed to pulmonary hypertension.\nPatient's neurological symptoms and signs improved after 2 months and after 7 months follow up, she was still free of symptoms. | [[40.0, 'year']] | F | {'16283095': 1, '3896208': 1, '18032765': 1, '29636921': 2, '19932381': 1, '9042010': 1, '11552036': 1, '10209662': 1, '27326368': 1, '24250841': 2} | {'5889254-1': 1} |
164,151 | 3829218-1 | 24,250,842 | noncomm/PMC003xxxxxx/PMC3829218.xml | Reversible therapy-related dysplastic hematopoiesis following Beta Interferon Therapy in Multiple Sclerosis Patients: Report of 2 Cases | A 39-year-old woman suffering from acute paresis of the right lower limb was referred to our clinic for evaluation. She had the symptoms for 8 years and the year before the evaluation, she had an episode of left optic neuritis which had been treated with high dose of steroids. She had recovered completely after 1 month. Neurological examinations revealed diplopia, limb ataxia, dysarthria and fairly clumsy tandem gait.\nGiven her history of two attacks, as well as MRI lesions matching the McDonald criteria for dissemination in space and time, other possibilities were ruled out and she was diagnosed as MS and accordingly, interferon β1b was started for the patient.\nShe had received interferon for 5 years without any significant side effects or unpredictable problems. During this period, she had 4 relapses for which she was treated with methyl prednisone pulse for each relapse. A few months prior to the time of this report, during routine evaluation of the patient, the lab data showed a reduction of WBC, Hb and platelets (WBC: 3000/dl, Hb: 9.8g/dl, PLT: 151/000dl- 2008/4). The interferon was stopped and hematology consultation was performed.\nBone marrow examinations showed dysplastic hematopoiesis, granulocytes displayed reduced segmentation (pseudo-Pelger-Huet abnormality) and reduced granulation.\nThe patient was treated with conservative therapy and gradually all hematologic measures returned to normal levels. The same beta interferon treatment was reintroduced. After more than 1 year of restarting the interferon treatment there were no abnormalities in the blood tests (WBC: 6900dl, Hb: 10g/dl, PLT: 301.000dl- 2010/10). | [[39.0, 'year']] | F | {'19577164': 1, '19770475': 1, '16764353': 1, '11503953': 1, '18946071': 1, '21136583': 1, '20838962': 1, '17345612': 1, '20874249': 1, '24250842': 2} | {'3829218-2': 2} |
164,152 | 3829218-2 | 24,250,842 | noncomm/PMC003xxxxxx/PMC3829218.xml | Reversible therapy-related dysplastic hematopoiesis following Beta Interferon Therapy in Multiple Sclerosis Patients: Report of 2 Cases | A 35-year-old woman, with no significant previous illness, had a history of five-day diminished vision in the right eye followed by full recovery that had occurred seven years ago. Two years following the incident, she was apparently suffering from paresthesia and weakness in both lower limbs with left side predominance. Since MRI of the brain was compatible with MS, after ruling out other possibilities, she was diagnosed with a case of relapsing MS, for which she was treated with a course of intravenous methyl prednisolone over five days. Two years later, during laboratory follow up, the CBC showed a decrease in WBC and hemoglobulin levels (WBC: 2900dl, Hb: 9/9g/dl, platelet: 168.000dl). Interferon was stopped and hematology consultation was performed.\nBone marrow examinations confirmed dysplastic hematopoiesis; granulocytes displayed reduced segmentation (pseudo-Pelger-Huet abnormality) and reduced granulation.\nAfter treatment with conservative therapy, gradually all hematologic measures returned to the normal levels (WBC: 4000dl, Hb: 11.1g/dl, PLT: 193.000dl- 2010/10). Beta interferon was restarted and after two years, no abnormalities have been observed in the blood tests. | [[35.0, 'year']] | F | {'19577164': 1, '19770475': 1, '16764353': 1, '11503953': 1, '18946071': 1, '21136583': 1, '20838962': 1, '17345612': 1, '20874249': 1, '24250842': 2} | {'3829218-1': 2} |
164,153 | 3829227-1 | 24,250,848 | noncomm/PMC003xxxxxx/PMC3829227.xml | Four cases of brown-vialetto-van laere syndrome from Iran: Clinical and electrophysiologic findings | A 17-year-old female, unmarried and student presented with speech problem and progressive hearing loss since the age of 12. She was admitted in our hospital in 1999 with liquid dysphagia and progressive weight loss in the last 6 months. She also reported irregularity in menstruation recently. Her parents were first cousins and four siblings had no problem. Systemic examination was unremarkable except left tympanic membrane perforation. She was mentally normal and there was bilateral facial and cervical flexor weakness. The tongue was atrophic with fasciculation and gag reflex was diminished and the limbs were atrophic with mild proximal weakness. Deep tendon reflexes (DTRs) and sensory exams were within normal limits. Biochemical lab tests revealed no abnormality; but on audiometry, there was severe bilateral sensorineural hearing loss. Electromyography and nerve conduction studies (EMG-NCV) were compatible with motor neuron disease with prominent involvement of cranial muscles; in addition, repetitive nerve stimulation was negative. Other investigations including chest X-ray, brain magnetic resonance imaging (MRI) and abdomino-pelvic sonography were normal. | [[17.0, 'year']] | F | {'10030685': 1, '2325091': 1, '1007898': 1, '20206331': 1, '16948939': 1, '7229669': 1, '16122634': 1, '22718020': 1, '1512615': 1, '24283429': 1, '24470831': 1, '10797435': 1, '16963409': 1, '1913372': 1, '12427524': 1, '16009552': 1, '3655850': 1, '18416855': 1, '11465021': 1, '12686396': 1, '24250848': 2} | {'3829227-2': 2, '3829227-3': 2, '3829227-4': 2} |
164,154 | 3829227-2 | 24,250,848 | noncomm/PMC003xxxxxx/PMC3829227.xml | Four cases of brown-vialetto-van laere syndrome from Iran: Clinical and electrophysiologic findings | This 17-year-old girl was admitted for the evaluation of slowly progressive dysphagia and choking from 6 months before admission in 2000.\nShe also complained of proximal weakness in upper extremities from 2 weeks ago. She had an episode of febrile seizure at the age of 3 and slowly progressive hearing loss from the age of 12. Her 3 brothers and 2 sisters were healthy and parents were non-consanguineous. Physical examination was normal. On neurologic exam, there was bifacial weakness, diminished gag reflex, atrophic tongue with fasciculation and proximal weakness. Routine laboratory tests, peripheral blood smear, creatine phosphokinase (CK), and lactate dehydrogenase (LDH) were all normal, as well as cerebrospinal fluid (CSF) analysis. There was bilateral low frequency sensorineural hearing loss on pure tone audiometry (PTA) and motor neuron involvement mainly in cranial innervated muscles on EMG-NCV. Other investigations including chest X-ray, brain MRI, Tensilon test, repetitive nerve stimulation (RNS) and abdomino-pelvic sonography were negative and genetic testing did not show deletion in SMN1. One year after the beginning of gabapentin, 900 mg/day, she reported some improvement in dysphonia and dysphagia, which continued for the next 4 years, when she was lost to follow up. | [[17.0, 'year']] | F | {'10030685': 1, '2325091': 1, '1007898': 1, '20206331': 1, '16948939': 1, '7229669': 1, '16122634': 1, '22718020': 1, '1512615': 1, '24283429': 1, '24470831': 1, '10797435': 1, '16963409': 1, '1913372': 1, '12427524': 1, '16009552': 1, '3655850': 1, '18416855': 1, '11465021': 1, '12686396': 1, '24250848': 2} | {'3829227-1': 2, '3829227-3': 2, '3829227-4': 2} |
164,155 | 3829227-3 | 24,250,848 | noncomm/PMC003xxxxxx/PMC3829227.xml | Four cases of brown-vialetto-van laere syndrome from Iran: Clinical and electrophysiologic findings | This 21-year-old female was admitted in December 2008 because of hoarseness, difficulty in swallowing, choking and fatigue in the recent 3 months. She had weight loss, difficulty in walking and bilateral hearing loss since 2 years ago which aggravated gradually. She also reported chronic bifrontal throbbing headache that was more prominent in mornings and history of several generalized tonic clonic seizures in the past few years. In the last months, she occasionally had mild dyspnea during sleep. Her 4 brothers and 1 sister were healthy and parents were non-consanguineous.\nShe was alert and of normal intelligence. There was bifacial weakness, wasted tongue with fasciculation, diminished palatal and left vocal cord movements and nasal speech. Weakness particularly in neck and proximal limb girdle and bilateral pes cavus were noted. Routine lab tests, creatine phosphokinase (CPK), lactate dehydrogenase (LDH) and acetylcholine receptor antibody disclosed no abnormality. Findings of brain MRI, chest CT-scan and abdomino-pelvic sonography were unremarkable. There was bilateral low frequency sensorineural hearing loss and electrodiagnostic study was compatible with anterior horn cell disease. | [[21.0, 'year']] | F | {'10030685': 1, '2325091': 1, '1007898': 1, '20206331': 1, '16948939': 1, '7229669': 1, '16122634': 1, '22718020': 1, '1512615': 1, '24283429': 1, '24470831': 1, '10797435': 1, '16963409': 1, '1913372': 1, '12427524': 1, '16009552': 1, '3655850': 1, '18416855': 1, '11465021': 1, '12686396': 1, '24250848': 2} | {'3829227-1': 2, '3829227-2': 2, '3829227-4': 2} |
164,156 | 3829227-4 | 24,250,848 | noncomm/PMC003xxxxxx/PMC3829227.xml | Four cases of brown-vialetto-van laere syndrome from Iran: Clinical and electrophysiologic findings | A 22-year-old female, presented with hoarseness, sore throat, dysphagia, and hearing loss from 3 years before our first visit in December 2008. In the last 2 months, weakness developed over lower and then upper limbs associated with muscle wasting, fasciculation and exertional dyspnea. She reported 2 episodes of seizures at the age of 11 and her parents were first cousins and all 4 sisters and her brother were healthy. She was mentally normal with bifacial weakness, wasted tongue and fasciculation (), palatal weakness, reduced motor force more in lower limbs, bilateral foot drop and generalized brisk DTRs. Plantar reflexes were downward. Sensory and cerebellar exams were unremarkable. Lab data revealed hypochromic microcytic anemia with normal serum iron and total iron binding capacity. In addition, brain MRI was normal. PTA showed bilateral low frequency sensorineural hearing loss and normal tympanometry. Nerve conduction studies were normal and EMG of limbs and tongue muscles was compatible with motor neuron disease. One year after the treatment with 900 mg gabapentin, her swallowing subjectively improved and motor strengths became completely normal. No change in speech and hearing was seen. | [[22.0, 'year']] | F | {'10030685': 1, '2325091': 1, '1007898': 1, '20206331': 1, '16948939': 1, '7229669': 1, '16122634': 1, '22718020': 1, '1512615': 1, '24283429': 1, '24470831': 1, '10797435': 1, '16963409': 1, '1913372': 1, '12427524': 1, '16009552': 1, '3655850': 1, '18416855': 1, '11465021': 1, '12686396': 1, '24250848': 2} | {'3829227-1': 2, '3829227-2': 2, '3829227-3': 2} |
164,157 | 3829232-1 | 24,250,856 | noncomm/PMC003xxxxxx/PMC3829232.xml | A rare case of facioscapulohumeral muscular dystrophy and myasthenia gravis | A 70-year-old man presented to our department with complaint of 15-day history of progressive difficulty in chewing and dysartheria. He had a 50-year history of slowly progressive asymmetrical weakness of proximal upper limb muscles.\nExaminations revealed reduction in forces of bilateral orbicularis oculi muscles, weakness and wasting of bilateral triceps muscles especially on right side and bilateral winging of scapula more prominent on right side. The legs and pelvic girdle muscles had normal forces. The reflexes were somewhat depressed throughout. Sensation and coordination were normal. The patient's gait was normal.\nSerum creatine kinase values and other laboratory data were normal. Computerized tomography of the thorax was normal. Nerve conduction studies showed decrement response on repetitive nerve stimulation. Concentric needle electromyography showed myopathic changes especially in proximal limb muscles. Edrophonium test was performed and dysartheria and chewing difficulty showed dramatic improvement but had no effect on limb weakness. Serum anti-acetylcholine receptor (AchR) antibody level was markedly elevated. Muscle biopsy showed myopathic changes with invariability in muscle fiber size, intramuscular infiltration of chronic inflammatory cells, mostly lymphocytes, few hyaline fibers and prominent fat infiltration. Subsequent genetic analysis confirmed the diagnosis of FSHD. Our patient's bulbar symptoms showed dramatic improvement following administration of choline-esterase inhibitor agents. | [[70.0, 'year']] | M | {'19019312': 1, '31579125': 2, '15389657': 1, '11676158': 1, '11985390': 1, '30215155': 1, '21872471': 1, '9008491': 1, '32813049': 1, '17986494': 1, '24250856': 2} | {'6763750-1': 1} |
164,158 | 3829233-1 | 24,250,857 | noncomm/PMC003xxxxxx/PMC3829233.xml | A rare presentation of medulloblastoma in adults as primary leptomeningeal involvement | A 22-year-old male presented to our department with a 3-months history of generalized headache, hearing loss, tinnitus and blurred vision. Physical examination of the patient revealed decreased visual acuity (right eye 20/80 and left eye one meter finger count), bilateral papillaedema, bilateral hearing loss and bilateral upward plantar responses. Other neurological examinations including muscle strength, sensory and gait were normal.\nBrain magnetic resonance imaging (MRI) with and without contrast showed intense dural enhancement of cerebellar folia and cerebral convexity, moderate hydrocephalus and intraparenchymal signal changes in right cerebellar hemisphere ( and ).\nLumbar punctures were done three times that had negative results for gram stain, culture, Wright, angiotensin-converting enzyme, Indian ink, cerebrospinal fluid (CSF) adenosine deaminase, polymerase chain reaction for tuberculosis, CSF cytology and human immunodeficiency virus (HIV) antibody. CSF pressure was extremely high (about 70 cm H2O). CSF analysis showed normal cellular counts but elevated protein level and decrease glucose level was significant. Complete blood count, biochemistry profiles were normal. Erythrocyte sedimentation rate was 11 and C-reactive protein result was negative. Serum HIV antibody, HBs antigen, HCV antibody were all negative. Tuberculin purified protein derivative (PPD) was performed that had negative result. Serum Wright, ANA, ds DNA, Antineutrophil cytoplasmic antibody (cANCA and pANCA) and antiphospholipid antibody were within normal limits, too. Paranasal sinus, chest, pelvic and abdominal CT-Scan with contrast all had normal results. Audiometric evaluation showed bilateral asymmetrical sensory neural hearing loss.\nA suboccipital craniotomy was performed and the posterior fossa dura, pia arachnoid and cerebellar hemispheres were subject to biopsy. Histological examination of biopsy material showed highly cellular neoplasm that is composed of cells with small to medium-sized, hyperchromatic nuclei and little apparent cytoplasm. Immunohistochemical stains performed on the biopsy material revealed positive reaction of tumor cells with neuron-specific enolase and glial fibrillary acidic protein and negative result with CD99. Synaptophysin shows weak positive reaction (–). | [[22.0, 'year']] | M | {'34194127': 1, '2795197': 1, '8988076': 1, '17992051': 1, '19695677': 1, '19537136': 1, '29683126': 1, '24250857': 2} | {} |
164,159 | 3829241-1 | 24,250,869 | noncomm/PMC003xxxxxx/PMC3829241.xml | An adult man with progressive dysarthria, dysphagia and disequilibrium | The patient was a 40 year old man, who referred to our clinic because of progressive dysarthria, dysphagia and disequilibrium for the previous 15 years. According to his medical history, he had bilateral cataract surgery when he was only 2 years old and mild mental retardation since early childhood.\nOn neurologic examination, he had severe dysarthria (anarthria) and jaw opening dystonia with drooling. Furthermore, he had bilateral hand dystonia and mild upper limb dysmetria. Deep tendon reflexes were brisk and there was bilateral Babinski and leg spasticity. Due to his severe dystonia, spasticity and ataxia, he had become bedridden and was unable to walk.\nThe brain MRIs are presented below ():What abnormalities are seen on brain MRI? What is the most probable diagnosis? Is there any treatment for this patient (other than symptomatic treatments)? | [[40.0, 'year']] | M | {'21243300': 2, '9578968': 1, '19373932': 1, '21825196': 1, '22869688': 1, '22146219': 1, '24250869': 2} | {'2999723-1': 1} |
164,160 | 3829248-1 | 24,250,864 | noncomm/PMC003xxxxxx/PMC3829248.xml | Multifocal inflammatory leukoencephalopathy induced by accidental consumption of levamisole: A case report | A 53-year-old man was admitted to the Neurology Department of Farabi Hospital (Kermanshah, Iran) with walking inability and recognition disorder. Patient history showed that he had referred to hospital with vomiting, vertigo and headache 8 months before after consumption of two sachet of levamisole (for veterinary use) which each sachet contained 1.5 gram of levamisole hydrochloride. One month later, he had been stricken by progressive walking inability and recognition disorder up to administration to our hospital. The patient had not any previous illness.\nOn neurologic examination, he was confused and did not establish a good relationship with the bystander. On mental and cognitive power examinations, using the Mini Mental State Examination (MMSE), he earned 17 points (out of a total score of 30) with no signs of meningeal irritation (such as stiffness of neck). In addition, cranial nerves were normal. The power of limbs was within normal range but deep tendon reflexes in all of four limbs had increased in conjunction with extensor plantar response and reduced abdominal skin reflex. The patient had primitive reflexes including grasp, snout and palmomental. On cerebellar examination, finger to nose test and heel to shin was impaired and the gait was ataxic.\nOn the initial laboratory tests, complete blood count (CBC), blood sugar, urea, creatinine, and liver enzymes were normal. In cerebrospinal fluid analysis, color, pressure, cells, and sugar were normal but protein was increased (69 mg/dl). Oligoclonal band (OGB) was negative.\nOn electroencephalography (EEG), bilateral paroxysmal slow waves were seen. In visual evoked potential (VEP), there was a bilaterally prolonged P100 latency. Brain magnetic resonance imaging (MRI) showed mild cerebral atrophy and multiple focal lesions distributed in periventricular and cerebellar white matter and also in pons and midbrain (). These lesions had low-signal intensity on T1-weighted images and high-signal intensity in fluid-attenuated inversion recovery (FLAIR) view and T2-weighted images.\nFollowing clinical examinations and ruling out of other causes, including infectious and vascular causes, trauma and metabolic, central nervus system (CNS) vasculitis and paraneoplastic syndromes; and according to the patient's history, the patient was diagnosed as multifocal inflammatory leukoencephalopathy following levamisole consumption. The patient did not give consent for brain biopsy.\nThe patient was treated with intravenous methylprednisolone (500 mg) every 12 hours for 7 days followed by two weeks oral consumption of the prednisolone (50 mg/day) during hospitalization. No change was noticed in cerebellar signs and gait disorder but a brief improvement was seen in mentality and cognition after 1 and 3 months. After a month of treatment, MRI did not show a reduction or remission of the lesions. () | [[53.0, 'year']] | M | {'7550929': 1, '9296206': 1, '7583711': 1, '8730185': 1, '19187474': 1, '7854541': 1, '26482228': 2, '8032957': 1, '12690653': 1, '8625249': 1, '24250864': 2} | {'4615875-1': 1, '4615875-2': 1} |
164,161 | 3829259-1 | 24,250,876 | noncomm/PMC003xxxxxx/PMC3829259.xml | Paget's disease of bone presented as normal pressure hydrocephalus: A case report and review of literature | A 66-year-old woman was admitted to Imam Khomeini Hospital with the chief complaint of gait difficulty since 6 years ago. She described the gait difficulty as a falling tendency while walking. She also complained of urinary incontinence. Furthermore, she expressed annoying memory problems. She had diabetes type II, hypertension, dyslipidemia, and hypothyroidism in past medical history. Moreover, she had ischemic heart disease and a previous angiography had revealed stenosis, which was treated by percutaneous coronary intervention. The drug history comprised the following medications: amlodipine, losartan, atenolol, nitrocontin, glibenclamide, atorvastatin, metformin, and levothyroxine. Her pulse rate was 90 per minute with blood pressure of 140/90. Her recent memory was disrupted. A slight facial paresis was detectable as asymmetric nasolabial fissure pattern. She also utilized hearing aids due to hearing problems. Assessing the cerebellar function, the finger to nose and heel to shin tests were normal, while the tandem gait was disrupted. Her gait was slow but normal for her age.\nCell blood count showed lymphocytosis of 42.1% with the white blood cell (WBC) count of 5500/µl. The brain CT scan revealed thickened calvaria (). Furthermore, hydrocephaly was detectable in all supratentorial ventricles, but the forth ventricle remained intact (),. Besides, emphysema was observable in all subcutaneous areas around the skull and outside calvaria (). MRI showed periventricular leukoencephalopathy and increased marrow signal (). In order to assess the thickened calvaria, whole body scan was performed and the serum levels of calcium, phosphorous, and alkaline phosphatase were assessed.\nIn order to investigate the problem, cerebral spinal fluid (CSF) sample was collected after lumbar puncture. After the lumbar puncture the patient's problems including recent memory deficits diminished for one day. Venereal disease research laboratory test (VDRL) and Wright test of CSF were negative. Other indicators of the CSF sample were normal. To investigate multiple myeloma, serum and urine proteins electrophoresis failed to show any specific abnormality. The serum B12 level was normal. Serum calcium and phosphorous levels were within normal limits. Serum alkaline phosphatase was 4723IU/L. The symptoms relieved dramatically after lumbar puncture. | [[66.0, 'year']] | F | {'16995808': 1, '11198695': 1, '233208': 1, '571551': 1, '7211510': 1, '8053279': 1, '15057532': 1, '7852484': 1, '15389972': 1, '15885393': 1, '24250876': 2} | {} |
164,162 | 3829261-1 | 24,250,881 | noncomm/PMC003xxxxxx/PMC3829261.xml | Etiopathophysiological assessment of cases with chronic daily headache: A functional magnetic resonance imaging included investigation | P. K., a 52-year-old married female, mother of two children, with MA educational level had suffered from chronic headache since 20 years ago. For many years, the headaches were mild to moderate with long intervals. Following an emotional stressor, she started to experience regular and more intense headaches since 8 years ago and turned to a case of CDH since 3 years prior to the current presentation. She mainly complained of nocturnal headaches aggravated by intense emotions. Headaches were most often unilateral on the left side. Upon attacks, she became nauseated and sensitive to photic or acoustic stimuli. The headache was refractory to various analgesics. The patient's past medical history was not significant. There was a positive family history of intense headache in her mother and sister. She had no medication history except analgesics. Likewise, she had received no prophylactic regimen for the headaches.\nNeurological examinations and conventional MRI were normal. On psychological assessments, she had normal cognitive performance status (MMSE and ACE); however, BAI, BDI-II and PSQI scales showed that she had moderate anxiety and depression as well as poor global sleep quality. The psychological assessment results of all four cases are outlined in .\nOff-headache EEG demonstrated scattered sharp wave activity. The repeated EEG evaluation during the maximal headache episode, turned out to reveal generalized paroxysmal epileptiform activity. illustrates her EEG patterns during off-headache and maximal headache episodes.\nTCD findings in headache-free evaluation indicated a diminished mean blood flow velocity in bilateral middle and posterior cerebral arteries (MCA and PCA). However, it showed an increase in mean blood flow velocity in left MCA upon maximal intensity headache (the headache site, by 50%). Routine lab data was within normal limits. After all, the clinical impression was chronic migraine headache. | [[52.0, 'year']] | F | {'15617293': 1, '19705061': 1, '20618816': 1, '19059349': 1, '18460006': 1, '16897620': 1, '20959433': 1, '22327509': 1, '16004846': 1, '15501092': 1, '19864908': 1, '12010386': 1, '9533664': 1, '15095562': 1, '10328249': 1, '2197679': 1, '15953273': 1, '21614577': 1, '22408655': 1, '19157973': 1, '19415430': 1, '25337368': 1, '16075452': 1, '10395332': 1, '20464577': 1, '18757883': 1, '12697628': 1, '24250881': 2} | {'3829261-2': 2, '3829261-3': 2, '3829261-4': 2} |
164,163 | 3829261-2 | 24,250,881 | noncomm/PMC003xxxxxx/PMC3829261.xml | Etiopathophysiological assessment of cases with chronic daily headache: A functional magnetic resonance imaging included investigation | S. S., a 32-year-old married female, no children, with MSc educational level who had the complaint of ‘on and off’ mild to moderate headache for many years. Her more intense and frequent headache attacks started 5 years ago and had been a case of CDH (over 15 days per month headache) over the past 3 years. Her headache bouts were almost always very intense (rated 8-10/10 in VAS) especially when she was physically tired and was partially alleviated by sleep. She reported a unilateral (mainly right hemispheric) throbbing headache with no concurrent nausea, vomiting, photophobia and phonophobia during the episodes. Presence of headache did not follow a diurnal pattern. The patient neither had a significant past medical nor a family history of headache. The medication and substance use history was negative except for simple analgesics in routine basis. General and neurological physical examinations, laboratory workups and brain MRI were within normal limits. Her psychological assessments demonstrated normal cognitive functioning (MMSE and ACE); however, a minimal anxiety and depression was detected based on BAI and BDI-II scales, respectively. PSQI showed an appropriate sleep quality ().\nEEG and TCD studies upon maximal and headache-free episodes were unremarkable, showing no quantitative and qualitative differences in both states as compared to each other. The clinical impression for this case was again, chronic migraine headache. | [[32.0, 'year']] | F | {'15617293': 1, '19705061': 1, '20618816': 1, '19059349': 1, '18460006': 1, '16897620': 1, '20959433': 1, '22327509': 1, '16004846': 1, '15501092': 1, '19864908': 1, '12010386': 1, '9533664': 1, '15095562': 1, '10328249': 1, '2197679': 1, '15953273': 1, '21614577': 1, '22408655': 1, '19157973': 1, '19415430': 1, '25337368': 1, '16075452': 1, '10395332': 1, '20464577': 1, '18757883': 1, '12697628': 1, '24250881': 2} | {'3829261-1': 2, '3829261-3': 2, '3829261-4': 2} |
164,164 | 3829261-3 | 24,250,881 | noncomm/PMC003xxxxxx/PMC3829261.xml | Etiopathophysiological assessment of cases with chronic daily headache: A functional magnetic resonance imaging included investigation | A. J. was a 53-year-old female, widow, with no children, and illiterate. She revealed the history of quite often headaches responsive to analgesics since 5 years ago. After the loss of her husband (three years ago) she started to have chronic headache which affected her for more than 15 days per month. The headache was mainly bilateral and retro-orbital and if unilateral, was in right side involving occipital and upper cervical regions. The pain had a constrictive nature however not accompanied by nausea, vomiting, photophobia and phonophobia. The headache was aggravated during emotional stresses and alleviated by rest. In the past medical history, she had infertility. She used to take non-steroidal anti-inflammatory drugs (NSAIDs) for her chronic headache, which was not any more effective Moreover, the patient had not been administered prophylactic regimens for the headaches. Family history was not significant. Apart from the body mass index of 28, general physical examination was normal. Neurological examination, lab data and brain MRI were also within normal limits. Psychological evaluations (despite the illiteracy issue) showed a normal cognitive profile (MMSE and ACE). BAI and BDI-II scales showed a minimal anxiety and depression. Her sleep quality was impaired based on PSQI (). EEG and TCD evaluations in maximal and headache-free episodes’ were normal. Lab data were inconclusive. The clinical impression we had, was the chronic tension type headache. | [[53.0, 'year']] | F | {'15617293': 1, '19705061': 1, '20618816': 1, '19059349': 1, '18460006': 1, '16897620': 1, '20959433': 1, '22327509': 1, '16004846': 1, '15501092': 1, '19864908': 1, '12010386': 1, '9533664': 1, '15095562': 1, '10328249': 1, '2197679': 1, '15953273': 1, '21614577': 1, '22408655': 1, '19157973': 1, '19415430': 1, '25337368': 1, '16075452': 1, '10395332': 1, '20464577': 1, '18757883': 1, '12697628': 1, '24250881': 2} | {'3829261-1': 2, '3829261-2': 2, '3829261-4': 2} |
164,165 | 3829261-4 | 24,250,881 | noncomm/PMC003xxxxxx/PMC3829261.xml | Etiopathophysiological assessment of cases with chronic daily headache: A functional magnetic resonance imaging included investigation | M. K. was a 54-year-old male, married, father of two children and with educational level of PhD. He reported mild transient headache since young adulthood, becoming a known case of migraine when he was 26 years old. He used to take ergotamine–C upon headache during those years. Due to severity and frequency of episodes, he was given prophylactic regimens since the age of 40; however, became refractory in a matter of few years. He was labeled as CDH since 5 years ago. The headache had been intrusive in over 20 days per month lasting 15 hours per day in average. Headaches are mostly bilateral, causing photophobia and phonophobia and accompanied by nausea and vomiting in severe instances. The headache timing did not follow a distinct pattern; however, was more intense at nights. Pain was partly alleviated by sleep. His past medical history was negative. He revealed a family history of migraine in her mother. Over the past few years, he experienced various medications including prophylactic tetracyclic antidepressant, benzodiazepines, antiepileptic, beta blockers and lithium carbonate to all which he failed response. He had recently been taking sumatriptan and ergotamine as abortive medication upon headache episodes, with a very modest response. His general and neurologic examinations as well as the conventional brain MRI with and without contrast were normal. His psychological assessments indicated a normal neuro-cognitive state (MMSE and ACE); however, with a minimal anxiety and depression based on BAI and BDI-II. His sleep quality was evaluated poor, as per PSQI ().\nHe had no significant findings during maximal and minimal headache EEG and TCD evaluations. After all assessments, our impression was medication overuse headache (MOH). His acute phase medications were discontinued and interestingly, after many years, his headache turned into less intense with an episodic pattern, once or twice a week. | [[54.0, 'year']] | M | {'15617293': 1, '19705061': 1, '20618816': 1, '19059349': 1, '18460006': 1, '16897620': 1, '20959433': 1, '22327509': 1, '16004846': 1, '15501092': 1, '19864908': 1, '12010386': 1, '9533664': 1, '15095562': 1, '10328249': 1, '2197679': 1, '15953273': 1, '21614577': 1, '22408655': 1, '19157973': 1, '19415430': 1, '25337368': 1, '16075452': 1, '10395332': 1, '20464577': 1, '18757883': 1, '12697628': 1, '24250881': 2} | {'3829261-1': 2, '3829261-2': 2, '3829261-3': 2} |
164,166 | 3829678-1 | 24,250,229 | noncomm/PMC003xxxxxx/PMC3829678.xml | Pulmonary adenocarcinoma with osseous metaplasia: a rare occurrence possibly associated with early stage? | A 60-year-old Chinese woman presented with the symptom of bloody sputum, which she had noticed for 2 weeks. Enhanced computed tomography (CT) showed an irregular abnormal soft tissue mass located in the left upper lobe that was approximately 1.7 cm× 0.8 cm in size and obviously enhanced with contrast medium (). The CT value in the enhanced arterial phase was approximately 40–60 Hounsfield units, while the venous phase CT value was approximately 72 Hounsfield units. Minimal calcification was not apparent in the tumor. The patient denied any history of gastric carcinoma or digestive symptoms. On the basis of her history and imaging studies, the patient was diagnosed with a malignant pulmonary tumor and underwent lobectomy. The tumor had a heterogeneous off-white appearance and was solid with unclear boundaries. No depressions or varicose veins were found in the pleura.\nHematoxylin and eosin-stained sections showed that the alveolar structure had disappeared within the tumor and that the tumor cells were distributed into round or oval glands with a central lumen. There was no mucin in the tumor cell cytoplasm or glandular cavity. The tumor cell nuclei were ovoid and dark-stained, with prominent nucleoli. The mitotic activity was approximately two mitoses per ten high-powered fields. New bone formation was observed at the center of the tumor (approximately 1.25 mm × 0.85 mm, ). The bone island consisted of mature bone tissue and was surrounded by osteoblast cells that were accompanied by proliferating fibroblasts (). No bone marrow cells were present in the bone tissue. Immunohistochemical staining showed that the tumor cells were positive for cytokeratin-7 () and thyroid transcription factor-1 (), but the metaplastic bone tissue was negative for these factors. However, the tumor cells were negative for caudal-related homeodomain protein 2, which ruled out the possibility of gastrointestinal adenocarcinoma metastasis to the lung, and the Ki-67 labeling index was approximately 35%. An epidermal growth factor receptor exon 19 deletion mutation was found in this patient, but the echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase rearrangement was not found. On the basis of histologic and immunohistochemical findings, this tumor was diagnosed as an invasive pulmonary adenocarcinoma with a predominant acinar pattern, accompanied by osseous metaplasia in tiny lesions and without lymphatic metastasis. This diagnosis was based on the International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society classification system for standard lung adenocarcinoma. | [[60.0, 'year']] | F | {'10879031': 1, '11150957': 1, '14989424': 1, '20168113': 1, '15782573': 1, '19543517': 1, '20555058': 1, '9444652': 1, '23892935': 1, '7586747': 1, '21418396': 1, '3931607': 1, '11026714': 1, '22396294': 1, '7801415': 1, '15965172': 1, '18080136': 1, '16218421': 1, '22228122': 1, '21862118': 1, '11107069': 1, '14588103': 1, '22393100': 1, '24250229': 2} | {} |
164,167 | 3830136-1 | 24,250,063 | noncomm/PMC003xxxxxx/PMC3830136.xml | Use of a combined retroperitoneoscopic and transperitoneal laparoscopic technique for the management of renal cell carcinoma with level I tumor thrombi | A 70-year-old man was referred to our department with an 11 × 10 × 8 cm stage T3b (2009 TNM classification system) right renal tumor extending into the vena and was evaluated with contrast enhanced computed tomography (CT). The radiology department reported that the tumor thrombus in the renal vein extended 2 cm into the vena cava and that there was no evidence of hilar lymphadenopathy []. In addition, a second tumor measuring 3 × 3 × 3 cm was detected at the upper pole of the left kidney. The patient's thorax CT and bone scan were negative. After obtaining the consent of the patient, we decided to perform a LRN using a combined retroperitoneoscopic and transperitoneal technique. | [[70.0, 'year']] | M | {'12544294': 1, '19440023': 1, '15725928': 1, '15476504': 1, '17548146': 1, '17445647': 1, '15716200': 1, '12187230': 1, '20406459': 2, '17095065': 1, '18710749': 1, '20846783': 1, '19498412': 1, '12885352': 1, '33224010': 1, '12809912': 1, '19119807': 1, '21367518': 1, '10737509': 1, '33919290': 1, '20490982': 1, '24250063': 2} | {'3830136-2': 2, '2873261-1': 1, '2873261-2': 1} |
164,168 | 3830136-2 | 24,250,063 | noncomm/PMC003xxxxxx/PMC3830136.xml | Use of a combined retroperitoneoscopic and transperitoneal laparoscopic technique for the management of renal cell carcinoma with level I tumor thrombi | A 46-year-old man presented with right upper quadrant abdominal pain. His CT and subsequent magnetic resonance imaging (MRI) revealed a 13 × 10 × 10 cm renal mass and a renal vein thrombus extending 1.5 cm into the vena cava. The metastatic work-up using a thorax CT and bone scan was negative. After obtaining the consent of the patient, surgery using the “combination technique” was planned. | [[46.0, 'year']] | M | {'12544294': 1, '19440023': 1, '15725928': 1, '15476504': 1, '17548146': 1, '17445647': 1, '15716200': 1, '12187230': 1, '20406459': 2, '17095065': 1, '18710749': 1, '20846783': 1, '19498412': 1, '12885352': 1, '33224010': 1, '12809912': 1, '19119807': 1, '21367518': 1, '10737509': 1, '33919290': 1, '20490982': 1, '24250063': 2} | {'3830136-1': 2, '2873261-1': 1, '2873261-2': 1} |
164,169 | 3830137-1 | 24,250,064 | noncomm/PMC003xxxxxx/PMC3830137.xml | Stump appendicitis: A rare clinical entity | An 18-year-old boy was admitted by a physician with a 1 day history of severe periumbilical pain radiating to the right iliac fossa with loss of appetite. There was no history of vomiting, fever, altered bowel habits or urinary symptoms. Patient had undergone laparoscopic appendectomy 2 years back and had an uneventful recovery, but the details of the operative findings and histopathology were unavailable. Positive clinical findings included a right lower quadrant tenderness and leukocytosis i.e. 15,000 cells/mm3 (reference normal range 4-11,000 cells/mm3). A computed tomogram of abdomen showed only small collection in right iliac fossa [] and initial conservative management was planned by the treating physician.\nSurgical consultation was sought after two days as the clinical condition of the patient deteriorated. The patient developed fever, tachycardia and guarding in the right iliac fossa. The patient was subsequently posted for a Diagnostic Laparoscopy after informed consent.\nIntra operative findings included dense adhesions around the ileocecal region. There was a 3cm long inflamed perforated appendicular stump with abscess formation (~ 30-40 ml pus) [Figures and ]. The appendicular stump was defined and divided at the base with an Endo Stapler []. The specimen was sent for histopathology and showed suppurative appendicitis with perforation. Patient had port site wound infection in post operative period and was discharged on 4th post operative day. | [[18.0, 'year']] | M | {'13998581': 1, '25596290': 1, '16981278': 1, '33088403': 1, '24985784': 1, '15471026': 1, '18427031': 1, '28275759': 2, '15520153': 1, '29849750': 1, '8807521': 1, '34584721': 1, '31462849': 2, '15728024': 1, '34085112': 1, '10966030': 1, '16536249': 1, '10915703': 1, '20157645': 2, '21985727': 1, '27503615': 1, '14605929': 1, '24250064': 2} | {'2821303-1': 1, '5336632-1': 1, '6688392-1': 1} |
164,170 | 3830138-1 | 24,250,065 | noncomm/PMC003xxxxxx/PMC3830138.xml | Standard laparoscopic cholecystectomy for malposition of the gallbladder caused by right-sided ligamentum teres | A 31-year-old female patient was admitted to the surgical clinic because of recurrent right upper quadrant pain during the last 2 months. Clinical examination and laboratory analysis were normal. Stones in the GB were detected on abdominal ultrasonography. She was taken into the operating theatre with a diagnosis of cholelithiasis. At exploration, the GB was absent from its normal location, and it was found just left to LT []. It had edematous and hydropic appearance with an impaction of a calculus at the neck. With the standard localization of ports and a LT lift, it was possible to perform cholecystectomy via laparoscopically in a retrograde manner. During the operation, it was found that there was a short and wide cystic duct joining to the common bile duct on the right side, and the cystic artery with anterior and posterior branches originating normally from the right hepatic artery. She was discharged uneventfully at the first postoperative day. Pathologic examination showed chronic calculous cholecystitis.\nMagnetic resonance cholangiopancreatography and angiography were performed to understand the biliary and portal venous system anomalies. This showed the first branch of the portal vein (PV) running to the right posterior segment, and then formation of the main trunk of the left and right anterior PVs []. The latter vein formed saccularly dilated umbilical portion of PV and finally joined to LT []. | [[31.0, 'year']] | F | {'18330492': 1, '22353517': 1, '9609896': 1, '19660232': 1, '14755792': 1, '18333151': 1, '18081230': 1, '16121888': 1, '11796904': 1, '9060583': 1, '24250065': 2} | {} |
164,171 | 3830139-1 | 24,250,066 | noncomm/PMC003xxxxxx/PMC3830139.xml | Single-port laparoscopic cholecystectomy in situs inversus totalis using the E.K. glove port | A 65-year-old man presented with 1-year history of intermittent epigastric and left upper quadrant discomfort and concomitant digestive problems. Abdominal ultrasonography revealed gallstones, and that the liver and gallbladder were located in the left upper quadrant, whereas the spleen and stomach were located on the right side. A pre-operative chest X-ray showed dextrocardia []. Laboratory data were normal. After obtaining the patient's informed consent, surgery was performed.\nThe patient underwent general anaesthesia and was positioned supine on the operating table. The surgeon stood on the right side of the patient with the assistant on the left side of the surgeon. The scrub nurse and the monitor were on the left side of the patient []. A standard 10 mm, 30o angled rigid laparoscope with a vertical light cable was used. One articulating laparoscopic grasper (roticulator endo grasp, Covidien), for the left hand and standard rigid 5 mm laparoscopic instruments for the right hand were used in this operation.\nA 2.5 cm completely intra-umbilical, vertical skin incision was performed. The incision was deepened to enter the peritoneal cavity. The inner flexible ring, fitted with the glove was then introduced into the abdomen. The open end of the glove was then wrapped around the outer rigid ring []. Co2 pneumoperitoneum was induced and the patient was then put in reverse Trendelenburg position and tilted slightly right laterally for the remainder of the procedure.\nSIT was confirmed with the telescope inserted via the E.K. Glove port[] in the umbilicus. The liver and the gallbladder were confirmed to be on the left-side [], whereas the spleen, the stomach and the heart beat were seen on the right.\nA tuft or bun was made with the tail end of the No.1-0 nylon suture. The needle was passed through the fundus of the gall bladder, care being taken to pass the needle through the serosa without puncturing the lumen. It was next passed through the peritoneum below the diaphragm. The needle was then brought out through the left subcostal region. When the thread was pulled from outside and fixed with a haemostat, a good retraction of the gallbladder imitating retraction accordance to conventional technique for safe cholecystectomy was achieved []. The entire gallbladder, except for the fundus was covered with dense adhesions, which were lysed using the Maryland grasper and monopolar diathermy current. The cystic artery and duct were identified, dissected [] and clipped with 10 mm clip applicators separately and divided with a pair of scissors.\nNext, the gallbladder was grasped with the left hand grasper and retracted in various directions so that it could be dissected from the liver bed by hook electrocautery in an infundibulum-to-fundal direction.\nThe specimen was retrieved through the E.K. Glove port.[] The fascial defect was closed using 1-0 Prolene (Ethicon) and the skin was approximated using 3-0 polyglycolic Rapide suture (Ethicon) []. The procedure took 70 min and the operative blood loss was minimal. Our patient had an uneventful post-operative course and was discharged on the second post-operative day. Pathologic examination confirmed cholelithiasis with chronic cholecystitis. The patient was followed up and has remained well. | [[65.0, 'year']] | M | {'22472363': 2, '21626341': 1, '15790219': 1, '27226919': 1, '32273670': 1, '34306867': 2, '21966139': 1, '25349766': 1, '22468065': 1, '28458815': 1, '21902984': 1, '22679325': 1, '17171807': 1, '29882522': 2, '28417652': 2, '24250066': 2} | {'5536415-1': 1, '6001295-1': 1, '8294112-1': 1, '3337794-1': 1} |
164,172 | 3830140-1 | 24,250,067 | noncomm/PMC003xxxxxx/PMC3830140.xml | Laparoendoscopic single-site cholecystectomy in a pregnant patient | A 33-year-old woman in the 16th week of her first pregnancy experienced two episodes of upper abdominal pain suggestive of biliary colic. Hematological and biochemical parameters were normal but ultrasonography showed previously undiagnosed multiple small gallbladder calculi. Two weeks later she experienced another episode of abdominal pain during which the liver function tests including bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase were marginally elevated. An endoscopic ultrasound (EUS) showed a patulous ampulla indicative of a recently passed bile duct stone and normal calibre bile ducts. At this point she was referred for a surgical consultation and was counselled regarding a LESS-chole. While awaiting her surgery scheduled 3 days later she developed another episode of abdominal and back pain. The serum amylase and lipase were elevated but the white cell count, liver function tests, serum calcium, and lactate dehydrogenase (LDH) were normal. This episode of mild acute pancreatitis settled within 48 h and a repeat EUS was normal. A LESS-chole was undertaken during the same admission. At the time of surgery she was in the 20th week of her pregnancy. An obstetric consultation was obtained and she was started on inj. terbutaline (Bricanyl, Astra-Zeneca, Mumbai, India) 5 mg subcutaneously on the evening before the surgery. Fetal heart monitoring was initiated on the morning of surgery and continued at an interval of 2 h in the postoperative period until discharge. | [[33.0, 'year']] | F | {'21938570': 1, '21471779': 1, '28116209': 2, '14769301': 1, '17713817': 1, '21197237': 1, '22173546': 1, '9751939': 1, '24250067': 2} | {'5220453-1': 1, '5220453-2': 1, '5220453-3': 1} |
164,173 | 3830149-1 | 24,251,258 | noncomm/PMC003xxxxxx/PMC3830149.xml | A Case of Congenital Lobar Emphysema in the Middle Lobe | A 3-week-old male baby weighing 2300 g was referred to our neonatal intensive care unit for asphyxia with respiratory distress not responding to medical management in regional hospital. His mother did not have any follow-up during her pregnancy. He was delivered as a full term with delayed cry and respiratory distress.\nPhysical examination revealed a tachypneic baby with flaring of alae nasi and sub costal retraction, the cyanosis was generalized (oxygen saturation spO2 was 70% in air). On examination of the respiratory system, decrease breath sound on the left hemithorax was noted. The cardiac auscultation was normal.\nThe chest X-ray showed hyperinflation on the right side, and right basithoracic opacity []. computed tomography (CT) scan of the thorax supported the X-ray []. There was hyperinflation on the right middle lobe with tracheal and mediastinal shift to the left side. The blood parameters were normal. On the echocardiography, there was no evidence of congenital cardiac anomalies.\nAfter hemodynamic stabilization of the child, surgical intervention was performed. The right middle lobe looked emphysematous at time resection []. Post-operative chest X-ray showed expansion of the right upper and lower lobes, with no emphysema or mediastinal shift.\nHistopathological examination of the excised right middle showed alveolar distension without fibrosis [].\nThe child was discharged 7 days post-surgical intervention, and he was seen as an out-patient for follow-up. He had normal O2 saturation in room air and he was feeding well. | [[3.0, 'week']] | M | {'19643792': 1, '16769334': 1, '20075537': 1, '18726590': 1, '21808403': 2, '23189104': 1, '27381542': 1, '27609589': 1, '15769700': 1, '34225689': 1, '12789097': 1, '24251258': 2} | {'3141155-1': 1} |
164,174 | 3830150-1 | 24,251,259 | noncomm/PMC003xxxxxx/PMC3830150.xml | Congenital Malaria with Atypical Presentation in a Preterm Neonate | A 16-day-old male child was admitted with complains of refusal to feed and poor activity. The baby was delivered at the gestational age of 32-34 weeks, in the same hospital by cesarean section. Activity, Pulse, Grimace, Appearance, respiration score at 1 min and 5 min was 7/10. The mother was primigravida. He had been admitted on 1st day of life for low birth weight (1,500 g) and poor activity. Rooting and Sucking reflex was poor. There was no organomegaly. The baby was not taking mother′s breast milk but was tolerating spoon feeding. Sepsis screen was negative and Hb% was 14 g%. The baby was treated with intravenous antibiotics and fluids for probable sepsis and was discharged after 4 days of admission on repeated requests of parents. The baby came in the out-patient department on 10th day of life for follow-up. The baby was still on spoon feeding and there was no weight gain (weight = 1,480 g). In order to find the cause of failure to gain weight in the baby, admission of the baby was advised, but parents refused. Hence, sepsis screen was performed on the out-patient basis and it came out to be negative. On present admission, the child was lethargic and was not tolerating even spoon feeding. Cry was very weak. Weight was 1,420 g. Pallor was marked. Except for mild tachycardia, vital signs were stable. On abdominal examination, hepatosplenomegaly was present. On 2nd day of admission, the baby developed icterus. The direct fraction of serum bilirubin (T = 9.6 mg/dl, D = 4.6 mg/dl, ID = 5.0 mg/dl) was elevated. The jaundice was pathological. Sepsis screen (total leukocyte count = 8500/mm3, platelet count = 96300/mm3, C-reactive protein = negative, band cells = 5%) was again negative. Hb% had decreased to 11 g%. The peripheral blood smear examination showed the presence of plasmodium vivax. A provisional diagnosis of CM was made. This prompted us to take the gestational history once again. The mother then gave a history of fever with chills at third trimester of pregnancy, for which she was treated with some drugs. The documented evidence of the laboratory reports and drugs were not available. Furthermore, the family was a resident of a malaria endemic area. The baby was treated with oral chloroquine at the standard cumulative dose of 10 mg/kg given in divided doses over 3 days. Blood transfusion with packed cell was also carried out. After completion of the course of chloroquine, the baby showed marked improvement in activity. The icterus disappeared. He started to take mothers breast milk normally. There was a decrease in spleen size. The baby was discharged on nutritional supplements and was on regular follow-up. After 1 month of discharge, the baby had significant weight gain (weight = 2,700 g), pallor subsided (hemoglobin% (Hb%) =17.6 g/dl), spleen was not palpable and the baby was active and playful and was on a full breast feeds. | [[16.0, 'day']] | M | {'21727650': 1, '9475682': 1, '17984408': 1, '17430603': 1, '17233887': 1, '23661831': 1, '24251259': 2} | {} |
164,175 | 3830151-1 | 24,251,260 | noncomm/PMC003xxxxxx/PMC3830151.xml | Solitary Crossed Renal Ectopia with Vesicoureteric Reflux Presenting with Impaired Renal Function in a Neonate | A 15-day-old male neonate was brought to us by parents with an antenatal ultrasound scan suggestive of right sided hydronephrosis and hydroureter. At the time of presentation, the general and systemic examination of the neonate was normal. His renal functions were deranged (blood urea nitrogen (BUN): 16.2 mmol/L [8.0-16.4 mmol/L] and serum creat: 331 μmol/L 50-110 μmol/L]). Patient was having grade V VUR. There were no associated, cardiovascular and vertebral abnormalities.\nRoutine urine examination revealed plenty of pus cells and urine culture showed growth of Escherichia coli. Ultrasound of abdomen showed right sided hydronephrosis with right upper hydroureter with non-visualization of the left kidney. There were mobile internal echoes in urinary bladder. Patient was catheterized perurethrally and urinary tract infection (UTI) was treated with intravenous antibiotics.\nRenal radionucleotide scintigraphy, technetium-99m-L, L-ethylenedicysteine (EC scan) was done which was suggestive of absent left kidney and incomplete pelviureteric junction obstruction on the right side with adequate cortical function [].\nAfter obtaining a sterile urine culture report, a voiding cystourethrogram (VCUG) was done. It revealed grade IV VUR into the left ureter. The VCUG showed the ureter crossing the midline and entering the kidney on the right side [Figure and ]. Magnetic resonance urography, done to confirm the anatomy, revealed a solitary right kidney with the ureter crossing midline and opening on the left side of urinary bladder along with presence of hydroureteronephrosis []. Diagnostic cystoscopy revealed absent right ureteric orifice and a wide left ureteric orifice with left hemitrigone confirming the diagnosis of SCRE.\nPatient was managed initially with conservative treatment (antibiotics and catheterization). Once renal functions improved (BUN: 8 mg/dL and serum creatine: 1.2 mg/dL), the patient was discharged on chemoprophylaxis. However, in view of breakthrough UTIs with VUR in a solitary functioning renal unit, ureteric reimplantation was done at 6 months of age. Patient is asymptomatic and renal functions are normal at follow of 16 months. | [[15.0, 'day']] | M | {'6164143': 1, '10663865': 1, '671645': 1, '10415306': 1, '3999200': 1, '19595632': 1, '13794746': 1, '25829677': 2, '19362344': 1, '5479708': 1, '9463293': 1, '28228880': 1, '2678982': 1, '1746088': 1, '26167315': 2, '24251260': 2} | {'4360465-1': 1, '4488548-1': 1, '4488548-2': 1} |
164,176 | 3830165-1 | 24,250,049 | noncomm/PMC003xxxxxx/PMC3830165.xml | Challenges in the management of a case of tuberous sclerosis | A 16-year-old adolescent male, a Sikh by religion and educated up to 2nd standard, belonging to a middle socio-economic status with non-vegetarian dietary habits was brought to our psychiatry outpatient department by parents with chief complaints of generalized tonic-clonic seizures since 2 years of age, low-intelligence since childhood and behavior problems like stubbornness and aggression since past 5-6 years.\nHistory of present illness revealed uneventful prenatal and perinatal course along with delayed motor, speech, and adaptive milestones. The patient had his first episode of grand-mal seizures at around 2 years of age and has been having them regularly since then but with variable frequency and duration. There has been no seizure free period since the onset of seizures. The patient started going to a school at around 6 years of age but discontinued studies after 2 years of age due to poor performance at school and being ridiculed by his peers for poor performance and for marks on his face. The patient would spend most of the time at his home playing with his younger siblings and occasionally playing with other younger children in his neighborhood. For the past 5-6 years the parents have noticed increasing behavior problems like stubbornness and not following parental instructions along with frequent episodes of verbal aggression and occasional episodes of physical aggression mostly directed towards parents and younger siblings generally when his wishes were thwarted or demands were not met.\nThe patient had been shown to many doctors ever since his seizures started and his treatment prescriptions showed that for past 1 year he had been taking orally sodium valproate 500 mg twice daily, phenobarbital 60 mg twice daily, carbamazepine 200 mg thrice daily, and clonazepam 0.5 mg twice daily. The family reported only a small decrease in seizure frequency even after taking these medications. There was no history of any co-morbid medical and surgical illness in the patient or any history of similar features in any of the family members.\nGeneral physical and systemic examination was within normal limits apart from the findings of facial angiofibromas [] in the facial region. His body weight was 65 kg. Mental status examination was suggestive of low cognitive profile and did not reveal any other psychopathology.\nComputed tomography scan and magnetic resonance imaging of the patient displayed multiple subependymal nodules and small multifocal discreet lesions in bilateral cerebral hemispheres suggestive of cortical and sub-cortical tubers [Figures and ]. Electroencephalogram (EEG) of the patient was non-specific.\nManagement of the patient was carried out keeping in mind the following objectives:\nControl of grand mal seizures through optimization of treatment regime Assessment of patient's cognitive abilities and achievement of optimum level of adaptive functioning according to patient's cognitive abilities Behavioral modification aimed at reduction of undesirable behaviors and promotion of adaptive and socially desirable behaviors Detection and timely treatment of other manifestations of tuberous sclerosis to prevent complications.\nAs part of the management plan, the patient's medications were optimized and he was started on a single anti-epileptic drug sodium valproate at the dosage of 1000 mg/day (15 mg/kg/day). The rationale behind this step was that the patient's current medications regime comprised of multiple anti-epileptics medications two of which were enzyme inducers, i.e., carbamazepine and phenobarbital, which were reducing the effective dose of sodium valproate as well as carbamazepine resulting in reduced plasma levels. It was decided to subsequently adjust the dose of sodium valproate during subsequent follow-ups and to increase the dose gradually depending on the patient's tolerability and response to a maximum of 60 mg/kg body weight. Valproate was increased to 2 g/day in divided doses. Though, the patient's seizure frequency decreased markedly on this dose but he was not completely seizure free. Any effort to increase the dose of valproate resulted in intolerable gastrointestinal (GI) side-effects. Therefore, clobazam 10 mg/day was added to valproate and this resulted in complete improvement of patient's seizures. Currently, he is seizure free for past 2 months.\nThe patient's cognitive assessment (for Intelligence Quotient (IQ) assessment first parents were interviewed for development behavior on “Vineland social maturity scale” and then child was evaluated first on “Seguin form board test” and then on “Colored progressive matrices.” For cognitive assessment “bender gestalt test” and “Weschler memory scale” were done) revealed an IQ of 45, i.e., moderate mental retardation and a mental age of approximately 7 years with relative strength in visual-spatial domain. Parents and family members were psycho-educated regarding the patient's limited cognitive abilities and to lower down their expectations from the patient to bring it in coherence with the patient's cognitive abilities. Behavior therapy was started to reduce the frequency and duration of undesirable behaviors and to promote desirable behaviors by using the principles of negative and positive re-enforcement. The patient was given remedial education and was started from his current level of knowledge. After 3 months of behavior therapy and remedial education, there was marked improvement in the patient's behavior as evidenced by reduced frequency and duration of anger episodes and reduced need for help in daily routine activities. By the end of 3 months, the patient was able to read road signs in English and Hindi and write his name in both the languages and was able to do simple addition and subtraction problems.\nThe patient also underwent following investigations: Complete hemogram, liver function tests, renal function tests, ultrasonogram whole abdomen, echocardiography, and ophthalmic examination including, retinal and fundus examination. This was carried out to detect any other systemic manifestations of tuberous sclerosis, which might need treatment. These investigations were within normal limits.\nA dermatological consultation was also carried out for the treatment of cosmetically disfiguring facial angiofibromas since that was adding to the social embarrassment of the patient. The patient was started on tacrolimus 0.1% w/w ointment for topical application on the affected area. This resulted in visible reduction in the facial angiofibromas. No major adverse effects were noted except transient burning sensation at the site of application. | [[16.0, 'year']] | M | {'15505165': 1, '15595939': 1, '21931059': 1, '2039137': 1, '11063078': 1, '15798777': 1, '17637444': 1, '15563009': 1, '15269473': 1, '21915260': 1, '18722871': 1, '17304050': 1, '17003820': 1, '24250049': 2} | {} |
164,177 | 3830166-1 | 24,250,050 | noncomm/PMC003xxxxxx/PMC3830166.xml | Augmenting amisulpride with clozapine had led to unmasking of akathisia | A 20-year-old man presented with akathisia with psychomotor agitation. He had a 5-year history of schizophrenia and was previously partially controlled on risperidone 6 mg with trihexyphenidyl 4 mg in two equally divided doses daily in the last 2 years. Then he was switched to amisulpride 200 mg twice daily, that initially controlled the akathisia and agitation symptoms. However, this dose of amisulpride (400 mg in two divided doses) for 2 months did not achieve full symptom remission although he was better than before with akathisia remitted and psychomotor agitation controlled but still had disorganized behavior, fleeting delusion and hallucination. In an attempt to achieve complete symptom remission the patient was switched to amisulpride 200 mg thrice daily (600 mg/day) for next 6 weeks. Unfortunately, the patient did not achieve any further symptom remission, but did not deteriorate either. At this juncture, clozapine was definitely a strong choice. However, as the patient has already partially responded to amisulpride without much side-effect and amisulpride augmentation of clozapine is a proven effective procedure,[] to achieve further clinical improvement this augmentation strategy were thought of. Here reverse augmentation strategy i.e., to augment amisulpride with clozapine (25 mg to start with, which then escalated to 75 mg with 25 mg increments every 3 days) was tried, with an expectation of achieving symptom remission, as these two medicines may have synergistic effect. However, within 2 weeks this patient presented severe akathisia, restlessness, hypertonia along with sialorrhoea and tachycardia. These were managed with propranolol 120 mg and trihexyphenidyl 4 mg, but with modest success for 1 week. As clozapine was the medication last introduced, it was withdrawn and the patient continued the other medications, i.e., amisulpride 600 mg/day in three divided doses along with propranolol 120 mg and trihexyphenidyl 4 mg. Moderate improvement of akathisia and agitation symptoms was noted after 1 month, but it did not reach the base level, which were present before start of clozapine. Sialorrhoea was completely subsided on this regime. In order to achieve total side effect remission, amisulpride was completely withdrawn under the cover of lorazepam 6 mg and propranolol 120 mg. In another 2 weeks, akathisia symptoms drastically remitted but psychotic symptoms like aggressiveness, disorganized speech and behavior, use of abusive language severely increased.\nIt is known that clozapine has one of the least tendencies to cause akathisia symptoms on its own[] and withdrawal of clozapine did not remit akathisia and agitation completely, led to a hypothesis that it may not be clozapine per se, but its interaction with amisulpride might be instrumental in generation of the akathisia symptoms. So it was decided to give clozapine as a mono therapy a try, as it is a proven effective agent in treatment resistant schizophrenia. Hence clozapine was reintroduced without amisulpride at 50 mg/day, which was increased to 150 mg/day with small increments of 25 mg weekly. This regime showed very significant symptom control without any akathisia, along with propranolol 120 mg and lorazepam 4 mg. Even after slow withdrawal of supportive medications like propranolol and lorazepam the patient maintained effective symptom control without any akathisia or other unwanted side effect. | [[20.0, 'year']] | M | {'14750045': 1, '11772117': 1, '25878393': 2, '10823308': 1, '15667440': 1, '16160629': 1, '15056484': 1, '34239749': 2, '18203048': 1, '21845006': 1, '24250050': 2} | {'4386142-1': 1, '8235956-1': 1, '8235956-2': 1, '8235956-3': 1} |
164,178 | 3830168-1 | 24,250,052 | noncomm/PMC003xxxxxx/PMC3830168.xml | Tokophobia: A dread of pregnancy | A 43-year-old married housewife of high socioeconomic status presented to the psychiatry out-patient department with a 2 years history of morbid dread of pregnancy. This started 2 years after marriage when she contacted a gynecologist for menstrual irregularity. She asked the physician about the complications of pregnancy. On hearing the dreaded complications like having a deformed fetus, change in body figure, eclampsia, caesarean, and even death, she developed excessive fear of pregnancy. When also informed that no contraceptive method is fully protective, she started avoiding sexual contact with husband. On stopping all sexual activity, she gradually developed sad mood, hopelessness, helplessness, worthlessness, difficulty in falling asleep, weeping spells, loss of appetite and suicidal ideation. She also started having less interaction with husband, parents, and other relatives. Even after being counseled by relatives and two obstetricians, she could not get rid of the fear of pregnancy. There was no past or family history of mood disorder, schizophrenia, epilepsy, or drug dependence. Her vitals, routine investigations, and physical examination were normal.\nOn mental state examination, she was a tidy, cooperative lady of pyknic build. There were no disturbances in orientation or memory. Her mood was sad with reduced psychomotor activity and monotonous low volume speech. There were ideas of hopelessness and worthlessness and also, feeling of guilt and suicidal ideation. There was no formal thought disorder. Insight and judgment were intact.\nShe was diagnosed as a case of tokophobia with major depressive disorder. She was started on fluoxetine, 20 mg once daily and clonazepam 0.5 mg at night and counseling (including psycho education) weekly for about 2 weeks but there was no improvement. The dose of fluoxetine was increased to 40 mg daily and over the next 4 weeks, there was reduction in her morbid fear of pregnancy along with symptoms of depression. She started having normal sexual activity. At follow-up after 3 months while still on medication, there was no recurrence of symptoms. | [[43.0, 'year']] | F | {'12051188': 1, '10661607': 1, '34429733': 1, '10789333': 1, '9435734': 1, '12138933': 1, '8883751': 1, '13679545': 1, '12694113': 1, '11264605': 1, '10776242': 1, '24250052': 2} | {} |
164,179 | 3830236-1 | 24,250,088 | noncomm/PMC003xxxxxx/PMC3830236.xml | Metastasis of lung adenocarcinoma to the mandible: Report of a case | A 55-year-old white man, presented with an 8 week history of pain and non-fluctuant swelling at right submandibular area []. He had his right molar tooth extracted and a partial denture was made 10 years ago. One month before our examination, he had a swelling on the affected site and he was prescribed 300 mg clindamycin phosphate IM antibiotics for 5 days by his general dentist. Previous to this, he had paresthesia in the right lower lip for 3 days. Otherwise, the patient had no important medical history. He did not take any systemic medications regularly.\nExtraoral physical examination revealed a right mandibular swelling involving the ramus and the body. Vital signs were normal with hydrated skin and no neck adenopathy present.\nThe intraoral physical examination revealed anesthesia over the peripheral distribution of the inferior alveolar nerve on the affected side with decayed lower and upper canines. The intraoral mucosa was intact and a smooth surfaced non-tender lesion measuring about 2 × 2 cm was noted in the right mandibular premolar-molar area. The orthopantomography showed an ill-defined radiolucent osteolytic lesion of the right molar region under the inferior alveolar canal [].\nThe lesion has an irregular radiolucent area mimicking a dentoalveolar infection located in the corpus of the mandible just below the mandibular canal in the radiographical evaluation.\nThe incisional biopsy under local anesthesia was performed and a histopathological diagnosis of low differentiated adenocarcinoma of the mandibule was given. It was stated in histopathological report that there was a malignant tumoral tissue consisting of solid islands composed of atypical epithelial cells in desmoplastic stroma []. Nuclear pleomorphism in the tumoral islands was marked and cytoplasmic small vacuoles were seen []. This tumoral configuration is compatible with poorly differentiated adenocarcinoma. However, this morphology is not common in oral cavity tumors, including salivary gland tumors. For this reason, it was thought that the tumor was primarily metastatic. This high-degree adenocarcinoma was thought to be originated from the lung, gastrointestinal system, or breast. However, breast was excluded because the patient was male. Classical colorectal carcinoma morphology[] was not seen in this tumor but glandular morphology of gastric adenocarcinoma was more evident. The focus of this tumor was thought to be primarily lung according to the solid island configuration and focal cytoplasmic vacuolization.\nAfter obtaining the report of the biopsy, the patient had consulted the medical oncology department whereour histopathological diagnosis of lung cancer was approved. There was a mass on the left upper lobe of the lung in posteroanterior chest radiogram []. Enlarged aorticopulmonary, subcarinal, left hilar lymph nodes and a mass on superior segment of the left upper lobe of lung on a thorax computed tomography was noted []. However, the patient refused treatment of lung cancer for 1 year. On September 8, 2006, the patient appealed to medical oncology department because his condition became worse. Etoposide 50 mg/day for 21 days, ondansetron 8 mg 3 × 1 IV/po, or granisetron 3 mg 2 × 1 IV/po, or tropisetron 5 mg 1 × 1 IV/po as chemotherapy was initiated but unfortunately, the patient died 5 months after the start of the chemotherapy. | [[55.0, 'year']] | M | {'18061527': 1, '26980970': 2, '20031269': 1, '15337187': 1, '23196066': 1, '25756018': 1, '25999632': 2, '16940489': 1, '12576032': 1, '19464643': 1, '16473498': 1, '9327288': 1, '30567274': 1, '24250088': 2} | {'4430894-1': 1, '4774295-1': 1} |
164,180 | 3830238-1 | 24,250,090 | noncomm/PMC003xxxxxx/PMC3830238.xml | Centroblastic variant of diffuse large B-cell lymphoma: Case report and review of literature | A 55 year old male patient reported to the dental hospital in the year 2007 with a complaint of painless swelling in the lower right body of the mandible for the last 4 months. The swelling was insidious in onset and gradually increased in size. Facial asymmetry was seen on the right side. Examination revealed a nontender, solitary diffuse swelling measuring 3.5 cm × 3.5 cm in the lower right body of the mandible. The swelling was fixed, firm to hard in consistency. Intraorally, the swelling extended from 44 to 48 regions obliterating the buccal vestibule, with buccal cortical plate expansion. Computed tomography (CT) of mandible showed an osteolytic lesion with soft tissue density in the right body of the mandible at the mental foramen region with break in the cortical plates both on buccal and lingual side []. Incisional biopsy showed the lesion to be composed of abnormal large lymphoid cells with high nuclear cytoplasmic ratio. These large lymphoid cells were arranged in diffuse pattern, with the large cells having coarse chromatin and inconspicuous nucleoli []. Mitotic figures were also evident. The above mentioned findings favored the diagnosis of DLBCL.\nInvestigations like chest X-ray, ultrasonography of abdomen and pelvis, and bone scan of whole body were done. Bone scan showed minimal increase in uptake in the right mandible anteriorly indicating slow bone destruction. There was no evidence of distant bone involvement. Clinical examination and investigations classified the disease under stage IAE. Following this, immunohistochemical analysis was done for the expression of pan B-cell markers like CD45 (leukocyte common antigen), CD20 (selective marker that recognizes a subpopulation of B-cells), and CD3 (marker for T-cells and natural killer cells). CD45 [] and CD20 [] were positive and CD3 was negative. Based on immunohistochemistry report the lesion was diagnosed as DLBCL of the mandible. Centroblastic, immunoblastic, T-cell/histiocytic-rich, anaplastic, and plasmablastic variants are the five histopathological subtypes of DLBCL according to WHO classification.[] Histopathological examination of our case revealed centroblastic variant of DLBCL with few immunoblast like cells. Centroblasts are large noncleaved cells, with round to oval centrally placed nuclei and peripherally located nucleoli []. They have moderate to scanty cytoplasm with fragmentation of nucleoli being quite common among these cells. Based on histopathological examination and immunohistochemistry study, the following lesions under differential diagnosis were ruled out; Hodgkin's lymphoma, large cell lymphoma of T-Cell type, Burkitt's lymphoma, follicular lymphoma, undifferentiated carcinoma, and amelanotic melanomas.\nBased on the final diagnosis, chemotherapy was advised by the oncologist and a total of six cycles were suggested at the gap of every 3 weeks. The treatment regimen followed was that of cyclophosphamide, hydroxydoxorubicin, oncovin, and prednisone (CHOP) therapy comprising of cyclophosphamide, doxorubicin, vincristine, and prednisolone. Patient is being examined periodically once in 2 months and he has had no recurrences from past 3 years and is disease free.\nNHL arises primarily within the lymph nodes; however extranodal presentations are common in patients with NHL. Oral manifestations presented in only 3-5% of cases of NHL and are rarely the initial manifestation of the disease.[]\nOf the NHLs that occur in the oral cavity, 15-45% occur in the maxilla and mandible.[] A review of oral NHL shows upper jaw maxilla (11%), mandible (8%), palatal soft tissue (8%), vestibule, and gingiva (7%) to be the most common locations.[] Isolated mandibular NHL accounts for only 0.6% of the cases reported. Such cases when occur commonly mimic odontogenic infections leading to delay in diagnosis and therapy for the patients. To be classified as a primary NHL of bone there must be no evidence of visceral or lymphatic involvement and no distant metastases for at least 6 months following diagnosis.[] The peak incidence for primary NHL of jaws is in the 4th-5th decade. Equal sex distribution is usually reported with few cases showing female predominance.[] Mandibular NHL may involve any site with Gusenbauer et al.,'s series involving the body of the mandible followed by ramus, angle and symphysis region.[] In our case, the patient had undergone extraction, following which he developed a nontender swelling in the right mandibular body. Some authors reported paresthesia (about 20-100% ofcases) along the inferior alveolar nerve to be common in NHL involving the mandible.[]\nThere are no pathognomonic radiographic features for NHL involving the mandible. Features of osteolysis are usually suggestive with other radiological findings of destruction of the alveolar bone, diffuse trabecular pattern, mottling appearance, and resorption of roots of teeth. CT scan of our case showed an osteolytic lesion with soft tissue density in the right body of mandible at the mental foramen region with break in the cortical plates involving both buccal and lingual cortical sides. Histology coupled with immunophenotyping and cytogenetic evaluation can suggest the subtypes of NHL and thus help in rendering prompt treatment and aid in better survival rates of lymphoma patients.\nThe primary NHL involving the mandible for most of the times is of intermediate to high grade malignancy although it tends to remain localized at times of diagnosis with stage IAE presentation.[]\nDLBCL constitutes a heterogeneous group of lymphoid neoplasm's that is characterised by diverse spectrum of clinical and morphological features, response to therapy and survival. Morphologically DLBCLs replace the normal architecture of lymph nodes in a diffuse pattern. Neoplastic cells are at least twice the size of normal lymphocytes with vesicular nuclei, prominent nucleoli, and basophillic cytoplasm.[] DLBCL may be arising de novo, or as a primary tumor or as a result of transformation of a less aggressive lymphoma of lower grade such as lymphocytic, follicular, or marginal lymphoma.[]\nTwenty-eight percent of DLBCL's depict chromosomal translocations and molecular rearrangements such as translocation of t (14;8) (q32;q21) involving the Bcl-2 gene. Several classification systems have categorized DLBCL into its morphologic and phenotypic variants in the past.\nWHO Revised European American Lymphoma (REAL) classification of NHL according to clinical aggressiveness; groups DLBCL under the aggressive lymphomas.[]\nThe 2001 WHO classification being an update of REAL classification is given below.[]\nDLBCL subtypes according to 4th edition of the WHO classification of tumors of the hemopoietic and lymphoid tissues.\nCentroblastic Immunoblastic Anaplastic\nMolecular subgroups\nGerminal center B-cell like (GCB) Activated B-cell like\nImmunohistochemical subgroups\nCD5-positive DLBCL GCB Non-germinal center B-cell like (non-GCB)\nDLBCL subtypes/entities\nPrimary mediastinal (thymic) large B-cell lymphoma T cell/histiocyte rich large B-cell lymphoma Intravascular large B-cell lymphoma Primary DLBCL of the central nervous system (CNS) Primary cutaneous DLBCL, leg type DLBCL associated with chronic inflammation Anaplastic lymphoma kinase (ALK) positive DLBCL Large B-cell arising in human herpes virus (HHV) 8-associated multicentric Castleman disease Plasmablastic lymphoma and primary effusion lymphoma\nB-cell lymphoma, unclassifiable with features intermediate between DLBCL and Burkitt's lymphoma.\nB-cell lymphoma unclassifiable, with features intermediate between DLBCL and classical Hodgkin lymphoma.\nHistopathologically, our case was diagnosed as centroblastic variant having medium to large sized lymphoid cells with oval to round vesicular nucleus with fine chromatin and 24 membrane bound nuclei, the cytoplasm being amphophillic to basophilic. The tumor represented a monomorphic pattern with more than 90% comprising of centroblastic cells. Centroblastic DLBCL being the most common variant is composed of cells that resemble their normal counterparts in the reactive germinal centers.[] Variable number of immunoblasts may be found admixed, but generally comprises less than 90% of the tumor cell population.[]\nHistopathology, immunohistochemistry, immunophenotyping, and genetic studies help to categorize DLBCL further, in order to direct a specific regimen of therapy. DLBCL usually express pan B-cell markers such as CD19, CD20, CD75, CD79a, PAX5, and CD22; but may lack one or more of these. Surface and or cytoplasmic immunoglobulins (IgM > IgG > IgA) can be demonstrated in 50-75% of cases.[] CD20 expression by B-cells from mature precursor B-cell until the preplasma cell stage of differentiation is highly specific for B-cell lineage and mostly DLBCL show homogeneously bright staining for this as seen in our case.[]\nBcl-6 is selectively expressed by germinal center B-cell like GCB cells in normal lymphoid tissues and in DLBCL at about 57-100%, but with unclear biological significance with reports suggesting Bcl-6 expression related to oncogenesis.[]\nPatients with DLBCL have variable clinical courses and prognosis depending on many clinical, morphological, phenotypic, and genetic parameters. International prognostic index (IPI) is widely used as a predictive model in DLBCL patients of all ages and clinical stages. The IPI combines patient's age with easily measured clinical parameters which can serve as surrogate markers of tumor burden. Performance status, extranodal involvement, serum lactate dehydrogenase levels, stage of disease, and Bsymptom status are significantly associated with survival.[]\nA 5 year disease free survival was 53.2% for patients with centroblastic and 26.9% for patients with immunoblastic NHL.[] Patients with germinal center B-cell like lymphoma had the highest 5 year survival rate. DLBCLs of germinal center B type have a better prognosis than those derived from activated B-cell type.[]\nEarly stage disease care in DLBCL patients involves either chemotherapy alone or a combination of chemotherapy and radiotherapy. The chemotherapy usually involves three cycles of CHOP. The role of surgery is severely limited in treatment of DLBCL. Current treatment of DLBCL usually begins with multiagent chemotherapy, typically CHOP as done in our present case with 6 cycles of CHOP.[] Recently, anti-CD20 monoclonal antibody (rituximab) has been added to this regimen and has been found to improve failure-free survival.[] With the well-accepted addition of rituximab to the typical large B-cell lymphoma chemotherapeutic regimen, a revalidation of any survival differences between large B-cell lymphoma subtypes is necessary. So far, only a few studies have been published and we need more investigations in this field.[]\nLocalized (stage 1 and stage II) low grade extranodal lymphomas in the head and neck are treated primarily with radiation therapy. Patients with localized intermediate grade lymphomas should be treated with combination chemotherapy as done in our case. There is evidence that CHOP regimen could be curative for this subset of patients. Radiation therapy alone was the mainstay of treatment for these disorders until curative combination chemotherapies were developed. High grade and advanced stage NHL should be treated with aggressive chemotherapy regimen.[]\nTreatment options with combination chemotherapy alone CHOP had no recurrences seen in patients with NHL similar to our case.[] | [[55.0, 'year']] | M | {'12402391': 1, '16129841': 1, '17604660': 1, '9413361': 1, '20533006': 1, '19642739': 1, '9331243': 1, '1447619': 1, '16012407': 1, '26261675': 1, '19097355': 1, '21892315': 2, '2179495': 1, '6584818': 1, '24250090': 2} | {'3161690-1': 1} |
164,181 | 3830239-1 | 24,250,091 | noncomm/PMC003xxxxxx/PMC3830239.xml | Primary systemic amyloidosis of tongue with chondroid metaplasia | A 26-year-old male, who is an iron molding laborer, was diagnosed with multiple myeloma in 2007. He was managed with thalidomide, dexamethasone, external beam radiotherapy to pelvis, and analgesics. He underwent autologous peripheral blood stem cell transplant in 2010.\nTwo years later, in January 2012, he presented with dysphagia and dysarthria.\nClinical examination showed two nodules measuring 2 cm on either side of hard palate. Whole tongue was enlarged, hard with multiple nodules extending from the tip to the base of tongue and further down. Regional lymph nodes were not enlarged. Laboratory investigations revealed anemia, raised serum creatinine, and kappa light chain levels. Other parameters were within normal limits.\nIncisional biopsy was done from one of the nodular lesions in the tongue with the diagnostic possibilities of carcinoma tongue/myeloma infiltration. Histopathology showed tissue lined by hyperplastic squamous epithelium with subepithelial deposits of eosinophilic amorphous material admixed with chondroid areas [Figures and ]. Congo red staining showed apple green birefringence of eosinophilic amorphous material in polarizing microscopy, thus confirming the presence of amyloid []. Bone marrow biopsy was done which showed sheets of immature plasma cells []. | [[26.0, 'year']] | M | {'31965113': 1, '11535160': 1, '19550104': 1, '7598857': 1, '18462447': 1, '3459126': 1, '20107570': 2, '6724579': 1, '9256271': 1, '1745517': 1, '24250091': 2} | {'2809435-1': 1} |
164,182 | 3830240-1 | 24,250,092 | noncomm/PMC003xxxxxx/PMC3830240.xml | Chondrosarcoma of the maxilla: A case report and review of literature | A 29-year-old male patient was referred to our department for evaluation and treatment of a swelling in the left anterior maxillary region. The patient complained of a slow growing swelling over the left cheek which had increased over a period of 1 year. The patient had noticed an intraoral swelling 25-30 days back for which he had consulted his dentist. He also noted teeth displacement over a period of 1 year. The patient denied any history of trauma and was asymptomatic.\nThe patient's medical and family history was unremarkable. He had the habit of chewing tobacco and areca nut since 5 years. Clinical examination revealed a diffuse swelling on the left side of the face extending from the ala of the nose up to the zygomatic region measuring approximately 3 × 3 cm. On palpation, the swelling was hard with defined borders. The overlying and adjacent skin was normal; no regional lymphadenopathy was noted.\nOn intraoral examination, an irregular lobulated swelling was noted involving the entire left side of the palate, which had crossed the midline []. Labially the swelling extended from 21 to 24 with obliteration of the labial vestibule; the teeth in this region were displaced with mobility in relation to 21 and 22. The consistency was firm to hard and the mucosa was intact.\nWater's view showed a well-corticated radiolucent lesion destroying the inferior border of the maxillary sinus on the left side. A mixed lesion was seen in 22 and 23 region in continuity with the above mentioned lesion. Intraoral periapical radiographs showed displaced teeth i.r.t 21, 22, and 23. Computed tomography (CT) imaging showed an irregular soft tissue mass causing osteolytic destruction of left upper maxillary alveolus, floor and lateral wall of left maxillary sinus, medial wall of right maxillary sinus, and posteromedial part of right orbit [].\nThe differential diagnosis included odontogenic tumors since lesions like adenomatoid odontogenic tumor are common in this location and present a mixed appearance radiographically and therefore was considered. The clinical features such as displacement and mobility of teeth and the radiographic extent of the lesion suggested that it may be a non-odontogenic tumor of the bone.\nFine needle aspiration biopsy smears showed a matrix dominated lesion with moderate cellularity. The matrix was chondromyxoid in nature. Cells either single or in groups were embedded in the matrix. The cells showed abundant to moderate amounts of well-defined cytoplasm. The cytoplasm was eosinophilic and vacuolated. Binucleation and trinucleation was seen. Moderate degree of nuclear pleomorphism was noted. Some cells showed large nuclei with increased nuclear cytoplasmic ratio. Cartilage with cells in lacunae were not seen []. In view of the clinical and radiological data, a diagnosis favoring well-differentiated chondrosarcoma was offered. Following this, an incisional biopsy was carried out. | [[29.0, 'year']] | M | {'28035300': 1, '27066425': 1, '34522670': 2, '8635057': 1, '3131505': 1, '26722246': 1, '25519205': 2, '34458183': 2, '24908254': 1, '19881362': 1, '25386536': 1, '3688300': 1, '2003006': 1, '20614285': 1, '24250092': 2} | {'4301862-1': 1, '8407635-1': 1, '8387074-1': 1} |
164,183 | 3830241-1 | 24,250,093 | noncomm/PMC003xxxxxx/PMC3830241.xml | Monostostic fibrous dysplasia with nonspecific cystic degeneration: A case report and review of literature | A 40-year-old female patient reported to our college, with a chief complaint of swelling in the lower right and left posterior teeth region since 6 years. The swelling was asymptomatic. Her medical history was noncontributory. Extraoral examination revealed a swelling on the right posterior region of the mandible. The swelling extended anteroposteriorly 1.0 cm from the commissure to 4.0 cm in front of the angle of the mandible and superoinferiorly 1.0 cm above the lower border of the mandible to 0.5 cm from the commissural line and measured 4.0 × 3.0 cm in dimension. It was ill-defined, hard, and nontender; with overlying normal skin []. Intraorally, the swelling extended from the mesial aspect of 44 to the distal aspect of 47 with slight obliteration of the buccal vestibule. The lingual cortex showed slight expansion. The overlying mucosa was stretched but intact.\nExtraoral examination revealed a diffuse swelling on the left lower border of the mandible extending 2.0 cm behind the angle of the mouth to 5.0 cm from the angle of the mandible and measured 3.0 × 2.0 cm in dimension, was hard and nontender with overlying normal skin []. Intraorally, the swelling extended from mesial aspect of 34 to distal aspect of 37 with no obliteration of the buccal vestibule. The overlying mucosa was normal. Submandibular lymph nodes were palpable on both sides, solitary, mobile, and nontender.\nThe orthopantomograph showed a well-defined multilocular radiolucency with specks of radiopacity in the right and left posterior mandible. Radiolucency extended from 43 region to the ramus of the mandible on right side and from 34 to 37 region on the left side of the mandible, 36 was missing. The lower border of the mandible was intact [].\nOcclusal radiograph showed expansion of the buccal and lingual cortices on both right and left side of the mandible. Ground glass appearance of the mandible was visible []. Computed tomography (CT) scan revealed well-defined lytic lesion with radiopacities involving right and left posterior mandible region with buccal and lingual cortical expansion [].\nRoutine blood and urine investigations along with serum examination for alkaline phosphatase activity and calcium profile were performed and the values were within normal limits.\nUnder general anesthesia, a degloving incision was placed on the right side and the lesion was surgically recontoured. The lesional tissue did not separate out from the bone easily. The same procedure was followed on the left side and cystic cavities were seen which were empty [] and the lesion did not separate out easily. Hemostasis was achieved, betadine wash given, and primary closure was achieved. Specimens were submitted for histopathological examination with a clinical diagnosis of fibro-osseous lesion. Patient was kept under postoperative observation and recovered without any postsurgical complications. The healing was uneventful. | [[40.0, 'year']] | F | {'20614314': 1, '14824189': 1, '14263965': 1, '8336219': 1, '2797736': 1, '5770409': 1, '14569813': 1, '12703030': 1, '31321219': 2, '16085630': 1, '9403710': 1, '10503865': 1, '19895712': 1, '32995343': 2, '30510951': 2, '24250093': 2} | {'6561353-1': 1, '6264999-1': 1, '7494708-1': 1} |
164,184 | 3830242-1 | 24,250,094 | noncomm/PMC003xxxxxx/PMC3830242.xml | Leiomyoma: A rare tumor in the head and neck and oral cavity: Report of 3 cases with review | A 25-year-old female patient reported to out-patient department with a chief complaint of swelling in the right lower portion of the ear since 6 months. The swelling was painless, asymptomatic, slow growing and esthetically unacceptable for the patient.\nThe swelling was solitary, ovoid in shape, involving the right ear lobe, measuring about 1.5 cm × 1 cm, covered by normal appearing skin, which was stretched and mobile. It was firm in consistency having well-defined margins. Trans-illumination test was negative [].\nSurgical resection was planned with an excisional biopsy. An elliptical incision was placed and the lesion was excised under local anesthesia []. The post-operative period was uneventful with 1 year follow-up and there was no sign of recurrence.\nThe tissue specimen showed a non-encapsulated and well-circumscribed lesion. The cells were arranged in whorls and fascicles []. The cells were spindle shaped with eosinophilic cytoplasm and centrally located basophilic, cigar shaped nucleus. Prominent vascular spaces were seen. There was no evidence of nuclear atypia between the smooth muscle bands; or necrosis or hemorrhage. Thus, the histological diagnosis of solid variant of leiomyoma was made. | [[25.0, 'year']] | F | {'13520698': 1, '29696477': 1, '34083983': 2, '29238412': 2, '34106410': 1, '29375922': 2, '2358952': 1, '6722737': 1, '27668116': 2, '27162753': 2, '22238716': 1, '32148989': 2, '28500121': 1, '9135966': 1, '34352902': 1, '28439152': 1, '21731289': 2, '28913307': 2, '27887011': 1, '18581112': 1, '11688572': 1, '12221390': 1, '17909665': 1, '29386803': 2, '1122481': 1, '24250094': 2} | {'3830242-2': 2, '3830242-3': 2, '8123251-1': 1, '3125644-1': 1, '4860377-1': 1, '4860377-2': 1, '5030417-1': 1, '5767993-1': 1, '5742511-1': 1, '7053474-1': 1, '5712643-1': 1, '5556748-1': 1} |
164,185 | 3830242-2 | 24,250,094 | noncomm/PMC003xxxxxx/PMC3830242.xml | Leiomyoma: A rare tumor in the head and neck and oral cavity: Report of 3 cases with review | A 24-year-old female patient reported to out-patient department with a chief complaint of growth on the right pinna and ear lobule since 3 months. Two separate growths were seen associated with pinna and lobule of the right ear respectively; both of which were painless and had a gradual onset.\nClinical examination showed ovoid swellings measuring 2 cm × 1 cm and 1 cm × 1 cm respectively with well-defined margins []. Overlying skin appeared normal. Swellings were firm in consistency, non-tender and did not elicit fluctuation or translucency. The lesions appeared to be fixed to the underlying cartilage.\nMedical history and family history was not contributory and thus syndromic or hereditary association was ruled out.\nSurgical resection of both swellings was performed under local anesthesia. Resected specimens were sent for histopathological examination. Regular follow-up for a period of 3 years did not show any signs of recurrence.\nThe histopathological examination of the hematoxylin and eosin stained slides showed moderately cellular lesional tissue comprising of spindle cells with indistinct cytoplasmic membrane and nuclei having blunt ends []. Both longitudinal areas running in fascicles (hypercellular) and cross-sectional areas (hypocellular) were evident with numerous endothelial lined blood vessels []. There were no features of cellular atypia or necrosis. Thus, a histological diagnosis of solid variant of leiomyoma was given. | [[24.0, 'year']] | F | {'13520698': 1, '29696477': 1, '34083983': 2, '29238412': 2, '34106410': 1, '29375922': 2, '2358952': 1, '6722737': 1, '27668116': 2, '27162753': 2, '22238716': 1, '32148989': 2, '28500121': 1, '9135966': 1, '34352902': 1, '28439152': 1, '21731289': 2, '28913307': 2, '27887011': 1, '18581112': 1, '11688572': 1, '12221390': 1, '17909665': 1, '29386803': 2, '1122481': 1, '24250094': 2} | {'3830242-1': 2, '3830242-3': 2, '8123251-1': 1, '3125644-1': 1, '4860377-1': 1, '4860377-2': 1, '5030417-1': 1, '5767993-1': 1, '5742511-1': 1, '7053474-1': 1, '5712643-1': 1, '5556748-1': 1} |
164,186 | 3830242-3 | 24,250,094 | noncomm/PMC003xxxxxx/PMC3830242.xml | Leiomyoma: A rare tumor in the head and neck and oral cavity: Report of 3 cases with review | A 48-year-old male patient was referred to our department with a chief complaint of swelling in relation to right upper molar teeth since 2 months.\nOn examination, a solitary swelling was noted on the right side of the posterior palate associated with right upper second premolar and first molar measuring 1 cm × 1.5 cm. Overlying mucosa was pale pink in color and appeared normal. The swelling was a sessile, firm, dome shaped mass fixed to the underlying tissues [].\nAspiration biopsy was performed, which ruled out a vascular lesion. Radiographic picture showed no changes associated with underlying bone. The lesion was provisionally diagnosed as a minor salivary gland tumour. Excisional biopsy was performed and excised mass was sent for histopathologic examination [].\nThe lesional tissue present in the deeper stroma was well-circumscribed and non-encapsulated and the cells were arranged in a streaming pattern around the blood vessels []. They formed whorls, which were separated by collagen bands. Numerous vascular spaces were seen surrounded by proliferating spindle cells []. The lesional cells were spindle in shape with blunt ended nucleus and had a moderate amount of cytoplasm with indistinct outline. There was no evidence of mitosis or necrosis. Thus, a diagnosis of angioleiomyoma was made.\nNote: Special stains were done using Mallory's Phosphotungstic Acid-Hematoxylin for all the above three cases and the cells exhibited dark blue intracytoplasmic fibrils []. Masson trichrome staining exhibited smooth muscle cells (pink) in longitudinal and transverse sections with intervening collagen fibers (blue) [Figures –]. | [[48.0, 'year']] | M | {'13520698': 1, '29696477': 1, '34083983': 2, '29238412': 2, '34106410': 1, '29375922': 2, '2358952': 1, '6722737': 1, '27668116': 2, '27162753': 2, '22238716': 1, '32148989': 2, '28500121': 1, '9135966': 1, '34352902': 1, '28439152': 1, '21731289': 2, '28913307': 2, '27887011': 1, '18581112': 1, '11688572': 1, '12221390': 1, '17909665': 1, '29386803': 2, '1122481': 1, '24250094': 2} | {'3830242-1': 2, '3830242-2': 2, '8123251-1': 1, '3125644-1': 1, '4860377-1': 1, '4860377-2': 1, '5030417-1': 1, '5767993-1': 1, '5742511-1': 1, '7053474-1': 1, '5712643-1': 1, '5556748-1': 1} |
164,187 | 3830243-1 | 24,250,095 | noncomm/PMC003xxxxxx/PMC3830243.xml | Concurrent occurrence of adenoid cystic carcinoma of the salivary glands with small cell carcinoma of the liver: A rare case report | A 28-year-old female was referred from the surgical department of our college with a swelling in the cheek for the duration of 1 month.\nHer medical history revealed that she was diagnosed of SCC of liver confirmed by radiographic, histopathologic, and immunohistochemical investigations; 3 months earlier.\nPatient presented a diffuse swelling of about 2 cm in the left cheek region extraorally below the zygomatic area [].\nExtraoral clinical examination showed that the swelling had indistinct limits and there were no surface alterations of the skin over the growth. Palpation of the left side of the cheek identified a firm, nontender mass that was subcutaneously mobile; but partly attached to the underlying structures. The skin covering the tumor was normal. Intraoral examination showed normal mucosa without any surface changes. The mass was palpable from intraoral aspect and was not attached to the mucosa. Initial clinical diagnosis of metastatic tumor in the oral cavity was made. Subsequently, biopsy was performed in the cheek region.\nOral biopsy specimen showed islands with basaloid, medium cells with oval hyperchromatic nuclei, distinct nucleoli, and scanty eosinophilic cytoplasm. Atypia was mild to moderate. The subsequent deeper section showed evidence of few cribriform islands with eosinophilic coagulum. The lumina of the islands are surrounded by cells with eosinophilic cytoplasm. Moreover, rare small cysts and pseudo glandular structures filled with mucous material were seen. In addition to cribriform pattern [], there were also islands of basaloid, hyperchromatic cells were evident in tissue sections.\nThe histopathology of liver biopsy was in favor of SCC [Figure and ]. Since the oral biopsy showed areas of ACC, to confirm the diagnosis, the tissue sections were subjected to immunohistochemistry. The markers used were cytokeratin (CK)-5-6, high molecular weight CK anitbody (HMWA), vimentin, S-100, smooth muscle actin (SMA), Bcl2, neuron specific enolase (NSE), synaptophysin, and c-KIT (CD 117) and CD 10 to differentiate ACC from SCC and other salivary gland tumors. Immunohistochemically, tissue section from the cheek region reacted strongly with anticytokeratin antibodies such as CK5-6 [], including high molecular weight antibody (HMWA), vimentin, S100 [], Bcl2, c-KIT, CD 10 and Anti SMA whereas neuroendocrine markers such as synaptophysin, and NSE did not show positivity. | [[28.0, 'year']] | F | {'27407943': 1, '12118104': 1, '14694981': 1, '11914618': 1, '15542802': 1, '15545668': 1, '16325513': 1, '9374223': 1, '18159605': 2, '18091382': 1, '11870247': 1, '25328295': 1, '29492062': 1, '208752': 1, '19669327': 1, '24250095': 2} | {'2628196-1': 1} |
164,188 | 3830244-1 | 24,250,096 | noncomm/PMC003xxxxxx/PMC3830244.xml | Cartilaginous choristoma of tonsil: A hidden clinical entity | A 24-year-old male presented to the Ear, Nose, and Throat (ENT) Department with history of recurrent sore throat, pain, fever, and painful swelling. On examination, tonsils were persistently enlarged and white flakes were present on the tonsil. A clinical diagnosis of tonsillar keratosis was made. Tonsillectomy was performed and the specimen was sent for histopathological examination. Both the specimens from the right and left tonsils measured approximately 3 cm × 2 cm × 1.5 cm. Cut-section was grey in color and gritty to cut. Microscopic examination revealed lining of stratified squamous epithelium which at places had invaginated into the deeper tissues forming blunt ended crypts []. The subepithelial region contained numerous lymphoid follicles showing follicular hyperplasia with adjacent fibrocollagenous tissue. Numerous islands of mature cartilage were seen embedded in the fibrocollagenous tissue []. A diagnosis of cartilaginous choristoma was given. | [[24.0, 'year']] | M | {'16274810': 1, '4506720': 1, '25587459': 2, '18830169': 1, '30774688': 2, '26788483': 2, '30967722': 2, '15025369': 1, '8763392': 1, '12487669': 1, '15763299': 1, '3472154': 1, '1745517': 1, '30069128': 1, '16304874': 1, '24250096': 2} | {'6421904-1': 1, '4283443-1': 1, '6358567-1': 1, '4710887-1': 1, '4710887-2': 1} |
164,189 | 3830245-1 | 24,250,097 | noncomm/PMC003xxxxxx/PMC3830245.xml | Apert's syndrome: Report of a rare case | A 14-year-old boy presented with the complaints of malaligned teeth, difficulty in chewing food, and facial deformity. His past medical history revealed that he had undergone suturotomy surgery for relieving craniosynostosis 11 years ago and plastic surgery for relieving syndactyly 5 years ago. His chest radiograph revealed no abnormality. He had hypochromic microcytic anemia since 11 years and experienced seizures occasionally since 1 year. He had bilateral optic disc edema since birth, for which the treatment was still ongoing. He also suffered from severe acne last year for which treatment lasted for 7-8 months. Prenatal history revealed that he had premature birth by 40 days. His parents were nonconsanguineously married in their 3rd decade. No other family members were affected by same features.\nOn examination, the boy was found to have a flattened occiput with frontal prominence, abnormal contour of head (brachycephaly), shallow and downward slanting orbits with bilateral proptosis, hypertelorism, retruded midface, and prognathic mandible [Figures and ]. Intraoral examination showed normal mouth opening with anterior open bite and a high arched (V-shaped) palatal vault. Maxillary alveolar ridges were thick with crowding of maxillary teeth. Mandibular teeth were normally aligned []. He had symmetrical syndactyly with complete fusion of all digits of hands (except thumb) and feet []. The systemic examination revealed that patient has some ophthalmologic, ear, and central nervous system abnormalities.\nOn investigation, Water's view radiograph showed deformity of maxilla with malaligned maxillary teeth and deviated nasal septum []. Lateral cephalogram showed concave profile with retruded midfacial bone and fusion between cervical vertebra C5, C6, and C7 []. CT scan of the brain revealed premature fusion of coronal and lamdoid sutures with bilateral proptosis, deviation of nasal septum, and turricephalic skull. It also revealed a bone defect in the vault of skull due to previous operative procedures []. Magnetic resonance imaging (MRI) of brain also revealed abnormal skull shape with similar changes. Due to these typical features and presence of the triad of craniosynostosis, syndactyly of hands and feet with maxillary hypoplasia, patient was diagnosed with AS. Patient was advised orthodontic treatment with orthognathic surgery for correction of the facial dysmorphisms. As patient was not ready for any interventional procedures, only oral prophylactic measures were taken and he was kept under regular follow-up. | [[14.0, 'year']] | M | {'5479478': 1, '10635279': 1, '28811814': 2, '29053644': 1, '501671': 1, '19642754': 1, '17622301': 1, '16549440': 1, '28058401': 2, '15915098': 1, '28316926': 1, '19077386': 1, '29753329': 2, '29973408': 1, '19186770': 1, '12435011': 1, '10926435': 1, '18215098': 1, '24250097': 2} | {'5206464-1': 1, '5949149-1': 1, '5510146-1': 1} |
164,190 | 3830246-1 | 24,250,098 | noncomm/PMC003xxxxxx/PMC3830246.xml | Desmoplastic ameloblastoma with osteoplasia: Review of literature with a case report | A 26-year-old female reported with a swelling in relation to the upper front teeth. The swelling was slow in growth and present since 4 months. She had also noticed a slight downward movement of the affected teeth and had mild pain. On examination, a bony hard swelling was seen in relation to 21, 22 and 23 on the buccal aspect measuring about 2.5 cm × 1.5 cm and extending into the palate. It was non-tender. Grade I mobility of 21 and 22 was also noticed.\nRadiographs revealed the presence of irregular radiolucencies with faint radio-opacities in the periapical region of 22 and 23. Lamina dura of the teeth was hazy and teeth were seen to be displaced []. A provisional diagnosis of benign fibro-osseous lesion was made and an incisional biopsy was done.\nBoth hard-tissue and soft-tissue were received. The specimens showed few irregular epithelial islands in a densely fibrous connective stroma. The islands consisted of peripheral cuboidal cells and central spindle cells. Some of the islands showed cystic degeneration []. Extensive desmoplasia was seen throughout the stroma compressing the epithelial islands []. Areas of osseous metaplasia with active osteoblasts were also noted []. With the above picture, a diagnosis of DA with osteoplasia was made. | [[26.0, 'year']] | F | {'17938502': 1, '26557637': 1, '10834533': 1, '25298945': 2, '8233435': 1, '33037797': 1, '11140898': 1, '3472145': 1, '8464613': 1, '14756940': 1, '15660085': 1, '10052385': 1, '26984790': 2, '20971659': 1, '19631576': 1, '22676988': 1, '10549030': 1, '19400611': 1, '11377234': 1, '6593446': 1, '18355614': 1, '17221066': 1, '24250098': 2} | {'4181134-1': 1, '4793556-1': 1} |
164,191 | 3830247-1 | 24,250,099 | noncomm/PMC003xxxxxx/PMC3830247.xml | A massive sinonasal psammomatoid variant of juvenile ossifying fibroma: Report of a rare entity | A 20-year-old female patient reported with a painless progressive swelling in the left cheek region and difficulty in breathing since 1 year. Past medical history revealed that the patient underwent surgery in a private dental clinic 5 years back for the impacted tooth 23 which was associated with pathology. She had no noteworthy family history. Gross facial asymmetry was noted on left side of the face. The swelling was 6 × 4 cm in size approximately extending anteroposteriorly from ala of the nose to 5 cm from tragus of the ear on the left side. Nasal polyp was seen in the left nostril with obliteration of left ala of the nose [].\nIntraoral examination presented a swelling extending anteroposteriorly from the distal aspect of 21 to mesial aspect of 26; medially till the mid palatine raphe and laterally the buccal vestibule was obliterated and the swelling extended from 21 to 26. On palpation, the swelling was hard in consistency with no fluctuation.\nParanasal sinus (PNS) X-ray revealed haziness in the left maxillary sinus. Computed tomography (CT) scan confirmed well-defined mixed radiolucent and radiopaque areas with calcifications extending superoinferiorly from infraorbital rim to alveolus and anteroposteriorly from the nasal septum to post zygomatic buttress on left side [].\nHistopathological examination of incisional biopsy revealed connective tissue stroma with numerous spherical/irregular ossifications interspersed with cellular fibrous tissue []. The ossifications showed peripheral brush border surrounded by an eosinophilic rimming []. Haemorrhagic areas were also seen. The constellation of clinical, radiological, and histopathological features of this lesion supported an interpretation of psammomatoid variant of JOF.\nUnder general anesthesia, a Weber-Ferguson incision was given to expose the complete lesion. Subtotal maxillectomy was performed and the tumor mass along with nasal and ethmoidal polyps were removed with the help of a chisel and mallet. After complete removal of the mass, borders were carefully osteotomized to avoid the chances of recurrence []. The excised specimen was sent for histopathological examination [] and the diagnosis of PsJOF was confirmed. Postoperative facial appearance and oral function were satisfactory. Follow-up examination of the patient showed no signs of recurrence. | [[20.0, 'year']] | F | {'21840246': 1, '1899514': 1, '22144839': 2, '22654369': 1, '9544629': 1, '1843064': 1, '1908971': 1, '9010430': 1, '11925539': 1, '4687883': 1, '8630892': 1, '16632273': 1, '8263214': 1, '24250099': 2} | {'3227263-1': 1, '3227263-2': 1} |
164,192 | 3830248-1 | 24,250,100 | noncomm/PMC003xxxxxx/PMC3830248.xml | Malignant inflammatory myofibroblastic tumor of the maxillary sinus | In January 2012, a 29-year-old apparently healthy man was admitted to the Department of Oral and Maxillofacial Pathology, with 1 month history of left facial numbness, swelling and pain radiating to the left maxillary sinus, upper teeth, and zygomatic region. Pain was severe, aggravated during the night and relieved on medication. There was no nausea, vomiting or hypopsia. Clinical examination revealed a firm, diffuse swelling involving the left midfacial area, extending into the oral cavity, accompanied by pain in the left upper teeth.\nThe patient's medical history was otherwise unremarkable. No enlarged cervical lymph node was palpable and laboratory tests suggested no significant abnormality.\nIntraorally, both right permanent maxillary premolars and the first molar were luxated. The covering mucosa was normal. There were no signs of infection such as, erythema, purulent drainage, fluctuance or indurated swelling of the surrounding soft tissues.\nAn urgent computerized tomography (CT) scan revealed a homogenous soft tissue mass involving the left maxillary sinus. The mass destructed the anterior and inferior walls and extended further downward, until the alveolar bone was destroyed. Furthermore, cortex was destroyed from both buccal and palatal sides. No obvious calcification or ossification was noted []. The clinical and radiological impression was one of a malignant maxillary sinus tumor.\nThe patient therefore underwent an excisional biopsy via an extraoral approach under general anesthesia. The intraoperative findings revealed a highly vascular, friable lesion occupying the left maxillary sinus. The whole mass was excised.\nHistopathologically, this tumor was composed of diffuse storiform proliferation of spindle-shaped fibroblasts and myofibroblasts in a predominantly fibromyxoid stroma interspersed with dense bands of collagen. This was accompanied by inflammatory cells which included lymphocytes, plasma cells, and foamy histiocytes [Figures and ]. Mitotic figures were rare, but the cellularity of the tumor together with hyperchromatism, variations in the size of nuclei and the invasive quality of the tumor, indicated malignancy.\nImmunohistochemical analysis revealed that the spindle-shaped cells were strongly and diffusely positive for vimentin, smooth muscle actin, anaplastic lymphoma kinase (ALK), and revealed a high proliferative index (Ki-67 = 60%) []. None were positive for desmin, pancytokeratin, S-100 protein, CD57, CD34, and CD68. All immunohistochemical studies that have been performed are summarized in . Special stains revealed no acid fast bacilli, other microorganisms or foreign materials.\nOn the basis of the above histopathologic and immunohistochemical findings, a diagnosis of IMT with malignant transformation was established. There was no clinical evidence of local or distant metastatic spread.\nThe patient was referred to an oncologist for further treatment. As the patient did not keep his appointment with the dental school, no additional follow-up information is available. | [[29.0, 'year']] | M | {'15823818': 1, '18830608': 1, '17467217': 1, '17331689': 1, '17457491': 1, '15821353': 1, '12406189': 1, '12944561': 1, '11237978': 1, '12574774': 1, '28289810': 1, '25932089': 1, '15602716': 1, '26818898': 1, '16292226': 1, '12625580': 1, '15220822': 1, '17414097': 1, '15486877': 1, '19900638': 1, '25763286': 2, '32102989': 1, '33897928': 1, '24250100': 2} | {'4339865-1': 1} |
164,193 | 3830249-1 | 24,250,101 | noncomm/PMC003xxxxxx/PMC3830249.xml | A rare case of angiolymphoid hyperplasia with eosinophilia in the submental region | A 22-year-old man reported with a complaint of a hard disfiguring swelling in the chin region. The swelling had gradually increased in size to attain the present size and had hardened in consistency to attain the present consistency. Patient had first noticed the swelling 1½ years back and complained of mild associated pruritis. The patient gave a history of trauma to the same region twice, the first about 10 years ago, which was associated with significant bleeding and had required suturing and the second about 2 years ago. His medical history was non-contributory. He had no tissue abuse or tobacco abuse habit.\nOn extra-oral examination, a single, well-defined, non-tender nodular swelling measuring about 2.5 cm Χ 1.5 cm in size with firm to hard consistency was present in the submental region []. The nodule was movable in nature. The temperature over the nodule was normal. Intra-orally there was no abnormality detected apart from moderate gingival recession with lower left central incisor.\nPeriapical, occlusal and panoramic radiographs were obtained and were non-contributory. The laboratory investigations that were advised for the patient included complete blood count, bleeding time, clotting time, random blood sugar, hepatitis B surface antigen test and human immunodeficiency virus test. All the reports were within the normal limits except for differential leukocyte count, which showed marked increase in eosinophils to 8% (normal 1-6%). The lesion was surgically excised and sent for histopathological examination []. | [[22.0, 'year']] | M | {'3116865': 1, '17592625': 2, '18510751': 2, '5763634': 1, '12205289': 1, '15888166': 1, '19882016': 1, '10890984': 1, '15981816': 1, '21382284': 1, '3456143': 1, '12395376': 1, '17020619': 1, '26097322': 2, '21434541': 1, '16445506': 1, '4008683': 1, '2281680': 1, '7611073': 1, '16020984': 1, '24250101': 2} | {'2427016-1': 1, '1913531-1': 1, '4451652-1': 1} |
164,194 | 3830250-1 | 24,250,102 | noncomm/PMC003xxxxxx/PMC3830250.xml | Intramuscular sinusoidal hemangioma with Masson's lesion | A 20-year-old male patient presented with a chief complaint of swelling below the chin since 5 days. On extraoral examination, the swelling was located in the external submental and submandibular region extending from symphysis up to 1 cm superior to the thyroid cartilage. The swelling was ovoid, soft and compressible with well-defined margins, which moved on deglutition.\nThe mandibular occlusal radiograph showed a radiopaque mass in relation to submandibular duct indicative of sialolith.\nBased on the clinical and radiographic appearance a provisional diagnosis of an obstructive salivary gland pathology was given.\nOn grossing, the cut-surface of the specimen consisted of blood filled spaces with multiple septae and two calcified masses.\nMicroscopically, connective tissue stroma with numerous skeletal muscle bundles was seen. In between the skeletal muscle bands, large dilated vascular spaces were seen lined by endothelial cells [Figures –]. Areas of proliferating endothelial cells were seen []. The vascular spaces were sinusoidal and in some areas surrounded by smooth muscle cells. Few areas showed numerous papillary projections in an organizing thrombus within a vessel wall indicative of Masson's lesion [Figures and ]. Extravasated red blood cells were present in the sinusoidal spaces in few areas. Few arterioles, adipose tissue and numerous normal skeletal muscle bundles (in transverse and longitudinal sections) were seen. | [[20.0, 'year']] | M | {'9805543': 1, '5061701': 1, '2013460': 1, '24250102': 2} | {} |
164,195 | 3830251-1 | 24,250,103 | noncomm/PMC003xxxxxx/PMC3830251.xml | Clear cell change in a lower lip mucocele | A 74-year-old man was referred presenting an asymptomatic nodular lesion on his lower lip with 1 month duration. The clinical diagnosis was oral mucocele. The medical history was noncontributory and the extra-oral examination did not show alterations. Microscopic sections, at lower magnification, showed a dense population of clear cells surrounding an inner cavity [Figure and ], which contained sparse to absent mucoid material. At the periphery, the clear cells displayed irregular infiltration into adjacent minor salivary gland parenchyma as broad sheets and cords, being supported by a dense fibrous stroma. In high-power, the cells showed clear cytoplasmic vacuolation with shrunken, pyknotic peripheral nuclei [] and a SRC appearance, intermingled with a delicate network of small vessels []. Periodic acid-Schiff and mucicarmine stains revealed focal areas with homogeneous mild positivity, consistent with intracellular mucin []. Despite these diagnostic approaches, definitive diagnosis still could not be achieved, because both epithelial cells and macrophages may contain cytoplasmic mucin. Therefore, immunohistochemical analysis was indicated, which showed strong positivity for CD68 (KP1) and CD163 [], whereas AE1/AE3 pan-cytokeratin, S100, HMB-45 and CD1a were negative, supporting a macrophage lineage cell. The post-surgical evaluation did not reveal any abnormality and after 3 years of follow-up the patient is well without complications. | [[74.0, 'year']] | M | {'9845723': 1, '18280759': 1, '15533232': 1, '20118912': 1, '20868985': 1, '12940782': 1, '12823721': 1, '11393085': 1, '11474456': 1, '20708324': 1, '21813157': 1, '19101492': 1, '24250103': 2} | {} |
164,196 | 3830252-1 | 24,250,104 | noncomm/PMC003xxxxxx/PMC3830252.xml | Maxillary sinus osteoma: From incidental finding to surgical management | A 39-year-old man was referred by his general dental practitioner for an incidentally found round radio-opaque tumor in the left maxillary sinus on the orthopantomogram (OPG) []. The patient was asymptomatic, but very concerned about the nature of the tumor. Otherwise he was in good health, particularly he did not complain of any gastrointestinal or skin symptoms. The extra- and intraoral examinations were unremarkable. The dentition, especially in the upper left quadrant was unremarkable and vital on cold test. Computed tomography (CT) of the head and paranasal sinuses was performed, which revealed a solitary exophytic osseous tumor that was pedunculated and attached to the dorsolateral wall of the maxillary sinus []. We removed the tumor from the left maxillary sinus by “modified Caldwell–Luc” approach under general anesthesia [Figures and ]. The osseous tumor was visible after the bony window from the anterior wall of the maxillary sinus was lifted []. The stalk of the tumor was separated from the dorsal aspect of the sinus by a chisel and the tumor was mobilized. Because of its large size, it had to be divided inside the sinus cavity. The osseous tumor measuring 2.1 cm in diameter was finally removed in three parts []. The defect of the anterior wall was easily closed by suturing back the bony window of the maxillary sinus with absorbable sutures. The final histopathology report confirmed the diagnosis of the maxillary sinus osteoma with no signs of malignancy [Figures and ]. Our patient remained asymptomatic at his 3rd-month of follow-up. | [[39.0, 'year']] | M | {'17307307': 1, '18602294': 1, '16799437': 1, '17138161': 1, '4506814': 1, '15979316': 1, '12420263': 1, '18154576': 1, '6938210': 1, '21493269': 1, '24250104': 2} | {} |
164,197 | 3830253-1 | 24,250,105 | noncomm/PMC003xxxxxx/PMC3830253.xml | Nasopalatine duct cyst developed in association with dental implant treatment: A case report and histopathological observation | A 45-year-old male patient visited our clinic in May 2005 due to detachment of a porcelain-fused-to-metal crown on the left maxillary central incisor, which had been connected at another clinic in 2000.\nThere were no special findings in his physical and extraoral conditions. On intraoral examination, mesiodistal fracture lines were found on the remaining tooth structure. A swelling and slight redness were observed on the peripheral soft tissue, but there were no acute symptoms such as purulence or pain [Figure and ].\nRadiographic examination showed no inflammatory symptoms, such as an increased periapical space, bone resorption, or periapical radiolucency, thus, the inflammation was judged confined almost exclusively in the gingival tissue. A nasopalatine foramen was found adjacent to the apex of the maxillary left central incisor [].\nThe maxillary left central incisor had a root fracture and required extraction. After a careful consultation about various treatment options, the patient desired implant treatment. Because there existed no obvious signs of acute inflammation or any other symptoms of the soft and hard tissue, postextraction immediate implant placement was planned. Prior to the implant treatment, the patient was subjected to meticulous scaling of all the remaining teeth and oral hygiene instruction session.\nIn May 2005, the maxillary left central incisor was extracted. After careful curettage of the extraction site, the mucoperiosteal flap was reflected. There was no resorption of the labial bone and an implant (TiOblast, Astra Tech, Mölndal, Sweden, ø 4.5 mm, length 13 mm) was placed into the fresh extraction socket with good primary stability. The osteotomy was made so that the implants would be located centrally in relation to the socket; however, careful drilling was conducted in order to preserve the buccal wall. The gap between the fixture and the socket wall was filled with autogenous bone particles collected during the surgery. The wound was closed after a releasing incision. On the periapical radiograph taken immediately after implant surgery, the implant appeared to interfere with the nasopalatine canal [].\nThe implant was restored with the definitive crown in November 2005. No abnormality was found during quarterly maintenance visits after the implant surgery, however, at the maintenance visit in November 2007, the patient complained about swelling on the palate. Clinical examination detected pulsation on the palate and an oval-shaped radiolucency having unclear boundary around the apex of the dental implant detected on the periapical radiograph. A computed tomography (CT) scan confirmed the radiolucency of a size of 10 mm × 10 mm × 9 mm, which surrounded the apical portion of the implant, reaching to the nasopalatine canal [Figure –]. Although the patient had no spontaneous pain, the lesion seemed to be enlarging and it was judged that early removal of the cyst was necessary. Because the implant was immobile, with no signs of peri-implant bone resorption, it was decided not to remove the entire implant but to resect the apical portion of the implant lodged inside the cyst, and remove the entire lesion. The surgery was performed in November 2007. Flap incision was designed to be away from the expected lesion area so that the incision will not overlap with the bone defect after the cyst removal. Mucogingival flap was elevated and resorption of the labial bone was observed. After removing the thinned cortical bone and detaching the cyst wall on the palatal side, the apical portion of the implant (approximately 3 mm) lodged inside the cyst was resected using a carbide bur. Thereafter, the entire cyst, including the resected implant, was removed en bloc. It was evident that the nasopalatine neurovascular bundle was incorporated into the cyst []. The wound was closed by repositioning the mucoperiosteal flap, and no bone grafting materials were used to fill the defect.\nThe histopathological findings showed that the wall of the cystic lesion comprised of cuboidal, ciliated columnar and stratified squamous epithelium with underlying connective tissue. The cysts that form adjacent to oral mucosa of the incisal foramen was lined mainly by stratified squamous epithelium, whereas the lining close to the incisal foramen was lined by cuboidal and ciliated columnar epithelium, and there were no signs of inflammatory cell localization within the observed biopsy []. Thus, based on the clinical and histological findings, the lesion was diagnosed as nasopalatine duct cyst developed in association with the dental implant placement.\nAfter the cyst removal, the patient has been carefully followed by clinical, radiographic examinations (both periapical and CT) during maintenance visits scheduled every 4 months. The current status after 28 months after the cyst removal shows no signs of implant mobility, marginal gingival recession, or peri-implant inflammation. Compared with the radiographic findings before the cyst removal, the radio-opacity of the original lesional area seemed to have increased. The bone defect measured on the CT after the cyst removal is 4 mm × 3 mm × 4 mm, comparably smaller to the preoperative radiograph, suggesting a favorable healing []. | [[45.0, 'year']] | M | {'34522664': 1, '17465352': 1, '12704955': 1, '20009600': 1, '12400727': 1, '18545048': 1, '11737103': 1, '11315428': 1, '8620395': 1, '22126353': 1, '27011942': 1, '15841583': 1, '24779952': 1, '19663967': 1, '13665452': 1, '1995816': 1, '32244843': 1, '19537472': 1, '26557434': 1, '19681935': 1, '19298293': 1, '11168243': 1, '10716000': 1, '18498588': 1, '15665234': 1, '3271698': 1, '9663096': 1, '20657882': 1, '32403226': 1, '24250105': 2} | {} |
164,198 | 3830254-1 | 24,250,106 | noncomm/PMC003xxxxxx/PMC3830254.xml | Central odontogenic fibroma of the maxilla | A 24-year-old female patient came with the complaint of a swelling over the right cheek region for the past 1 year. There was a slow growing swelling in the middle one-third of the face on the right side. It measured about 3 × 5 cm in size and obliterated the nasolabial fold. It was hard in consistency and asymptomatic. Intraoral examination revealed a well-defined, bony swelling measuring, about 3 × 5 cm in size in the right side of the maxilla, extending from canine to second molar in the anteroposterior direction. There was buccal cortical expansion and grade I mobility of 14 and 15 [].\nOrthopantomogram (OPG) showed an ill-defined, mixed radiolucent, and radio-opaque area; extending from the distal surface of canine to the distal aspect of second molar []. Occlusal radiograph revealed a well-defined radiolucent lesion in the hard palate extending from the incisor to the second molar. It also showed buccal cortical expansion with radio-opaque flakes on the buccal aspect of 14, 15, and 16 []. From the above findings, a provisional diagnosis of a fibro-osseous lesion was arrived at the clinical level.\nThe incisional biopsy showed a highly cellular, fibrous connective tissue stroma with plump fibroblasts and long strands, islands and nests of odontogenic epithelium seen scattered throughout the lesion and it exhibited mild eosinophilic to clear cytoplasm [Figure –, and ]. Numerous cementum-like hematoxyphilic calcifications of various sizes were seen []. These calcified structures demonstrated basophilic lamellated spherules to acellular eosinophilic materials akin to dentin or acellular cementum. In focal areas, loose fibrous connective tissue with fine collagen fibrils and stellate shape fibroblast were observed. The diagnosis of COF (epithelial-rich variant) was made because it was the predominant feature, although areas of the simple type were also seen focally.\nThe lesion was surgically excised and was not encapsulated. The cut surface appeared grayish-white and gritty. The X-ray finding of the excised specimen was suggestive of a fibro-osseous lesion []. The histopathology of the postoperative tissue was consistent with the incisional biopsy diagnosis. | [[24.0, 'year']] | F | {'1702150': 1, '25506436': 2, '25646136': 2, '26752885': 2, '31583206': 2, '8986968': 1, '21751042': 1, '26457211': 2, '10513876': 1, '7898916': 1, '2004076': 1, '3133430': 1, '26125006': 2, '7600224': 1, '21684774': 1, '24250106': 2} | {'6761066-1': 1, '6761066-2': 1, '4592713-1': 1, '4483617-1': 1, '4691995-1': 1, '4259130-1': 1, '4311396-1': 1} |
164,199 | 3830255-1 | 24,250,107 | noncomm/PMC003xxxxxx/PMC3830255.xml | Filarial abscess in the submandibular region | A 25-year-old lady presented to dental out-patient services with swelling and pain in the right side of the face. Local examination showed a fluctuant swelling measuring 5 mm × 3 cm over the right side of the angle of mandible []. The swelling was warm and tender on palpation with signs of impending rupture. Clinical examination of the orofacial region did not reveal any odontogenic or non-odontogenic foci of infection. Patient's vitals were in the normal limits. All the hematological parameters were normal except for borderline leukocytosis and a low hemoglobin level. Incision and drainage (I and D) of the abscess was carried out under local anesthesia. As the patient was in her 12th week of gestation, antibiotics were prescribed in consultation with the gynecologist.\nOn a follow-up visit after 2 weeks, a painless indurated swelling at the same site was noted [, inset]. Pus culture carried out during the incision and drainage had not revealed any bacterial growth. As the condition was not resolving, a fine needle aspiration cytology (FNAC) was advised in consultation with the pathologist, to rule out tubercular infection.\nAspirate from the swelling yielded purulent material. The smears were moderately cellular and showed abundant necrotic debris within which were seen polymorphs and histiocytes. One of the smears revealed the presence of a single microfilaria of W. bancrofti, which was rounded anteriorly and tapered posteriorly []. The caudal end of the microfilariae had a clear space free of nuclei. After the aspiration, the patient was admitted and a midnight blood sample was taken. The wet mount preparation showed motile microfilariae, which confirmed the diagnosis of filariasis.\nSince, the patient was in the first trimester of pregnancy, decision was taken to start the anti-filarial drugs after delivery. | [[25.0, 'year']] | F | {'28182103': 2, '8629415': 1, '18417874': 1, '8453019': 1, '6349200': 1, '19446380': 1, '24250107': 2} | {'5259939-1': 1} |
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