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164,400 | 3841599-2 | 24,339,578 | noncomm/PMC003xxxxxx/PMC3841599.xml | Benign occipital lobe seizures: Natural progression and atypical evolution | A 14-year-old boy presented with history of seizures involving all four limbs since the age of 7 years.\nThe current clinical seizures are characterized by initial grunting and face turning to the right followed by jerking of all four limbs lasting for a few minutes. The boy remains in a confused state for at least 30 min after seizures. He was treated with VAP 300 mg BD, carbamazepine (CBZ) 200 mg BD and clonazepam (CLN) 0.5 mg: 1-0-2 at the time of presentation []. The working diagnosis at this time was primary generalized seizures. EEG then showed evidence for bilateral occipital spike and wave discharges, which led to further questioning and this revealed additional blurring of vision preceding the generalized seizures and also independent brief episodes with just blurring of vision, which actually started well before the generalized clinical seizures.\nA diagnosis of occipital seizures was made and drugs modified. CBZ was increased to 300 mg BD and CLN reduced to 1 mg OD (noc) and VAP to 500 mg OD (noc).\nImaging studies were normal [].\nSeizures are better controlled now with reduction from weekly seizures to one seizure in the last 3 months. | [[14.0, 'year']] | M | {'12614400': 1, '6802526': 1, '3148690': 1, '16822650': 1, '17442007': 1, '16950946': 1, '15519916': 1, '10386532': 1, '12773298': 1, '10403229': 1, '17442005': 1, '10756414': 1, '6810202': 1, '17888075': 1, '16338676': 1, '6410006': 1, '16105750': 1, '1889978': 1, '24339578': 2} | {'3841599-1': 2, '3841599-3': 2} |
164,401 | 3841599-3 | 24,339,578 | noncomm/PMC003xxxxxx/PMC3841599.xml | Benign occipital lobe seizures: Natural progression and atypical evolution | A 15-year-old boy suffered with two episodes of un-responsiveness lasting many hours once when he was 7 years and then when he was 9 years old. On both occasions, patient was travelling in a train with family.\nDuring these prolonged episodes, the boy suddenly went un-responsive and blue according to the mother. He also vomited during the first episode. There were no visual symptoms or jerking of limbs reported during both these events. This patient only underwent one routine EEG in 2005, which showed evidence for bilateral posterior spike and wave discharges. He responded well to CBZ []. Despite stopping anticonvulsants 2 years ago he has remained seizure free. The previous 4 years on medication were also seizure free. An EEG performed in 2012 as follow-up was normal. The diagnosis of occipital seizures/PS was made retrospectively based on the previous history and EEG changes. | [[15.0, 'year']] | M | {'12614400': 1, '6802526': 1, '3148690': 1, '16822650': 1, '17442007': 1, '16950946': 1, '15519916': 1, '10386532': 1, '12773298': 1, '10403229': 1, '17442005': 1, '10756414': 1, '6810202': 1, '17888075': 1, '16338676': 1, '6410006': 1, '16105750': 1, '1889978': 1, '24339578': 2} | {'3841599-1': 2, '3841599-2': 2} |
164,402 | 3841600-1 | 24,339,579 | noncomm/PMC003xxxxxx/PMC3841600.xml | Recurrent prolonged fugue states as the sole manifestation of epileptic seizures | A 15-year-old female, presented with 10 years history of recurrent episodes of acute onset, prolonged confusional states, accompanied by excessive somnolence, lasting for 15-24 h or more. The patient was a full-term normal delivery, with normal developmental milestones. The attacks first manifested at 5 years of age with a frequency of 1-2 per month, the current frequency being 2-3 per month. The attacks were stereotyped in nature and characterized by a prolonged fugue like state which would descend all of a sudden without any prior warning. During the attacks, the patient would appear dazed and become clumsy and ataxic. She displayed excessive sleepiness and remained confined to bed most of the day but remained partially responsive, answering in monosyllables, drinking and eating food when offered and would also attended to her toilet needs with assistance. The attacks were not accompanied by any jerks, tonic-clonic contractions, automatisms, or incontinence. The attacks would terminate as suddenly as they started and the patient would then resume her normal day to day activities as before. Interictally, her behavior was normal but her overall school performance was poor. There was no history of absence attacks, complex partial seizures (CPS), myoclonic jerks, or generalized tonic-clonic seizures. There was no history of head injury or family history of seizures. She had received valproate (600 mg/day) for 7 years following the onset of these attacks without any significant change in the frequency or duration of the attacks.\nOn examination, at the time of presentation, she was fully conscious and alert. Her minimum mean square error score was 27/30. On detailed higher mental function assessment, her fund of knowledge was poor and frontal lobe performance (literal fluency, mental flexibility, motor programming) was impaired. New learning ability, verbal memory tasks, and constructional ability was also impaired. There was no motor or sensory deficit.\nRoutine investigations including haemogram, blood biochemistry, and magnetic resonance imaging brain were normal. An interictal electroencephalogram (EEG) done at 8 years of age, showed normal background activity with frequent intermittent short lasting bursts of generalized 2.5-3 Hz spike wave discharges lasting for 4-s []. An ictal EEG done at 12 years of age revealed continuous generalized 2.5-3 Hz spike wave discharges throughout the trace without any discernable background activity []. A current EEG done 2 days following the last attack, revealed 3-4 Hz slow background activity with frequent intermittent bursts of generalized, bilateral symmetric and synchronous, high voltage slow wave activity intermixed with spike discharges and at places 3 Hz spike and wave discharges suggestive of a generalized seizure disorder []. Video EEG monitoring in the immediate postfugue state did not reveal any evidence of typical or subtle clinical absence attacks.\nOn the basis of the history and EEG findings, a diagnosis of prolonged fugue states or AS as the sole manifestation of epileptic seizures was made. In view of a history of lack of response to valproate, she was started on levetiracetam (1.5 g/day). Lacosamide (100 mg/day) was added subsequently because of persistence of epileptiform discharges in EEG after 1 week. There was, however, no decrease in frequency of attacks even after 1 month. However, on adding clobazam (30 mg/day) during one of the fugue states she became more responsive with improvement in her sensorium and the duration of attack was significantly reduced to 6 h. Subsequently, clobazam was continued and she remained seizure free over a 4 months follow-up period. | [[15.0, 'year']] | F | {'18093147': 1, '479114': 1, '3187298': 1, '3295588': 1, '12076103': 1, '3241475': 1, '6802525': 1, '17307710': 1, '31186974': 2, '10937158': 1, '17205231': 1, '4501885': 1, '13351159': 1, '34908691': 2, '3365642': 1, '24339579': 2} | {'6521420-1': 1, '8611604-1': 1, '8611604-2': 1, '8611604-3': 1} |
164,403 | 3841601-1 | 24,339,580 | noncomm/PMC003xxxxxx/PMC3841601.xml | Opercular myoclonic-anarthric status epilepticus: A report of two cases | A 75-year-old, right-handed male patient presented with acute onset of abnormal, involuntary movements of soft palate, tongue, lips and jaw for the last 3 days. He had speech disturbances and swallowing difficulty, occasionally associated with choking episodes. He had no difficulty in voluntary movements of facial, palatal muscles and tongue. There was no history of diabetes mellitus or hypertension. He was a chronic smoker (30 pack years) and occasionally consumed alcohol.\nOn general physical examination, vital data was normal except for elevated blood pressure (170/100 mmHg). Neurological examination revealed that speech was slow and dysarthric and bilateral, symmetrical, involuntary, continuous, repetitive and synchronized rhythmic myoclonus involving soft palate, lips, chin, tongue and jaw at a rate of 60-80/min []; rest of the neurological examination was unremarkable.\nLaboratory investigations including hemogram, serum biochemistry and 2D-echocardiogram were normal. Carotid/vertebral arterial Doppler study showed thrombosis of left internal carotid artery. Electroencephalogram (EEG) was normal []. Magnetic resonance imaging (MRI) of brain, diffusion weighted axial image (DWI) showed restriction in left frontal opercular cortex suggesting an acute infarct []. Magnetic resonance angiography (MRA) of the brain showed thrombosis of left internal carotid artery.\nHe was treated with oral clonazepam (0.5 mg twice daily), gabapentin (100 mg 3 times daily) for palatal myoclonus; oral aspirin (150 mg once daily) and rosuvastatin (5 mg once daily) for ischemic stroke; and oral amlodipine (2.5 mg once daily) for hypertension control. Long-term warfarin therapy was also prescribed. During hospital stay myoclonus improved over a period of 5-7 days []. Speech disorder gradually improved in 8-10 days. During the follow-up period of 1 year, the patient had no recurrence of myoclonus. | [[75.0, 'year']] | M | {'23476665': 2, '404996': 1, '7064190': 1, '7614913': 1, '1823535': 1, '21325126': 1, '7684439': 1, '3929672': 1, '3484855': 1, '30643669': 1, '16793572': 1, '1597690': 1, '6153606': 1, '24339580': 2} | {'3841601-2': 2, '3588394-1': 1} |
164,404 | 3841601-2 | 24,339,580 | noncomm/PMC003xxxxxx/PMC3841601.xml | Opercular myoclonic-anarthric status epilepticus: A report of two cases | A 72-year-old right-handed female presented with sudden onset of abnormal, involuntary movements of tongue, lips, lower jaw and larynx for the last 2 days. She had speech and swallowing difficulties, occasionally associated with choking episodes. She had no difficulty in voluntary movements of facial, palatal muscles and tongue. She was a known hypertensive for the last 6 years and was on irregular treatment.\nOn general physical examination, vital data was normal except for elevated blood pressure (180/100 mmHg). Central nervous system examination revealed that speech was slow and dysarthric and bilateral, symmetrical continuous, involuntary, repetitive and synchronized rhythmic myoclonus involving tongue, lips, chin, jaw and larynx at a rate of 90-110/min []; rest of the neurological examination was normal.\nLaboratory investigations including hemogram, serum biochemistry and 2D-echocardiogram were normal. Carotid/vertebral arterial Doppler study showed thrombosis of right internal carotid artery. EEG was abnormal and revealed diffuse theta slow waves and intermittent bursts of sharp and slow waves over posterior temporal, centro-parietal, occipital regions and occasionally generalized epileptiform discharges []. Single photon emission computerized tomography (SPECT) showed areas of intense radio-tracer uptake in right frontal region []. MRI brain-DWI showed restriction in right high frontal region suggesting acute infarct. MRA of brain showed thrombosis of right internal carotid artery.\nShe was started on oral clonazepam (0.5 mg twice daily) initially and later sodium valproate (20 mg/kg/body weight) was added. Myoclonic jerks were not controlled in 5 days. Then levetiracetam (20 mg/kg/body weight) and gabapentin (100 mg 3 times daily) were added. Oral amlodipine 5 mg once daily was started for control of hypertension; oral aspirin (150 mg once daily) and rosuvastatin (10 mg once daily) were started for the treatment of ischemic stroke. Long-term warfarin therapy was prescribed. During hospital stay, myoclonus improved over a period of 10-12 days []; swallowing difficulties and speech had gradually improved in 14-16 days. During the follow-up period of 2 months, the patient had no recurrence of myoclonus. | [[72.0, 'year']] | F | {'23476665': 2, '404996': 1, '7064190': 1, '7614913': 1, '1823535': 1, '21325126': 1, '7684439': 1, '3929672': 1, '3484855': 1, '30643669': 1, '16793572': 1, '1597690': 1, '6153606': 1, '24339580': 2} | {'3841601-1': 2, '3588394-1': 1} |
164,405 | 3841602-1 | 24,339,581 | noncomm/PMC003xxxxxx/PMC3841602.xml | Clinical and imaging perspective and unanswered questions in a case of metronidazole induced encephalopathy | We discuss the case of a 78-year-old male who developed slurring of speech and ataxia acute in onset for the last 3 days. During the hospital stay, he developed multiple episodes of focal seizures without secondary generalization involving the angle of mouth on the right side. The patient complained of headache not associated with vertigo, tinnitus or visual complaints. There was no recent history of toxin exposure or trauma. Five weeks prior to admission, the patient was admitted for amoebic liver abscess. He underwent percutaneous aspiration of abscess. The patient was prescribed oral metronidazole 800 mg thrice daily for 6 weeks and was discharged. At the time of admission, he had taken the drug for 5 weeks (35 days). On examination, the patient was well oriented. Sensory motor and cranial nerve examination were unremarkable. The patient had cerebellar signs in the form of ataxia dysdiadochokinesia and impaired co-ordination in both the upper and the lower limbs. Reflexes were within normal limits. The patient underwent MRI examination, which revealed symmetrical areas of altered signal intensity, appearing hyperintense on T2-weighted and fluid-attenuated inversion-recovery (FLAIR) images involving the dentate nuclei, dorsal pons and midbrain [Figures and ]. Diffusion-weighted/apparent diffusion coefficient (ADC) mapping was suggestive of T2 shine through due to cytotoxic edema rather than restricted diffusion [Figures and ]. Given the history of metronidazole and characteristic distribution of lesions on MRI, the patient was diagnosed as a case of MIE. The offending drug was discontinued immediately, after which the patient improved clinically. A follow-up scan was performed after 12 days, which showed complete resolution of the lesions [Figures and ]. | [[78.0, 'year']] | M | {'19346865': 1, '7396319': 1, '15778547': 1, '30826778': 1, '26894145': 1, '10588095': 1, '27504340': 1, '25990105': 1, '25391707': 1, '7898724': 1, '15824365': 1, '30536109': 1, '12736767': 1, '17885234': 1, '11098341': 1, '24339581': 2} | {} |
164,406 | 3841606-1 | 24,339,585 | noncomm/PMC003xxxxxx/PMC3841606.xml | Facio-brachio-crural dystonic episodes and drop attacks due to leucine rich glioma inactivated 1 encephalitis in two elderly Indian women | A 68-year-old woman presented to us with sudden jerky right sided movements of 10 days duration that were also causing her to fall. These movements had started acutely and predominantly involved the right sided arm and leg. They occurred multiple times a day and initially were spontaneous and brief lasting a few seconds. They interfered with walking and caused frequent falls. Observation of a few of these episodes revealed facial grimacing and brief right upper limb dystonic posturing lasting 1-2 s. While standing or walking, the movements occasionally involved the right leg causing buckling at the knee and falls. There was no significant past medical history and routine investigations including prolonged electroencephalography (EEG) monitoring and magnetic resonance imaging (MRI) brain were normal. She was diagnosed with late onset paroxysmal non-kinesogenic dyskinesia (PNKD), likely symptomatic and was put on clonazepam, phenytoin without significant improvement. She was discharged after 5 days. After 1 month, she was readmitted from the emergency room with drowsiness and hyponatremia (serum sodium 116 meq/l). After correction of Na and improvement in sensorium, she was noticed to have frequent bilateral alternating attacks up to 30-50/day involving the face, arm and legs. Carbamazepine, lamotrigine and sodium valproate were added to her regimen. She had some symptomatic relief, but the episodes persisted. Her falls abated, but she continued to have mild faciobrachial dystonic (FBD) attacks. Serum was stored for future analysis. She declined to be video graphed and was requested discharge from our facility. At telephonic follow-up 6 months later, she was asymptomatic and off on all medications. | [[68.0, 'year']] | F | {'21556879': 1, '21616043': 1, '26756036': 1, '27450643': 1, '21842591': 1, '21416487': 1, '26831002': 1, '24339585': 2} | {'3841606-2': 2} |
164,407 | 3841606-2 | 24,339,585 | noncomm/PMC003xxxxxx/PMC3841606.xml | Facio-brachio-crural dystonic episodes and drop attacks due to leucine rich glioma inactivated 1 encephalitis in two elderly Indian women | A 60-year-old woman was admitted to our ward with recurrent falls of 1 month duration. She was a long standing diabetic of 10 years duration on insulin and oral hypoglycemic agents. Her husband had noticed that she had developed a voracious appetite, eating every 2 h; although, there was no evident weight gain. For the past 3 days, the falls had increased in frequency and now she was falling 2-3 times a day. She complained of an abnormal sensation in the epigastrium followed by sudden buckling at the knee. She usually fell backward; although, she could fall to either side. On the day of admission, she had fallen 4 times and bruised her left side of the chest and sustained lacerations over the forehead and the occipital region []. She denied any palpitations or loss of consciousness during the episodes and was able to pick herself up immediately after the falls. There was no history of tongue bite or urinary or bowel incontinence associated with these episodes. She was admitted for further evaluation of drop attacks. Prolonged EEG monitoring was normal. Recurrent clinical episodes were recorded without any EEG correlate or recordable movement. MRI brain with contrast was normal. Holter monitoring was normal. Audiometry revealed mild sensorineural hearing loss bilaterally 1 week after admission; she continued to have recurrent falls with injury. Owing to hyponatremia (serum Na of 115 meq/l) and drowsiness, she was shifted to the intensive care unit for observation. At this time, she was noticed to have frequent brief alternating facial grimacing and upper limb dystonic posturing lasting a few seconds. Each of these episodes was preceded by the typical discomfort or aura that she experienced prior to fall and a feeling of weightlessness. These episodes were now noticed to occur every time she became drowsy or woke up from sleep (approximately 30 times a day) []. She was noticed to be very confused and disoriented. Her Addenbrooke's cognitive examination (ACE) score was 68/100 with prominent deficits in attention, concentration and recall. Patient was treated with 1 g of intravenous (IV) methylprednisolone for 5 days followed by oral prednisolone 40 mg/day. She was shifted back to the ward where her husband continued to notice milder attacks with occasional posturing of the leg on the side of the attacks []. The attacks gradually declined in frequency and by day 7 after initiation of therapy, she was asymptomatic and ambulant. Routine blood evaluation, liver function test, renal function test, thyroid function test and vasculitic work-up were normal. The cerebrospinal fluid study showed 0 cells and normal sugar and protein levels. Her ACE score had improved to 82/100. Serum was sent for anti LGi1 and contact in associated protein 2 (CASPR2) antibodies to Oxford University, UK. She tested positive for LGi1 antibody and negative for CASPR2. A second simultaneous sample sent to Statens Serum Institute Copenhagen was positive for LGi1 immunoglobulin G (IgG) antibodies at a titer of 1:320 and negative for LGi1 IgA & IgM, CASPR2, ANNA-1 (Hu), ANNA-2 (Ri), PCA-1 (Yo), Tr, Myelin-associated glycoprotein (MAG) antibody, myelin, PNMA1 (Ma/Tr), glutamic acid decarboxylase antibody (GAD), Amphiphysin, Aquaporin-4 (Aqp4), glycine receptor (GlyR), Abs, GABAbR, GluR (AMPA type) glutamate receptor and (GluR) (NMDA type) antibodies.\nOwing to financial constraints, the family declined further testing. She was discharged on oral prednisolone 40 mg/day. At follow-up 45 days later, there were no further falls or dystonic episodes; however, she complained of disabling persistent amnesia and her ACE score was 80/100 with predominant recent memory impairment.\nAfter review of the second case, serum of the 1st patient was sent to Oxford University for LGi1 and CASPR2 antibodies. Serum was positive for LGi1 antibodies and negative for CASPR2 antibodies. | [[60.0, 'year']] | F | {'21556879': 1, '21616043': 1, '26756036': 1, '27450643': 1, '21842591': 1, '21416487': 1, '26831002': 1, '24339585': 2} | {'3841606-1': 2} |
164,408 | 3841607-1 | 24,339,586 | noncomm/PMC003xxxxxx/PMC3841607.xml | Voltage gated potassium channel antibodies positive autoimmune encephalopathy in a child: A case report and literature review of an under-recognized condition | A 13-year-old, right handed, previously fit and healthy girl presented with a short history of generalised headaches and confusion. She had “flu-like” symptoms 4 weeks ago followed by complete recovery. There was no history of fever, drug ingestion, head injury, rash, tick bite or travel outside the country within last 6 months. Parents were non-consanguineous, Afro-Caribbean origin, and her father died at the age of 55 years from a “possible stroke.”\nOn admission, Glasgow Coma Scale was 13/15 and she was aggressive and disorientated. She was apyrexial with normal blood pressure and heart rate. There were no focal neurological signs, and general examination was unremarkable. Soon after admission she developed left focal motor seizures with secondary generalization, requiring intensive care treatment for the next 3 weeks. Seizures were difficult to control, and she had repeated episodes of status epilepticus, requiring multiple anticonvulsants. Repeated electroencephalogram (EEG) showed diffuse generalised slowing with no epileptiform discharges.\nInitial blood investigations were unremarkable, including full blood count and peripheral smear, baseline electrolytes, renal, liver and bone profile, haemoglobin electrophoresis, peripheral blood film for malarial parasites, investigations for tuberculosis, antibodies for Borrellia burgdorferi and human immunodeficiency virus. Highest C-reactive protein was 85 in the 1st week. Initial cerebrospinal fluid (CSF) was reactive with 34 white cells/mm3 (80% lymphocytes), normal glucose (more than 50% of blood glucose) and protein. Polymerase chain reaction (PCR) for Herpes, Enterovirus, Cytomegalovirus, Human herpes virus 6 was negative along with urine for toxicology. Blood, urine and CSF cultures were sterile. First MRI brain [] showed thickening of right temporal lobe gyrus, extending on to parietal lobe, with increased T2 signal within the cortex. There was associated restricted diffusion on diffusion-weighted imaging (DWI) []. She was treated for 2 weeks of third-generation antibiotics and acyclovir for probable encephalitis.\nPost-intensive care she remained confused, disorientated and had recurrent episodes of aggression and rage. She became mute and developed visual hallucinations. Sleep cycle was completely disrupted, and she was emotionally labile. Seizures were difficult to control initially but responded to a combination of Phenytoin and Levetiracitam. Repeat CSF examination was clear with normal biochemistry. PCR for Herpes and other viruses were negative.\nSerum VGKC-Abs were positive with titers of 1088 pM (normal < 100 pM). Further radiological investigations for possible underlying malignancy were negative. Treatment with high a dose oral prednisolone (60 mg) once daily for first 2 weeks followed by 4 weeks of weaning doses. The latency period from admission to immunotherapy was 3 weeks. There was slow but significant improvement in her symptoms following immunotherapy. The repeat serum VGKC-Abs titers after immunotherapy were negative, consistent with her clinical improvement. The neuropsychological evaluation before and after the immunotherapy suggested significant improvement in her cognition and behavior.\nRepeat MRI brain done after the treatment showed a reduction in the gyral thickening with improved grey-white matter differentiation and normal DWI. She received intense neurorehabilitation based at hospital and community following discharge. She has restarted in mainstream school after 6 months and has made near complete recovery. | [[13.0, 'year']] | F | {'19780798': 1, '11456313': 1, '15819715': 1, '14960497': 1, '20663977': 1, '20660916': 1, '18815385': 1, '28461817': 1, '21777830': 1, '20034278': 1, '20959359': 1, '18411052': 1, '19251579': 1, '24339586': 2} | {} |
164,409 | 3841622-1 | 24,339,601 | noncomm/PMC003xxxxxx/PMC3841622.xml | Electromyographic and histological features of postpartum hypernatremic rhabdomyolysis | A 20-year-old lady was admitted 2 weeks after first delivery with progressively declining word output for 10 days. She was disoriented for 3 days before admission with oliguria. She had normal tone and power with brisk tendon reflexes. EMG of right upper and lower limb muscles revealed fibrillations and positive sharp waves. Muscle power remained normal during hospital stay. Serum CK was 6,139 units/l at admission (normal range: 50-200. units/l); 4,175 units/l on the day of EMG and declined to 149 units/l at 1 month follow-up. Subsequently, she had uneventful second pregnancy and puerperium 1 year later. | [[20.0, 'year']] | F | {'19078619': 1, '20129624': 1, '19841484': 1, '34621362': 1, '18157396': 1, '16267412': 1, '15252172': 1, '10339709': 1, '19959721': 1, '25678154': 1, '19099134': 1, '11870710': 1, '19078759': 1, '24339601': 2} | {'3841622-2': 2, '3841622-3': 2, '3841622-4': 2} |
164,410 | 3841622-2 | 24,339,601 | noncomm/PMC003xxxxxx/PMC3841622.xml | Electromyographic and histological features of postpartum hypernatremic rhabdomyolysis | A 25-year-old lady was admitted 3 weeks after fourth delivery with 5 days progressive quadriparesis and disorientation with drowsiness for 3 days. She was bedbound and incontinent for 2 days and had symmetric proximally dominant quadriparesis and during recovery was found to have ataxia. Serum CK was 58,587 units/l at admission and reduced to 917 units/l on 15 days from the onset of symptoms when needle EMG was performed. EMG revealed moderate amount of fibrillation and positive sharp waves, which was prominent in proximal muscles. Myotonic discharges were seen in biceps brachii, quadriceps and tibialis anterior []. Left biceps brachii muscle revealed features of extensive rhabdomyolysis, a few regenerating fibers and areas of perivascular infiltration as shown in . Clinical evaluation was normal at 1 month follow-up and serum CK level was 90 units/l. | [[25.0, 'year']] | F | {'19078619': 1, '20129624': 1, '19841484': 1, '34621362': 1, '18157396': 1, '16267412': 1, '15252172': 1, '10339709': 1, '19959721': 1, '25678154': 1, '19099134': 1, '11870710': 1, '19078759': 1, '24339601': 2} | {'3841622-1': 2, '3841622-3': 2, '3841622-4': 2} |
164,411 | 3841622-3 | 24,339,601 | noncomm/PMC003xxxxxx/PMC3841622.xml | Electromyographic and histological features of postpartum hypernatremic rhabdomyolysis | This 18-year-old lady was admitted 16 days after her first delivery with progressive quadriparesis and irrelevant speech that started 6 days after delivery. She had symmetrical severe quadriparesis with hypoactive tendon reflexes at admission. Tendon reflexes were noted to be brisk when the weakness improved. Serum CK was 11,288 units at admission and declined to 144 units/l on 10th day after symptom onset when EMG revealed fibrillations and positive sharp waves in limb and paraspinal muscles. Myotonic discharges were seen in biceps brachii and extensor digitorum brevis. Evaluation at one month after discharge was normal including serum sodium and CK levels. | [[18.0, 'year']] | F | {'19078619': 1, '20129624': 1, '19841484': 1, '34621362': 1, '18157396': 1, '16267412': 1, '15252172': 1, '10339709': 1, '19959721': 1, '25678154': 1, '19099134': 1, '11870710': 1, '19078759': 1, '24339601': 2} | {'3841622-1': 2, '3841622-2': 2, '3841622-4': 2} |
164,412 | 3841622-4 | 24,339,601 | noncomm/PMC003xxxxxx/PMC3841622.xml | Electromyographic and histological features of postpartum hypernatremic rhabdomyolysis | A 20-year-old primiparous lady was admitted with status epilepticus, which occurred 2 weeks after uneventful delivery. Blood pressure was 110/80 and the Glasgow coma scale was 4/15. She was found to have proximally dominant flaccid quadriparesis when she became conscious following seizure control. Serum CK was 15,122 units/l on the 2nd day of admission. EMG performed 7 days later revealed moderate amount of fibrillations and positive sharp waves in biceps brachii, quadriceps and tibialis anterior. Limb muscle weakness had become nearly normal at the time of EMG and serum CK level had reduced to 7,559 units. She had mild limb weakness with bilateral cerebellar ataxia at discharge and was lost from follow-up. | [[20.0, 'year']] | F | {'19078619': 1, '20129624': 1, '19841484': 1, '34621362': 1, '18157396': 1, '16267412': 1, '15252172': 1, '10339709': 1, '19959721': 1, '25678154': 1, '19099134': 1, '11870710': 1, '19078759': 1, '24339601': 2} | {'3841622-1': 2, '3841622-2': 2, '3841622-3': 2} |
164,413 | 3841625-1 | 24,339,604 | noncomm/PMC003xxxxxx/PMC3841625.xml | Hot cross bun sign in HIV-related progressive multifocal leukoencephalopathy | A 37-year-old lady presented to us with subacute onset progressive ataxia, with tendency to sway toward the left, of 2 month duration. She had significant weight loss, anorexia, and recurrent fevers for 6 months. She was emaciated, had oral candidiasis, and hepatomegaly. Neurological examination revealed left gaze evoked nystagmus, incoordination involving the left extremities, and slurred speech. HIV serology done was positive with a CD4 count of 28/μL. Cerebrospinal fluid study revealed normal opening pressure, mild elevation of protein (65 mg%) with no cells and normal glucose.\nMRI of the brain multiplanar T1, T2, FLAIR, diffusion and postcontrast done on a 1.5 Tesla system (Avanto-SQ Engine, Siemens Medical Systems, Erlanger, Germany) revealed the classical HCB sign in pons. In addition, there were asymmetrical T2 hyperintense lesions involving the left middle and inferior cerebellar peducle extending into left cerebellar hemisphere with atrophy of the same structures []. The left cerebellar hemispheric hyperintensities were partially suppressible on FLAIR and not enhancing on contrast []. Magnetic resonance spectroscopy revealed reduction of N-Acetylaspartic acid peak with mild elevation of choline. Imaging features suggested a possible necrotic demyelinating process asymmetrically, involving the left cerebellar white matter and transverse pontine fibers consistent with PML. | [[37.0, 'year']] | F | {'11601421': 1, '25297924': 1, '19279286': 1, '2305051': 1, '29390551': 2, '21483137': 1, '9762957': 1, '34316636': 1, '33328971': 1, '9667563': 1, '19187260': 1, '24339604': 2} | {'5758253-1': 1} |
164,414 | 3841626-1 | 24,339,605 | noncomm/PMC003xxxxxx/PMC3841626.xml | Cerebral proliferative angiopathy: A rare clinical entity with peculiar angiographic features | An 18-year-old male presented with episodes of generalized tonic clonic seizures for 1 year. His compliance to treatment was not very good leading to poor seizure control. There was neither any history of headache, vomiting or any stroke like episode nor his neurological examination was suggestive of any focal neurological deficit.\nInitially magnetic resonance imaging brain was done elsewhere which revealed large left frontal parasagittal arteriovenous malformation (AVM) []. Subsequently cerebral digital subtraction angiography (DSA) was done at our center. DSA showed diffuse proliferative angiopathic changes suggestive of cerebral proliferative angiopathy (CPA) [].\nPatient was managed conservatively with antiepileptic drugs with strict adherence to compliance and was seizure free and doing well until he was lost to follow-up 1 month later. | [[18.0, 'year']] | M | {'29991310': 1, '26396618': 2, '1436409': 1, '18239181': 1, '9562595': 1, '24339605': 2} | {'4553743-1': 1} |
164,415 | 3841628-1 | 24,339,607 | noncomm/PMC003xxxxxx/PMC3841628.xml | Autosomal recessive bilateral frontal polymicrogyria with ectopia lentis and chorioretinal dystrophy | A 26-year-old female presented with epilepsy from 7 years of age. She also had a reduced vision from early childhood. Her initial generalized tonic clonic seizures later evolved as brief tonic right upper limb posturing suggestive of mesial frontal originating seizures. Magnetic resonance imaging (MRI) brain revealed BFP [Figure –]. EEG showed left parasagittal central-frontal spikes without focal slowing. Seizures were controlled on a combination of carbamazepine and clobazam.\nShe was born of second degree consanguineous parentage. Her antenatal, natal, and immediate postnatal periods were normal. There was a mild global delay in achieving some of her milestones. She completed her schooling with an average performance. There was no family history of similar illness in up to three generations other than her brother who had similar visual problems.\nShe had marfanoid body habitus. Head circumference was 54.5 cm, height 171 cm, and arm-span 177 cm. No skeletal or spinal deformities were evident. Cognitive skills were average without problems for routine daily activities. Neurologically, eye movements were normal. No focal neurological deficits were evident. Other systemic examination was normal.\nUncorrected visual acuity was counting finger close to face bilaterally. Slit lamp examination revealed infero-temporal subluxation of the lens in the right eye [Figure , and ]. Indirect ophthalmoscopy showed attached retina with optic disc pallor. There was diffuse retinal pigment epithelium (RPE) atrophy with tessellated background, arteriolar attenuation, and choroidal sclerosis in both the eyes []. There were no RPE clumps or bony spicules. At 3 weeks review, the previously subluxed lens in the right eye had dislocated into the vitreous. Full field electroretinogram (ERG) showed reduced amplitude of scotopic (75-80%) and photopic responses (60-70%).\nHemogram, renal and liver functions, serum homocysteine, arterial blood gas, ammonia, lactate, aminoacidogram (urine and serum), ultrasonography of abdomen, electrocardiogram and echocardiography were normal. | [[26.0, 'year']] | F | {'19734141': 1, '17568394': 1, '12730993': 1, '12049599': 1, '8334934': 1, '18509043': 1, '19200529': 1, '11845408': 1, '15159468': 1, '10634459': 1, '10894214': 1, '10690985': 1, '11941487': 1, '24339607': 2} | {} |
164,416 | 3841629-1 | 24,339,608 | noncomm/PMC003xxxxxx/PMC3841629.xml | Guillain Barre syndrome as a manifestation of neurological melioidosis | A 53-year-old gentleman, known diabetic of 8 years duration presented with a pain in both lower limbs of 15 days duration and weakness in the form of ascending quadriparesis involving proximal followed by distal group of muscles of 12 days duration. There were no cranial nerve and respiratory symptoms. There was history of malaise and low grade fever preceding this illness.\nOn examination at admission, vital signs were normal. General physical examination was normal. Higher mental functions and cranial nerve examination were normal. There was hypotonia in all four limbs with Medical research council (MRC) power of grade 4/5. The deep tendon reflexes were absent and he had bilateral flexor plantar response. Cerebrospinal fluid examination revealed albumino-cytological dissociation (Glucose 70 mg%, protein 88 mg%, no cells). Nerve conduction studies were suggestive of demyelinating polyradiculoneuropathy. He was detected to be HBs Ag positive and was seronegative for human immunodeficiency virus infection. Apart from elevated glycosylated hemoglobin A1C level of 7.8%, serum biochemical parameters including potassium levels were normal. He had neutrophilic leukocytosis (13,400/cmm, 88% neutrophils), blood cultures were sent and was empirically started on ceftriaxone. IV immunoglobulins of 0.40 g/kg/day were given for 5 days. During the course of the hospital stay, his blood sugars were kept under control with insulin.\nOn 2nd day of admission, patient developed bilateral facial weakness, power deteriorated to MRC grade 3/5. After 4 days of treatment, the patient developed respiratory distress requiring ventilatory support. Arterial blood gases report showed metabolic acidosis with raised lactate levels and hypoxia. Later, patient developed refractory septic shock and succumbed to death. Cultures grew B. pseudomallei and the diagnosis of melioidiosis presenting as GBS on a background of diabetes mellitus was considered. | [[53.0, 'year']] | M | {'16966405': 1, '10674641': 1, '9746040': 1, '1617057': 1, '10674639': 1, '460953': 1, '10780681': 1, '5945962': 1, '18240918': 1, '9781538': 1, '2708842': 1, '19121666': 1, '15372438': 1, '17642999': 1, '9127663': 1, '27506202': 2, '21448411': 2, '18506283': 1, '15614712': 1, '21963741': 1, '11049780': 1, '24339608': 2} | {'3063533-1': 1, '4977609-1': 1} |
164,417 | 3841630-1 | 24,339,609 | noncomm/PMC003xxxxxx/PMC3841630.xml | A case of peduncular hallucinosis presenting as a primary psychiatric disorder | A 63-year-old female patient was admitted to the psychiatry emergency clinic for hallucinations, nervousness and agitation, which had started abruptly before 2 days. She was described to be a little bit aggressive and conversable person before but neither the patient nor her family had a previous history of psychiatric disease. She was consulted to neurology as a late-onset psychiatric disorder to rule out an organic etiology. She had hypertension and had an ischemic cerebrovascular accident before and stopped taking acetylsalicylic acid treatment for 3 days.\nBefore 2 days, she had suddenly seen her sister was plastering the house she lived before and it had lasted nearly 5-6 min. After a few hours later, she had seen her dead mother calling her “come here” and this also had lasted nearly 5-6 min. After several hours, she had heard some voices calling “get out and walk” and she had walked aimlessly in the house. Then, she had become agitated and had thrown her grandson's toys around and had broken a window. After that she had attempted to jump down from the balcony and had slapped her daughter's face while she was trying to hold her. After she had calmed down, she had recognized these all as hallucinations and her children had brought her to the psychiatry emergency clinic.\nAt the neurological examination, she was cooperative, orientation for the person and the location was normal, but she was disoriented to time and couldn’t distinguish night and day. Cranial nerves were intact; there was no paresia other than a left upper monoparesia, which was the sequel of a previous ischemic cerebrovascular accident. She was aware of the hallucinations that she had.\nThere was no metabolic abnormality in blood examination; electrocardiogram and electroencephalogram (EEG) was normal, no acute pathology was found in cranial computed tomography. Acute infarction was found at the left side of pons with diffusion weighted magnetic resonance imaging (MRI) investigation [Figures and ].\nShe was diagnosed as a cerebrovasculer accident presenting with pedincular hallucinosis and was treated with heparin and 100 mg/day acetyl salicylic acid and ketiapin 50 mg/day was given for hallucinations. One week later, her hallucinations were resolved almost completely. | [[63.0, 'year']] | F | {'29867752': 1, '8146743': 1, '2812338': 1, '2360791': 1, '14941240': 1, '27403217': 1, '30046405': 2, '6684235': 1, '10070472': 1, '19333408': 1, '9798740': 1, '1552309': 1, '24339609': 2} | {'6037096-1': 1} |
164,418 | 3841631-1 | 24,339,610 | noncomm/PMC003xxxxxx/PMC3841631.xml | “Dry” and “wet” beriberi mimicking critical illness polyneuropathy | A 44-year-old non-alcoholic male was admitted with dyspnea, vomiting, upper abdominal pain, oliguria, and weakness of both the lower limbs of 3 days duration. He was admitted thrice in the previous 1 month for symptoms of heart failure at a peripheral hospital, with partial recovery each time upon conservative treatment. On admission, patient had tachypnea, unrecordable blood pressure, heart rate 136/min, elevated Jugular Venous Pressure (JVP), and bilateral pitting edema of legs. Systemic examination revealed right sided S3, systolic murmur of 3/6 intensity at the lower left sternal edge and 3 cm tender hepatomegaly. Bilateral lower limb power was 3/5 with sluggish deep tendon reflexes.\nElectrocardiography (ECG) revealed sinus tachycardia with ST depression in leads V3-V6. Arterial Blood Gas analysis showed severe metabolic acidosis []. 2D echocardiography on admission showed dilated Right atrium/Right ventricle (RA/RV) with mild tricuspid regurgitation and pulmonary hypertension []. A provisional diagnosis of right heart failure with the multiorgan dysfunction possibly due to sepsis or cardiac beriberi was made and he was managed conservatively with broad spectrum antibiotics, sodium bicarbonate infusion, inotropes, and thiamine infusion. Acidosis, shock, and renal failure recovered promptly over from 24 h to 48 h. However, his paraparesis worsened over the next 2-3 days and Nerve conduction study (NCS) suggested predominantly motor, axonal type of peripheral neuropathy []. With continued thiamine supplementation, his power in the lower limbs gradually improved and he was discharged in 2 weeks with near normal power in the lower limbs. | [[44.0, 'year']] | M | {'29213485': 1, '9741406': 1, '8868953': 1, '6147512': 1, '25781926': 1, '17346820': 1, '12682465': 1, '20987416': 1, '32551830': 2, '24339610': 2} | {'3841631-2': 2, '3841631-3': 2, '7791272-1': 1} |
164,419 | 3841631-2 | 24,339,610 | noncomm/PMC003xxxxxx/PMC3841631.xml | “Dry” and “wet” beriberi mimicking critical illness polyneuropathy | A 25-year-old lady who had delivered a baby 6 weeks back was admitted with generalized anasarca and paraparesis of 10 days duration. She had dyspnea and oliguria since 1 day. Deep tendon reflexes (DTR) suggested global areflexia and bilateral lower limb power was 3/5. Her thyroid function was normal and Anti-nuclear antibody (ANA) was negative. Her investigation results are tabulated in and NCS findings in . A diagnosis of heart failure with polyneuropathy was made and she was treated with IV thiamine infusion and supportive treatment. Edema disappeared over a week and she was discharged after 12 days with near normal power in lower limbs. | [[25.0, 'year']] | F | {'29213485': 1, '9741406': 1, '8868953': 1, '6147512': 1, '25781926': 1, '17346820': 1, '12682465': 1, '20987416': 1, '32551830': 2, '24339610': 2} | {'3841631-1': 2, '3841631-3': 2, '7791272-1': 1} |
164,420 | 3841631-3 | 24,339,610 | noncomm/PMC003xxxxxx/PMC3841631.xml | “Dry” and “wet” beriberi mimicking critical illness polyneuropathy | A 36-year-old alcoholic male was admitted withbilateral edema of legs andbilaterallower limb weakness of 3 weeks duration. He also had oliguria and vomiting of 4 days duration. Bilateral lower limb power was 4/5 and his echocardiography as well as NCV findings are enlisted in Tables and . Upon treatment with intravenous thiamine for 1 week followed by oral supplementation, his renal functions and acidosis recovered, edema disappeared. After 11 days he was discharged with complete recovery. | [[36.0, 'year']] | M | {'29213485': 1, '9741406': 1, '8868953': 1, '6147512': 1, '25781926': 1, '17346820': 1, '12682465': 1, '20987416': 1, '32551830': 2, '24339610': 2} | {'3841631-1': 2, '3841631-2': 2, '7791272-1': 1} |
164,421 | 3841632-1 | 24,339,611 | noncomm/PMC003xxxxxx/PMC3841632.xml | Osteomalacia induced peripheral neuropathy after obesity reduction surgery | A 25-year-old lady from a good socio-economic background presented with generalised body pains, cramps in limbs, paresthesias, and difficulty in getting up and climbing stairs for 10 days. She had undergone gastric sleeve surgery for morbid obesity 3 months before presentation. She was having recurrent vomiting and reduced oral intake after the surgery. Her weight had reduced by 21 kg over 2½ months after surgery. She had no co-morbidities. At the age of 11 years, the patient had experienced difficulty in walking and climbing stairs associated with body pains for the 1st time. She had genu valgum deformity and was chair bound for 2-3 months. At that time also, she was diagnosed to have osteomalacia. Neurophysiological evaluation had revealed a myopathic pattern. She had recovered completely with vitamin D and calcium supplementation. A similar episode a few years later also recovered with the same treatment.\nAt the time of current admission, her general physical examination was unremarkable except for obesity and mild pedal edema. Cardiorespiratory and abdominal examination was normal. Neurological examination revealed a waddling gait, hypotonic limbs without wasting and upper and lower limb weakness. Power was: upper limbs-3-4/5 proximally, 4-/5 distally; lower limbs-3/5 proximally, 4+/5 distally. Deep tendon reflexes were normal in upper and sluggish - Medical Research Council (MRC) grade 1 in lower limbs. There was no cranial nerve weakness and sensory examination was normal. A provisional diagnosis of limb girdle weakness of probable inflammatory or nutritional etiology was made.\nLaboratory investigations including hemogram, vitamin B12 (938 pg/mL; reference range: 220-960 pg/mL), and folate levels (5 ng/mL; reference range: 3-17 ng/mL) were unremarkable. However, serum calcium was 7.8 mg/dL, alkaline phosphatase 214 IU/L and parathormone level was raised (232 pg/mL; reference range: 14-72 pg/mL). The level of 25-hydroxy vitamin D was significantly low (2.58 ng/mL; reference range: 30-100 ng/mL). X-ray pelvis showed Looser zones in the pelvic bones []. Bone densitometry testing by a Dual energy X-ray absorptiometry (DEXA) scan showed a Frisk score of 6.9 (normal: 4.7 ± 1.4) suggestive of osteoporosis []. The diagnosis of post-gastric sleeve surgery with osteomalacic limb girdle weakness and hypoalbuminemia was made. Electrodiagnostic test carried out 3 months after surgery revealed reduced conduction velocities in the motor nerves of the lower limbs with normal sensory potentials suggestive of symmetrical motor polyneuropathy []. Electromyography (EMG) showed more proximal involvement with active denervation in the form of positive sharp waves and fibrillations in both vastii lateralis, high amplitude, and long duration motor unit potentials with decreased recruitment in proximal and distal muscles of both lower limbs consistent with neurogenic pattern of involvement.\nShe was started on a high protein, calcium, and vitamin rich diet and vitamin D and calcium supplementation. On evaluation after 1 week of treatment initiation, she had subjective improvement of 40% with respect to cramps and general well-being and had improved clinically by 10-15%. Power in the limbs had increased by one grade and mobility was better. Three months later, pain had subsided and she had only distal numbness over tips of thumb and index fingers. Power and mobility had further improved and finally she regained complete recovery of strength after 7 months of initiation of treatment. Nerve conduction parameters also normalized []. Serum levels of albumin, calcium, alkaline phosphatase, 25-hydroxy vitamin D, and parathormone returned toward normal. X-ray pelvis on follow-up showed disappearance of the Looser's zones []. Thus, this young female who had presented with severe degree of proximal weakness due to osteomalacia unmasked after bariatric surgery, finally recovered with treatment with vitamin D and calcium therapy-clinically, biochemically and neurophysiologically. | [[25.0, 'year']] | F | {'6058144': 1, '993799': 1, '47234': 1, '29623355': 1, '15505166': 1, '1119316': 1, '25445838': 1, '18497435': 1, '14262195': 1, '10919943': 1, '21088925': 1, '20842487': 1, '33504933': 1, '24339611': 2} | {} |
164,422 | 3841633-1 | 24,339,612 | noncomm/PMC003xxxxxx/PMC3841633.xml | Focal neuromyotonia as a presenting feature of lumbosacral radiculopathy | A 36-year-old man presented with back pain and cramp like pain in both lower limbs of 4 month duration. Pain was initially dull aching localized to the lower back, aggravate on walking and partially subside with rest and analgesics. Simultaneously, he developed cramp like pain in both calves along with stiffness, which he initially noticed while walking. Initially, he had to take pauses while walking. Later on, there was severe difficulty in walking. Since, 2 months, patient developed severe cramp like pain even at rest, affecting his sleep. Along with the muscle cramps, he noticed formation of a transient lumps in both calves due to focal muscular contraction. He did not complain of any radicular pain, tingling, numbness or any other sensory complaints. There was no excessive sweating. He noticed twitching in both calves since 2 months. There was no history of any weakness or thinning noticed in lower limbs. He did not have any complaints in upper limbs. Family history was not significant. His general examination was unremarkable. Higher mental functions and cranial nerves were normal. Upper limb examination was normal. Lower limb examination revealed mild thinning in the left leg. There was frequent rippling noted in both calves. Tone, power, and reflexes were normal. There was no sensory loss, but because of pain and cramps he had severe limitation of walking. Spine examination revealed tenderness and spasm in lower paraspinal muscles. There was no deformity. Straight leg-raising testing was positive on both sides. There was no evidence of autonomic involvement.\nHematological and biochemical tests including blood sugar, kidney function tests, serum electrolytes including calcium, thyroid profile were normal. Nerve conduction study revealed mildly reduced tibial compound muscle action potential amplitude with normal sural sensory nerve action potential. Electromyography (EMG) in bilateral gastronomies lateral head revealed spontaneous activity in the form of doublets, triplets and neuromyotonic discharges (160-200 Hz waning type of discharges with pinging sound). There was reduced recruitment, incomplete interference pattern along with polyphasic motor unit potentials (MUP) in bilateral L5, S1 innervated muscles (Tibialis anterior and hamstrings). Lumbar paraspinal EMG revealed fibrillation potentials. Bilateral H reflex testing didn’t show any recordable waveforms []. EMG in both quadriceps muscles was normal. Magnetic resonance imaging Lumbosacral spine revealed annular tear along with disc protrusion at L3-4, L4-5 with severe foraminal (right > left) and spinal canal stenosis along with compression of the nerve roots. There was contrast enhancement noted in the protruded disc and nerve roots suggestive of active inflammation []. Patient received intravenous methylprednisolone for 3 days, carbamazepine 200 mg twice a day, duloxetine 20 mg once a day and physiotherapy. There was marked relief in pain, stiffness and cramps after 10 days. Even the calf muscle rippling was drastically reduced. | [[36.0, 'year']] | M | {'10864615': 1, '20816272': 1, '11603366': 1, '10797387': 1, '21985744': 1, '1648679': 1, '11360270': 1, '21610902': 1, '23177040': 1, '16843723': 1, '17114847': 1, '7311989': 1, '12634577': 1, '19523866': 1, '24339612': 2} | {} |
164,423 | 3841634-1 | 24,339,613 | noncomm/PMC003xxxxxx/PMC3841634.xml | Acute myeloneuropathy: An uncommon presentation of Sjögren's syndrome | A 40-year-old female presented to our hospital with complaints of diffuse low intensity pain in all four limb since 20 days. She also noticed tingling sensation in all four limbs, which started distally and progressed proximally within 24 h. Simultaneously she noticed weakness in all four limbs, which started proximally and progressed to distal muscles over 24-30 h in all 4 limbs. She also complained of dysuria, urinary retention and incomplete emptying of the bladder. She had a history of gritty sensation in both eyes and dryness of mouth for last 8 months, for which she had to repeatedly take sips of water while having her food. Clinical examination revealed normal higher mental functions and cranial nerves. Hypotonia was noted in all four limbs. Power was Medical Research Council (MRC) grade 3/5 proximally and MRC grade 2/5 distally in both upper and lower limbs. Both superficial reflexes and deep tendon jerks were absent. Sensory examination was normal. No neck rigidity, local spinal deformity or nerve thickening was noted.\nInvestigations showed normal complete hemogram blood sugars (fasting and post-prandial), serum Vitamin B12 levels, thyroid function tests, renal function tests, enzyme-linked immunosorbent assay for human immunodeficiency virus, hepatitis B surface antigen and anti- hepatitis C virus tests. Both erythrocyte sedimentation rate and C-reactive protein were raised 24 mm at the end of 1 h and 19 mg/L respectively. Liver function tests were normal except serum albumin was low (1.9 g/dl) with reversal of globulin albumin ratio. Serum protein electrophoresis was normal. Magnetic resonance imaging (MRI) spine revealed diffuse T2 hyperintensity throughout the cord []. The nerve conduction studies revealed sensorimotor axonal polyneuropathy with absent F and H reflex []. Cerebrospinal fluid (CSF) analysis revealed mild pleocytosis with total cells of 20, predominantly lymphocytes (95%), CSF protein was raised (50 mg/dl) and CSF sugar was normal. CSF analysis for tuberculosis-polymerase chain reaction and virology (Epstein-barr virus, JE, cytomegalovirus and herpes simplex virus) was negative. Anti-nuclear antibodies were raised in the titre of 1:100. Anti-SS-A was positive, but anti –Sm was negative. Rheumatiod factor and anti-cyclic citrullinated peptide were negative. Histopathology of sural nerve biopsy showed mild perineural fibrosis, focal foamy changes in endoneurium with mild lymphocytic infiltration []. Wade Fite stain for Mycobacterium leprae was negative. Schirmer's test was positive in both eyes (2 mm/5 min in the right eye and 3 mm/5 min in the left eye). Patient didn’t give consent for salivary gland biopsy. She was treated with IV methylprednisolone 1 g/d for 5 days followed by oral prednisolone 50 mg/day. She received anti-cholinergic medications for urinary incontinence. The clinical improvement was seen in the patient with power improvement to MRC grade 4+ in proximal as well as distal muscle groups in all 4 limbs. Follow-up MRI study demonstrated normalization of altered signals on the spinal cord []. However, urinary incontinence persisted and subsequent uroflowmetry showed hypocontractile bladder with low compliance, which partly improved with anticholinergic drugs. | [[40.0, 'year']] | F | {'21808473': 2, '20976785': 1, '15342972': 1, '27110384': 1, '14710969': 1, '16049042': 1, '27011654': 2, '12006334': 1, '11868603': 1, '33208548': 1, '14717615': 1, '27293327': 1, '24339613': 2} | {'3141473-1': 1, '3141473-2': 1, '3141473-3': 1, '3141473-4': 1, '4782539-1': 1} |
164,424 | 3841635-1 | 24,339,614 | noncomm/PMC003xxxxxx/PMC3841635.xml | Two cases of medically-refractory spontaneous orthostatic headaches with normal cerebrospinal fluid pressures responding to epidural blood patching: Intracranial hypotension versus hypovolemia and the need for clinical awareness | A 31-year-old male presented in February 2009 with subacute onset occipital and sub-occipital moderate “pressure-like” headaches and neck pain for 2 years. The headache was precipitated by standing or walking and relieved on assuming recumbent position. There was no history of nausea, vomiting, photo-phonophobia, auras, seizures, loss of consciousness, neurological deficit, trauma, cranial/spinal surgery or fever. He had been evaluated at another hospital 1 year back where his MRI brain was normal, but CSF pressure was reported to be “low.” He had been treated with EBP, following, which he had shown good recovery. Clinical examination was normal. CSF opening pressure was 80 mm water. CSF analysis was normal. MRI brain revealed thin subdural hygroma, absence of meningeal enhancement, and mild tonsillar descent [Figure –]. Contrast MRI spine and myelography, and radioisotope cisternography did not reveal an area of CSF leak. Routine laboratory parameters were normal. He was given autologous EBP with reduction in headache by 40% after 5 days followed by complete relief over days without recurrence of headache since then. Follow-up MRI showed normalization of CSF space in the posterior fossa []. | [[31.0, 'year']] | M | {'28924323': 1, '31523146': 1, '21891924': 1, '10560599': 1, '18040112': 1, '12654957': 1, '1549206': 1, '21808479': 1, '16705110': 1, '21264139': 1, '9748027': 1, '14979299': 1, '20174499': 2, '11087775': 1, '15062528': 1, '12100320': 1, '24339614': 2} | {'3841635-2': 2, '2824935-1': 1} |
164,425 | 3841635-2 | 24,339,614 | noncomm/PMC003xxxxxx/PMC3841635.xml | Two cases of medically-refractory spontaneous orthostatic headaches with normal cerebrospinal fluid pressures responding to epidural blood patching: Intracranial hypotension versus hypovolemia and the need for clinical awareness | A 41-year-old male presented in Oct 2009 with subacute onset, severe bifrontal throbbing headaches for 1 month. It was precipitated within 10 min of standing and relieved after few minutes in the recumbent position. He was so incapacitated with his headache that he was very fearful of getting off his bed for activities of daily living. Rest of the history, clinical examination and routine laboratory parameters were unremarkable. On clinical suspicion of SIH, MRI brain was carried out, which revealed bilateral subdural hygromas [Figure –], diffuse meningeal enhancement [Figure ,], venous distension sign [], sagging of the brain and tonsillar herniation []. Contrast MRI spine did not reveal CSF leak. CSF opening pressure was 80 mm water. CSF analysis was normal. Patient did not respond to bed rest, analgesics and fluids. He responded remarkably to EBP with reduction of headache by 75% in 72 h, and was headache free after 4 weeks with no recurrence on follow-up. MRI after 3 months revealed resolution of findings [Figure –]. | [[41.0, 'year']] | M | {'28924323': 1, '31523146': 1, '21891924': 1, '10560599': 1, '18040112': 1, '12654957': 1, '1549206': 1, '21808479': 1, '16705110': 1, '21264139': 1, '9748027': 1, '14979299': 1, '20174499': 2, '11087775': 1, '15062528': 1, '12100320': 1, '24339614': 2} | {'3841635-1': 2, '2824935-1': 1} |
164,426 | 3841637-1 | 24,339,616 | noncomm/PMC003xxxxxx/PMC3841637.xml | Two case reports of an unusual association between Klippel-Feil syndrome and amyotrophic lateral sclerosis: Do they share same genetic defect? | Thirty-eight-year-old right-handed smoker male presented with progressive slurring of speech, difficulty in chewing and swallowing since 8 months. He complained of choking spells, nasal regurgitation, nonradiating neck pain, weakness and atrophy of right thumb and index finger along with muscle twitching in all limbs. There were no paresthesias, dyspnea, trauma, bladder, and bowel difficulties or significant family history. Examination revealed short neck, low posterior hairline, kyphoscoliosis with convexity to right, restricted neck movements on lateral flexion and extension with negative compression test. He had preserved language function with slurred, hypernasal speech. His right soft palate was sagging with absent gag reflex. Bilateral thenar and hypothenar muscles were atrophied. Fasciculation's were present in tongue, biceps, triceps, pectorals, and quadriceps. Brisk limb Deep Tendon Reflexes, extensor planters with normal sensory examination were present. Jaw jerk was absent. Magnetic resonance imaging (MRI) cervical spine revealed right kyphoscoliosis, partial fusion of C3-4 without cord compression and butterfly vertebra at C4 []. The Nerve Conduction Velocity-Electromyography (NCV-EMG) study showed low CMAP (Compound Motor Action Potential) in both facial nerves and denervation potentials in right upper limb suggestive of anterior horn cell disease. Audiometry, abdominal ultrasonography, echocardiography does not revealed other abnormalities. We examined his father and only daughter but could not find any evidence of Klippel-Feil syndrome (KFS) or amyotrophic lateral sclerosis (ALS). Final diagnosis was made as Klippel-Feil anomaly type II with definite ALS with bulbar presentation, using revised El-Escorial world federation of neurology criteria. Other possible differentials were excluded by relevant history, radiological, electrodiagnostic (EMG), biochemical (viz. Cerebrospinal Fluid, complete analysis, thyroid profile, lipid profile, S. calcium, Fasting Blood Sugar (FBS), T. proteins) and hematological [Complete Blood Count (CBC), Erythrocyte Sedimentation Rate (ESR)] investigations. | [[38.0, 'year']] | M | {'8187635': 1, '13225466': 1, '19917993': 1, '11391660': 1, '17485643': 1, '9055366': 1, '6747689': 1, '1093066': 1, '25634178': 1, '15948205': 1, '24339616': 2} | {'3841637-2': 2} |
164,427 | 3841637-2 | 24,339,616 | noncomm/PMC003xxxxxx/PMC3841637.xml | Two case reports of an unusual association between Klippel-Feil syndrome and amyotrophic lateral sclerosis: Do they share same genetic defect? | A case of 42-year-old right-handed male smoker presented with predominantly distal progressive asymmetrical weakness of all limbs, more on left, since 2 years. Also, slurred speech, difficult chewing and swallowing, choking spells, nasal regurgitation, limb cramps were present since 4 months. There were no paresthesias, dyspnea, trauma, bladder, and bowel difficulties. Examination revealed short neck, low posterior hairline, and restricted neck movements on lateral flexion with negative compression test. Speech was low volume, hypernasal with preserved language function. Bilateral atrophied thenar and hypothenar muscles, brisk DTR, extensor planters, fasciculation's of tongue, arm and thigh, absent jaw and gag reflex were evident. Sensory examination was normal. X-ray cervical spine revealed multiple fused vertebrae with wasp-waist sign. On MRI multiple block vertebrae C4-D1, butterfly vertebrae D2-3, cervical scoliosis without cord compression, wine glass appearance with loss of fibers of posterior third of internal capsule were evident [Figures and ]. The NCV-EMG study showed decreased amplitude in both facial nerves, denervation involving muscles of all limbs suggesting anterior horn cell disease. Digging into family history did not reveal any significant information. Final diagnosis was made as Klippel-Feil anomaly type I with definite ALS with bulbar involvement, using revised El-Escorial world federation of neurology criteria. Other possible differentials were excluded by relevant history, radiological, electrodiagnostic, biochemical (viz. CSF-complete analysis, thyroid profile, lipid profile, S. calcium, FBS, T. proteins) and hematological (CBC, ESR) investigations. | [[42.0, 'year']] | M | {'8187635': 1, '13225466': 1, '19917993': 1, '11391660': 1, '17485643': 1, '9055366': 1, '6747689': 1, '1093066': 1, '25634178': 1, '15948205': 1, '24339616': 2} | {'3841637-1': 2} |
164,428 | 3841640-1 | 24,339,619 | noncomm/PMC003xxxxxx/PMC3841640.xml | The combination of thermal dysregulation and agenesis of corpus callosum: Shapiro's or/and reverse Shapiro's syndrome | A 3.5-year-old girl was admitted to the Dokuz Eylul University Hospital with complaints of recurrent fever and vomiting. The patient had a history of hyperthermia episodes and vomiting, which started 4 months before admission. She had an axillary daily spiking fever up to 40°C. Fever and vomiting attacks lasted for 3-8 days. Vomiting did not accompany fever in all of the episodes. Besides these fever attacks, her mother mentioned that her child was also “becoming cold” during the day and this condition lasted approximately 1 h with accompanying diaphoresis. She had been investigated at other hospitals and had been treated with antibiotics for a presumed infection many times. She had agenesis of the corpus callosum, which was determined during the intrauterine period. She had psychomotor retardation. The parents were not consanguineous. There was no history of exposure to tuberculosis, cats, tick, insect bites, rash, arthralgia, arthritis, diarrhea, constipation, abdominal pain, or weight loss.\nOn physical examination, her weight, height, and head circumference were 10 kg (<3p), 88 cm (<3p), 46 cm (50-75p), respectively. Blood pressure was 90/55 mmHg. Body temperature was 40°C. Neurologic examination revealed strabismus, brisk deep tendon reflexes, and axial hypotonicity. Examination of the ears, nose, and throat was normal. She had normal lymphoid tissue with no adenopathy. Lungs were normal and cardiac examination revealed no murmur. There was no hepatosplenomegaly. The remainder of the physical examination was normal. The cause of fever with vomiting was unable determined in examination.\nInitial laboratory results were as follows: White blood cell count 9600/mm3 (4000-10300); hemoglobin 9.6 g/dL (12-14.5); platelet count 496000/mm3 (156000-373000); C-reactive protein 2.3 mg/L (0.1-8.2). Peripheral blood smear was normal. Renal and liver function tests, serum creatine kinase, electrolyte levels, and urine analysis were normal. The child was started with ceftriaxone. Cultures of blood and urine were negative. Serological work-up for toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus, ebstein barr virus, brucella, salmonella, mycoplasma pneumoniae, chlamydia, and hepatitis were negative. Evaluation for tuberculosis was also negative. After the elimination of infections, antiobiotherapy was stopped. Serum immunoglobulin A, M, G and complement (C3, C4) levels were normal. Anti-nuclear antibodies, anti-double stranded DNA antibodies, anti-neutrophil cytoplasmic antibodies, extractable nuclear antigens were negative. Mediterranean fever mutation analysis for familial mediterranean fever was negative. Level of serum Ig D for hyperimmunoglobulin-D syndrome was normal (18 IU/mL, N: 2-99.3). Abdominopelvic ultrasonography revealed normal findings. Brain magnetic resonance images (MRI) confirmed complete agenesis of corpus callosum []. Chest radiography and electroencephalography were normal.\nShe had normal serum levels of thyrotropin releasing hormon (2.82 μIU/mL) and free thyrotropin (1.22 ng/dL), cortisol (20.5 μg/dL), adrenocorticotropic hormon (15.9 pg/mL). Thus, infections, collagen vascular diseases, malignancy, hematologic diseases, some of periodic fever sydromes, hormonal disorder were excluded as the cause of her periodic hyperthermia with vomiting. Besides these fever attacks, during hospitalization, axillary body temperature of our case was observed to decrease to 34.3°C [] with accompanying diaphoresis, lasting for approximately an hour.\nPatient was evaluated in terms of possible metabolic causes of recurrent vomiting. A metabolic survey including analysis of serum tandem mass spectrometry and blood, urine amino acid assay found nothing specific. Serum lactic acid and ammonia level were normal. Venous blood gas analysis was normal during vomiting attacks. Thereby, metabolic diseases were excluded. In terms of recurrent vomiting, all investigations including analysis of serum and urine, abdominopelvic ultrasonography, MRI were normal. No specific cause of the recurrent vomiting was identified. Bowel obstruction was not considered because physical examination was normal and there was no symptom except for attack.\nIn our case, thermal dysregulation and vomiting was considered to may be associated with agenesis of corpus callosum. On the 15th day of the follow-up, she was discharged after resolving patient's fever and vomiting attacks. | [[3.5, 'year']] | F | {'7565067': 1, '5790256': 1, '16122637': 1, '11208537': 1, '19794103': 1, '16901417': 1, '2846402': 1, '1631258': 1, '21966219': 1, '22927684': 1, '16009897': 1, '554524': 1, '8179499': 1, '11160966': 1, '2910261': 1, '17250734': 1, '1639946': 1, '18203725': 1, '925703': 1, '19027594': 1, '6738818': 1, '10490044': 1, '9038041': 1, '4715189': 1, '6684246': 1, '21927958': 1, '8280447': 1, '24339619': 2} | {} |
164,429 | 3841642-1 | 24,339,621 | noncomm/PMC003xxxxxx/PMC3841642.xml | An unusual presentation of subdural empyema caused by Porphyromonas gingivalis | A 34-year-old male was admitted to Thammasat University Hospital, Thailand with 1 day of high fever, severe headache, photophobia, left hemiparesis, and repeated vomiting. He had had rhinorrhea, sore throat, facial pain, and low grade fever 2 weeks earlier and was treated with a short course of oral antibiotics.\nOn admission, he was alert and oriented. The patient had a temperature of 39°C, heart rate of 120 beats/min, and blood pressure of 130/90 mmHg. Neurological examination revealed nuchal rigidity and left hemiparesis grade 3 (medical research council scale). He had left facial weakness, upper motor neuron type with purulent nasal discharge, nasal turbinate swelling, and frontal sinus tenderness. His blood profile showed leukocytosis of 23,700 cells/mm3 with 95% neutrophils. His basic metabolic panel showed normal electrolytes, glucose, liver, and renal function. Computed tomography (CT) of the brain revealed crescent-shaped hypodense to isodense lesion at right frontal convexity and along right falx cerebri with 0.6 cm in maximal thickness at right frontal lobe suggestive of subdural effusion. The CT additionally revealed opacification at both frontal sinuses, both ethmoid sinuses and left maxillary sinus suggestive of sinusitis. A magnetic resonance imaging (MRI) was obtained and showed thin subdural collection over right hemispheric convexity and right interhemispheric fissure causing subfalcian brain herniation to the left for about 8 mm with bilateral frontal, ethmoid, and left maxillary sinusitis [].\nHe was diagnosed with subdural empyema and started on intravenous ceftriaxone 4 g daily divided every 12 h and metronidazole 1.5 g daily divided every 8 h and were continued for 6 weeks without dose adjustment. He received supportive care with neurosurgical consultation. On the 2nd day of admission he developed increased left hemiparesis (from grade 3 to grade 0) and his consciousness level deteriorated. Right frontoparietal craniectomy was performed. Antiepileptic drugs were started. Seizure prophylaxis was started as intravenous dilantin 300 mg daily divided every 8 h. Yellowish purulent material with a total volume of 100 ml was drained and sent for microbiological examination. No organisms were isolated in aerobic pus culture. Polymerase chain reaction (PCR) molecular identification for bacteria isolated Porphyromonas gingivalis. The 16S rRNA sequences of the genus Porphyromonas were selected from the taxonomy database of the National Center for Biotechnology Information (). The sequence of the forward primer, was 5’-GCGCTCAACGTTCAGCC-3’ (base pairs 612-628); the sequence of the reverse primer was 5’-CACGAATTCCGCCTGC-3’ (base pairs 664-679); and the sequence of the Taqman probe, was 5’-CACTGAACTCAAGCCCGGCAGTTTCAA-3’ (base pairs 634-660).[] Patient regained full consciousness 2 days after the surgery. Bilateral anterior ethmoidectomy and bilateral frontal sinectomy were also performed. On 15th day of admission, his consciousness deteriorated. MRI showed subdural empyema along bilateral falx cerebri and right parieto-temporo-occipital region. A second craniotomy was done and drainage tubes were placed at posterior midline parietal and occipital area, a total of 100 ml of yellow purulent material was drained. Patient gradually improved and was discharged after 6 weeks of the intravenous antibiotics. Dental consultations revealed no dental or root canal abscesses, no further work up for periodontal disease were carried out. At the time of discharge, his motor power was 5/5 with normal mental status. No signs of recurrent infection were detected on the follow-up 1 month after discharge []. | [[34.0, 'year']] | M | {'19707005': 1, '22144533': 1, '922397': 1, '21910623': 1, '15455734': 1, '28228396': 2, '3268746': 1, '9797247': 1, '23136260': 1, '22530835': 1, '589140': 1, '7916132': 1, '10522225': 1, '14605122': 1, '15013561': 1, '18327428': 1, '10069590': 1, '24339621': 2} | {'5337642-1': 1} |
164,430 | 3841662-1 | 24,339,463 | noncomm/PMC003xxxxxx/PMC3841662.xml | Triple protozoal enteropathy of the small intestine in an immunocompromised male: A rare histopathology report | A 43-year-old male was diagnosed in November 2008 as HIV-positive and was on regular ART. He was admitted to hospital with complaint of passing loose stools 8-10 times per day since 1 month without associated pain abdomen, passage of blood or mucus in stool. He had an episode of diarrhea about 6 months back. It was diagnosed as cryptosporidial diarrhea on stool examination and he was treated with nitrazoxamide successfully.\nThe patient had several associated comorbidities. He was a documented case of disseminated tuberculosis since August 2010 and was on ATT. Presently, he is also a patient of Herpes Zoster (T6-T10 dermatome) and is on acyclovir therapy. On general physical examination, he was found to be a thinly built, well oriented, afebrile with a supine blood pressure of 90/66 mmHg and a regular pulse rate of 88/min. He had a significant left cervical and axillary lymphadenopathy with matted nodes. No organomegaly on abdominal examination was seen. Upper GI endoscopy revealed essentially normal esophagus and stomach and first part of duodenum. The second part of duodenum showed nodular folds. Ultrasonography of abdomen and pelvis showed calcified areas in segment VII of liver and multiple hypoechoic focal lesions (? granulomas).\nThe laboratory investigations revealed hemoglobin-10.9 g/dl, total leucocytic count -4,200/μl, differential leucocytic count was lymphocytic predominant (54%), and a platelet count of 1.5 lakh/μl. His absolute CD4+ T lymphocyte count was 219 cells/μl and viral load was less than 400 copies/ml. His liver and renal function tests and urine examination were essentially normal. Upon stool examination no ova, cyst, acid-fast bacilli, or any other organism was discerned. Culture of stool showed no growth. Stool was also negative for fat globules.\nHistopathological examination of biopsy from second part of duodenum revealed mild atrophy in the form of blunting, shortening, and fusion of villi with crypt elongation at places. A focal disorganization of the epithelium, loss of nuclear polarity, cell crowding, and cell vacuolation was seen []. Lamina propria showed an intense lymphoplasmacytic infiltrate along with few eosinophils and occasional macrophages. Numerous enterocytes showed intracytoplasmic loose parasitophorous vacuoles containing isosporidia schizonts and merozoites. These organisms were seen in the basal part of cytoplasm below and around the nucleus. The single organisms were the schizonts. Focally on luminal surface of occasional enterocytes, small bluish intracellular but extracytoplasmic round to oval amphophilic structures resembling cryptosporidia were seen. Also noted were foci of occasional enterocytes containing intracytoplasmic vacuoles with small, round to oval, bluish supranuclear refractile spores resembling microsporidia []. No crypt destruction, dysplasia, or granulomas were seen. Lamina propria showed dilated vascular channels at places. Special histochemical stains to identify the parasites done were – Brown – Bren modification of Gram stain, PAS, Masson's trichrome, toluidine blue [], Giemsa, modified acid fast, and Gomori's methanamine silver (GMS) stains. A histopathology opinion of enteritis due to triple infection by isosporidia, cryptosporidia, and microsporidia was offered.\nBased on histopathology report, patient was put on tablets niazoxanide, Septran, Cifran, and Fluconazole. He has since improved and is under regular follow-up in the outpatient department and ART center of the hospital. | [[43.0, 'year']] | M | {'25763312': 2, '3487730': 1, '8218693': 1, '20739000': 1, '16509972': 1, '19822892': 1, '15458486': 1, '24339463': 2} | {'4334046-1': 1} |
164,431 | 3841663-1 | 24,339,464 | noncomm/PMC003xxxxxx/PMC3841663.xml | Pseudoepitheliomatous keratotic and micaceous balanitis | A 65-year-old male presented with a chronic nonhealing lesion over his penis since 6 months. It was associated with occasional itching, irritation, and burning sensation following micturition. There was no history of bleeding either spontaneously or following minimal trauma. Clinical examination, after retracting the prepuce, revealed a well-defined hyperkeratotic plaque with thick adherent micaceous scales surrounded by a slight erythematous halo []. There was no regional lymphadenopathy. Based on these findings, biopsy of the lesion was performed under local anesthesia with clinical differential diagnoses of verrucous/squamous cell carcinoma (SCC) and lichen sclerosus in mind. Histopathology of the lesion revealed epidermal hyperkeratosis, parakeratosis, acanthosis, and papillomatosis (features of pseudoepitheliomatous hyperplasia) with perivascular mononuclear cell infiltrate in the dermis []. There were no cellular dysplasia or frank neoplastic changes and the basement membrane was intact. Based on these clinical and histopathological findings, a diagnosis of PKMB was made. Patient is on treatment with topical 5-fluorouracil (5-FU; 5%) cream once-a-day [], and is being regularly followed-up. | [[65.0, 'year']] | M | {'21263246': 1, '20606894': 2, '8659009': 1, '27733889': 1, '21808443': 1, '3120984': 1, '30684817': 1, '3689682': 1, '3343410': 1, '15339089': 1, '10037403': 1, '33817603': 1, '14466728': 1, '21399489': 1, '591665': 1, '20826996': 1, '26557598': 1, '26793536': 1, '24339464': 2} | {'2887529-1': 1} |
164,432 | 3841664-1 | 24,339,465 | noncomm/PMC003xxxxxx/PMC3841664.xml | Bullous disorders as a manifestation of immune reconstitution inflammatory syndrome: A series of three cases | A 45-year-old, Hindu, male, truck driver was found to be HIV reactive 4 years back. Since then, he was on regular monitoring of CD-4 T-cell count at ART clinic. He had recurrent attacks of loose motion 3 months back. Investigations showed his CD4 T-cell count was 44/μL. Highly active antiretroviral therapy (HAART), comprising zidovudine, lamivudine and nevirapine was started after routine laboratory investigations. After 4 weeks, multiple flaccid bullous lesions appeared on the different parts of the body. Oral and genital mucosa were involved.\nClinical examination showed positive Nikolsky sign. Tzanck smear showed acantholytic cell under light microscope.\nInvestigation revealed increased CD4 T-cell count (252/μL). Incisional biopsy for histopathological examination (HPE) with hematoxylin and eosin stain showed intra-epidermal bullae [] and perilesional punch biopsy for the direct immunofluorescence (DIF) showed intra-epidermal deposition of immunoglobulin G (IgG). Considering all the findings, PV was diagnosed. | [[45.0, 'year']] | M | {'16553555': 1, '16051964': 1, '15750393': 1, '17255740': 1, '10975963': 1, '27190420': 2, '22169463': 1, '9727570': 1, '22310819': 1, '21270328': 1, '34540666': 2, '19815866': 1, '24339465': 2} | {'3841664-2': 2, '3841664-3': 2, '4857691-1': 1, '8444988-1': 1} |
164,433 | 3841664-2 | 24,339,465 | noncomm/PMC003xxxxxx/PMC3841664.xml | Bullous disorders as a manifestation of immune reconstitution inflammatory syndrome: A series of three cases | A 38-year-old known HIV positive, Hindu, male, gold smith had a history of sudden loss of weight for last 3 months. Investigations revealed the CD4 T-cell count was 53/μL. HAART was started. Bullous lesion appeared on the trunk and face, 3 weeks after the initiation of HAART. Clinical examination showed multiple erosions and crusted lesions present almost all over the body. The soft palate and inner side of lips were also involved. Nikolsky sign was positive. The CD-4 T-cell was found to be increased to 274/μL. Nevirapine was stopped immediately, but the lesions were persisting. Tzanck smear from fresh lesion showed acantholytic cell under light microscope. Histopathology from a fresh lesion showed intra-epidermal bullae. DIF from perilesional skin showed IgG deposition within the epidermis in lacy pattern. The clinical features and investigations point toward the diagnosis of PV. | [[38.0, 'year']] | M | {'16553555': 1, '16051964': 1, '15750393': 1, '17255740': 1, '10975963': 1, '27190420': 2, '22169463': 1, '9727570': 1, '22310819': 1, '21270328': 1, '34540666': 2, '19815866': 1, '24339465': 2} | {'3841664-1': 2, '3841664-3': 2, '4857691-1': 1, '8444988-1': 1} |
164,434 | 3841664-3 | 24,339,465 | noncomm/PMC003xxxxxx/PMC3841664.xml | Bullous disorders as a manifestation of immune reconstitution inflammatory syndrome: A series of three cases | A 42-year-old known HIV positive, Hindu lady showed CD4 T-cell count 50/μL during her 6 monthly routine follow-up. HAART was started with Zidovudine, Lamivudine and Nevirapine. After 8 weeks, she came to dermatology out-patient department with the complaints of multiple reddish, itchy rashes on the different parts of the body. They were transformed into bullous lesions within 2-3 days. Nevirapine was stopped immediately, but the lesions were persisting. Investigation revealed CD4 T-cell count was 260/μL. Clinical examination showed the multiple tense bullous having round margin and appeared on erythematous urticarial base on the skin. Mucosa were not involved. The bullous spread sign was positive, but Nikolsky sign was negative. Tzanck smear showed no acantholytic cell. HPE revealed sub-epidermal bullae [] with eosinophilic infiltrate. IgG and C3 deposition was found at the dermo-epidermal junction on DIF. Hence BP was diagnosed. | [[42.0, 'year']] | F | {'16553555': 1, '16051964': 1, '15750393': 1, '17255740': 1, '10975963': 1, '27190420': 2, '22169463': 1, '9727570': 1, '22310819': 1, '21270328': 1, '34540666': 2, '19815866': 1, '24339465': 2} | {'3841664-1': 2, '3841664-2': 2, '4857691-1': 1, '8444988-1': 1} |
164,435 | 3841665-1 | 24,339,466 | noncomm/PMC003xxxxxx/PMC3841665.xml | Myiasis in female external genitalia | A 17-year-old young unmarried female presented with a history of pain and swelling in the genitalia and also complaining of dropping of fly larva from vulva. She lived in the rural area with conditions of poor hygiene, which were compatible with high-risk of disease. Her non-hygienic toilet was outside the house and attracted many flies. Her hygiene was poor and wearing dirty clothes. She was accompanied by her aunt as her mother died in childhood and because of her shy nature, she didn’t report to any one until and unless she started having pain. There was a history of normal regular menstrual cycle prior to the onset of this painful swelling of genitalia. Patient did not use readymade sanitary napkins available in the market during the menstrual periods; instead, she used dirty ragged clothes during menstrual cycles. She used to hang the washed clothes and undergarments on a clothes line outside. There was no history of any trauma, insect bite, and sexual activity. There was no history of pain in the lower abdomen. No history of intake of any immunosuppressive or steroidal therapy. She also denied history of any chronic illness including tuberculosis, chronic urinary tract infection, and diabetes. Physical examination of the patient revealed a normal build (height 5 feet 2 inches, weight 52 kg) with vitals in normal range. General physical examination revealed that the patient was of sound physical and mental health and capable of caring herself. She was studying in 11th standard.\nOn local examination, both labia majora were tender, erythematous and swollen with the multiple discharging sinuses stuffed with crawling maggots of creamy-white color []. Labia minora were normal. Hymen was intact. No significant lymphadenopathy was present. Laboratory investigations revealed hemoglobin-9.8 g%, with a normal total and differential leucocytes count, blood sugar-98 g%, urine complete examination-within normal limits, her serology for HIV (Human immunodeficiency virus) and Syphilis (by Venereal Disease Research Laboratory test) was -Negative. Her urine examination and sonography was negative for pregnancy. She was hospitalized and was given injection ceftriaxone, injection metrogyl, injection gentamycin, tablet serratiopeptidase and tablet cetrizine empirically from the 1st day. Initially, on day 1, about 20 maggots were removed using non-toothed forceps and the wound was cleaned with betadine. On 2nd day, we applied Turpentine oil and more maggots were removed on 2nd and 3rd day. On the 4th day, maggots were completely absent. Lesions healed within a week time, patient was discharged and advised regarding personal hygiene to avoid re-infestation. | [[17.0, 'year']] | F | {'20883399': 1, '21976905': 2, '21063538': 1, '10888974': 1, '33747883': 2, '30693223': 1, '12715561': 1, '18159443': 1, '18978712': 1, '12625971': 1, '1589615': 1, '12205748': 1, '24339466': 2} | {'3183718-1': 1, '7951076-1': 1} |
164,436 | 3841666-1 | 24,339,467 | noncomm/PMC003xxxxxx/PMC3841666.xml | Papulonecrotic tuberculid of glans penis: A common disease at an uncommon site | A 65-year-old man presented with recurrent crops of multiple asymptomatic papulopustules over the glans penis since last 1 year. The lesions used to resolve spontaneously in a few days with scarring. He was treated with systemic antibiotics and various topical applications before referral. There was no history of trauma, drug intake, fever, cough, and constitutional symptoms. There was no personal or family history of TB. The patient denied history of unprotected sexual exposure. He denied any history of genital lesions or discharge in his wife. The patient was never vaccinated with Bacillus Calmette-Guérin (BCG).\nExamination revealed multiple, nonindurated, well-defined ulcers of size 0.5 cm × 0.5 cm over the ventral aspect of glans. Multiple irregular depressed scars were present around the ulcers []. The ulcers were nontender on touch and there was no bleeding on palpation of the ulcers. There was no clinical evidence of epididymo-orchitis. There was no significant inguinal lymphadenopathy. Mucocutaneous, appendageal and systemic examinations were normal. Patient's systemic examination was unremarkable.\nAll hematological and biochemical investigations were normal except for highly raised erythrocyte sedimentation rate (50 mm in the 1st h). Tuberculin (Mantoux) test was strongly positive (30 mm × 20 mm). Ziehl-Neelsen stain of the pus did not demonstrate any acid fast bacilli (AFB). X-ray chest did not reveal any radiological evidence of pulmonary TB. Urine sediment examinations for AFB and urine culture were noncontributory. Radiological and ultrasound evaluation of the genitourinary system was normal. Human immunodeficiency virus (HIV) antibodies test and Venereal Disease Research Laboratory test (VDRL) test were nonreactive. Systemic evaluation for any focus of TB was unremarkable.\nBiopsy from the edge of the ulcer (glans penis) showed dermoepidermal necrosis surrounded by a poorly formed granulomatous infiltrate composed of lymphocytes and macrophages []. Ziehl-Neelsen stain for AFB was negative. Tissue cultures for bacteria and fungus were negative. We were unable to perform tissue polymerase chain reaction (PCR) due to financial constraints.\nHe was treated with antituberculous treatment (ATT) for a period of 6 months. Four weeks after the initiation of therapy, the existing lesions over the glans had healed []. Further follow-up showed improvement in the condition and no recurrence. | [[65.0, 'year']] | M | {'17106609': 1, '13593873': 1, '10233340': 1, '3949057': 1, '11287704': 1, '16481728': 1, '16336535': 1, '24339467': 2} | {} |
164,437 | 3841667-1 | 24,339,468 | noncomm/PMC003xxxxxx/PMC3841667.xml | Condyloma lata in a preschooler: The dilemma of sexual abuse versus non-abuse | A 4-year-old girl was referred to our hospital for evaluation of peri-anal lesions. About 4 weeks back, she had developed sore-throat, fever and rash involving the trunk and extremities including the palms and soles. She was prescribed syrup cephalexin for 1 week by the pediatrician after which the fever and rash improved. Subsequently, the mother noticed peri-anal lesions and informed the pediatrician who referred the child to us. She was born of a full term normal uncomplicated delivery to a 31 years old woman who received no prenatal care. As both the mother and the child were normal and healthy–no need was felt to investigate either of them after the delivery. The child lived with her parents, two brothers and a sister. The child gave no history of her genitalia being touched by anybody else than her mother. According to the parents, the child did not exhibit any behavioral changes or concerns. Physical examination, at the time of referral revealed a malnourished child with generalized lymph node enlargement. Muco-cutaneous examination revealed condyloma lata in the peri-anal area with a few ulcerated papules in the vicinity []. There was no sign of sexual abuse. Systemic examination was normal. Dark-field examination of the lesions was negative for Treponema pallidum. Serology showed positive venereal disease research laboratory (VDRL) (titre-1:64), T.pallidum particle agglutination assay (>1:80) and negative human immunodeficiency virus (HIV). Cultures for Neisseria gonorrhoeae and Chlamydia trachomatis from the vagina and rectum were negative. She was diagnosed as secondary syphilis and administered benzathine penicillin, 50,000 U/kg in a single dose and her lesions resolved.\nVDRL titers of the mother and father were also positive 1:32 and 1:16 respectively. Father gave a history of unprotected extra-marital contact with a commercial sex worker 5 months back. After 3 weeks, he developed a genital sore which improved with medicines. Subsequently, he developed fever and rash, for which he was given antibiotics and paracetamol. 1 month after this, mother also developed fever, rash and warty lesions in the genital area for which she received no treatment. Both of them did not have any lesions at the time of examination. They were also treated with benzathine penicillin.\nPediatric, dermatologic and psychiatric work-up did not show any evidence of child abuse. After ruling out sexual abuse, we considered non-sexual transmission of syphilis in the child. Contact of the girl with her infected parents was hypothesized as the mode of infection. | [[4.0, 'year']] | F | {'31922108': 2, '9555811': 1, '6610855': 1, '5039114': 1, '1454437': 1, '26924909': 1, '2310968': 1, '6866786': 1, '9917484': 1, '24339468': 2} | {'6896382-1': 1} |
164,438 | 3841668-1 | 24,339,469 | noncomm/PMC003xxxxxx/PMC3841668.xml | Penile pyoderma gangrenosum | A 70-year old male, living with spouse presented with relatively asymptomatic ulcers over the penis of 1 month duration. He denied any extramarital contact. He was not a known diabetic or hypertensive.\nGeneral examination was within normal limits. Local examination showed two indurated ulcers 1.5 × 1 cm and 0.5 × 0.4 cm over the penis at the junction of foreskin and coronal sulcus. The ulcers bled on touch. There was no inguinal or femoral lymphadenopathy [].\nSquamous cell carcinoma penis, tuberculous ulcer, donovanosis, and Herpes genitalis (either because of immunocompromise or development of resistant mutation) were considered as the differential diagnosis. The following investigations: Routine blood and urine examinations, peripheral smear, ANA, rheumatoid factor, VDRL, ELISA-HIV, HBsAg, anti-HCV, Mantoux test, Chest X-ray PA view, Ultrasound abdomen, gram stain from the ulcer, and tissue smear for Donovan bodies were negative or within normal limits.\nA biopsy was done, and the patient was started on doxycycline 100 mg twice daily. Biopsy revealed a chronic ulcer with no evidence of malignancy. Tissue culture for mycobacteria and fungi were negative. Despite 3 weeks of doxycycline, the ulcers were found to be increasing in size and extent. A repeat biopsy was done, and the patient was circumcised to accelerate the healing process.\nThe second biopsy showed an ulcer with hyperplasia of the adjacent epidermis and a dense inflammatory cell infiltrate in the dermis composed of lymphocytes, neutrophils, Langhans, and foreign body type of multinucleate giant cells. Proliferation of capillary-sized blood vessels with perivascular accumulation of inflammatory cells was noted [].\nWith these histopathological findings and clinical correlation, an alternative diagnosis of PG was considered. He was started on 40 mg of prednisolone per day. The ulcer started healing on the third day. Prednisolone was tapered and stopped by 4 weeks. There has been no recurrence even 12 months after stopping treatment [].\nThis case is reported for its extreme rarity. PG is rare, and there are only very few reports of penile PG. | [[70.0, 'year']] | M | {'26396454': 2, '19470075': 1, '8609250': 1, '33102045': 1, '26392658': 2, '16021123': 1, '10188153': 1, '24339469': 2} | {'4553847-1': 1, '4555903-1': 1} |
164,439 | 3841692-1 | 24,339,493 | noncomm/PMC003xxxxxx/PMC3841692.xml | Aspergillus colonization in hydatid cyst: Addition of a case | A 52-year-old non-diabetic gentleman presented to this hospital with complaints of cough with productive sputum, anorexia and mild weight loss for the last four months. He had similar episodes of cough two years back for which he had been evaluated elsewhere. He did not have any other significant past medical history. General and systemic examination was unremarkable except for decreased breath sounds over the left lung fields. Hemogram was unremarkable. He was HBsAg and HIV negative.\nSputum culture did not reveal any specific findings. Pulmonary function test showed a combined restrictive and obstructive ventilation defect with mild airflow limitation. Chest X-ray showed a circumscribed cystic lesion in right lower lobe of lung. Tomogram chest showed soft tissue opacity in left mid and right lower zone with thickening of fissure on left side. Plain and contrast CT revealed a well-defined peripherally enhancing thick-walled cystic lesion of size 65 × 52 mm in the apical segment of left lower lobe []. The lesion showed tiny air pockets within the cyst (meniscus sign). Another similar smaller lesion was seen on right side. CT abdomen showed enlarged spleen with a lobulated non-enhancing lesion of size 31 × 42 mm near splenic hilum and similar smaller lesions anterior to bladder and rectum. With these findings a diagnosis of disseminated thoraco-abdominal hydatid disease was made.\nIn view of the present respiratory complaints, the patient was taken up for surgery, first on the left side. The thorax was opened via postero-lateral incision and the lesion was approached via the fifth intercostal space. The cyst was identified, pericyst was incised and cyst was anucleated. The specimen was submitted for histopathological evaluation. Grossly, the specimen measured 8 × 9 × 6 cm. The external surface was shiny. It yielded 10 cc of slimy turbid fluid. The inner surface was yellowish with focal brownish black granules [].\nHistological examination revealed lamellated hyaline eosinophilic membrane of hydatid cyst. The inner wall of the cyst showed dense lymphoplasmacytic inflammation and Splendore–Hoeppli composed of amorphous eosinophilic granular material with entrapped fungal hyphae. With Gomori's methanamine silver (GMS) stain, the fungal hyphae were slender, septate, branching at acute angles, morphologically compatible with Aspergillus species. The fungi were also stained with Masson's Fontana (MF) and Periodic Acid Schiff (PAS) stain []. The tissue was not submitted for culture.\nThe patient was prescribed 10 mg/kg/day of oral albendazole for 3 months. | [[52.0, 'year']] | M | {'33457026': 2, '20207859': 1, '18976399': 1, '7289939': 1, '18544065': 1, '19029047': 1, '1404546': 1, '19389072': 1, '16902888': 1, '4913991': 1, '11823982': 1, '26666549': 1, '18444973': 1, '18465032': 1, '8544222': 1, '8544224': 1, '13987495': 1, '17981484': 1, '24339493': 2} | {'7787855-1': 1} |
164,440 | 3841693-1 | 24,339,494 | noncomm/PMC003xxxxxx/PMC3841693.xml | Recovery of fluconazole sensitive Candida ciferrii in a diabetic chronic obstructive pulmonary disease patient presenting with pneumonia | A 55-year-old, female, bidi smoker, suffering from moderate COPD (GOLD guidelines) for 2 years, presented to the emergency room with progressive increase in dyspnea and cough with copious mucopurulent expectoration for 15 days and 10 days respectively. Before her exacerbation, her symptoms were well controlled with tiotropium and a fixed dose combination of formoterol and budesonide. On general examination, she was tachypneic (respiratory rate 30/min); had cyanosis and used her accessory muscles of respiration. Respiratory system examination revealed diminished vesicular breath sound with prolonged expiration on left lower zone; bilateral polyphonic rhonchi all over the chest and coarse biphasic crackles over bilateral lung bases more on the right side. Her peripheral oxygen saturation was 74% in room air during the admission and improved to 88-92% with oxygen through face mask at a flow of 8 L/min. Her arterial blood gas showed pH 7.43, PaO2 70 mmHg, PaCO2 36 mmHg, PaO2/FiO2 234, suggestive of acute lung injury. She was a known diabetic for 15 years and had needed insulin for the control of diabetes for the past 6 months. On admission blood culture; sputum for gram stain, Ziehl-Neelsen (Z-N) stain and pyogenic culture with sensitivity were asked for. She received piperacillin-tazobactum (4.5 g) 6 hourly and azithromycin (500 mg) once daily, along with nebulization by salbutamol + ipratropium, injectable deriphylline and intravenous fluids. Her chest X-ray showed bilateral lower zone heterogeneous opacity, more on left side with clear costophrenic angles on lateral chest X-ray suggestive of bilateral pneumonia []. Total leukocyte count was 11,700/mm3 with neutrophil 67%, lymphocytes 28%, eosinophils 2%, basophil 1% and monocytes 2%. Serum urea was 34 mg%, creatinine 0.7 mg%, sodium 138 mEq/L, potassium 3.5 mEq/L. Her glycosylated hemoglobin level was 11.8 indicating uncontrolled diabetes. Sputum gram staining and Z-N staining were negative. Since, her condition did not improve after 2 days a computed tomographic scan of thorax was requested for further evaluation, which revealed left lower lobe collapse with consolidation along with patchy pulmonary infiltrations in the right middle and lower lobe []. Fiber-optic bronchoscopy was carried out to know the cause of collapse, which showed patchy whitish lesion in the lateral wall of trachea just above the carina with a mucous plug occluding the lumen of the left main bronchus and purulent discharge from right main bronchus []. Bronchoalveolar lavage fluid (BAL) was taken from those segments with clearing of that mucous plug and BAL fluid was sent for cytological examination, gram staining, fungal staining, Z-N staining, malignant cells, mycobacterial culture, and fungal culture. The antimicrobial susceptibility test was performed by microbroth dilution method by VITEK-2. Fungal staining of BAL and mucosal biopsy specimen showed yeast forms suggestive of Candida species []. The fungal culture showed moderate growth of Candida ciferrii. Intravenous liposomal amphotericin B (150 mg daily) was initiated and changed to oral fluconazole (150 mg daily) after 4 days, when drug sensitivity revealed that the strain was fluconazole sensitive []. After 4 days, she showed remarkable recovery and maintained oxygen saturation on room air. Patient was discharged after 2 weeks on oral fluconazole 150 mg daily. Chest X-ray on follow-up after 6 weeks showed marked improvement []. Antifungal therapy stopped after 3 months. | [[55.0, 'year']] | F | {'10843984': 1, '19375640': 1, '8665465': 1, '16984866': 1, '11320905': 1, '14720566': 1, '19013346': 1, '31575637': 1, '30634716': 1, '26744644': 1, '15538834': 1, '9279244': 1, '17540785': 1, '24339494': 2} | {} |
164,441 | 3841694-1 | 24,339,495 | noncomm/PMC003xxxxxx/PMC3841694.xml | Internal mammary artery pseudoaneurysm: A rare fatal complication of tubercular empyema | A 15-year-old male had complaints of fever and cough with expectoration on and off for 8 months. On evaluation, sputum was found positive for acid fast bacilli and he was on anti-tubercular treatment (ATT, Directly Observed Treatment Short course, Category II) for the last 3 months.\nHe had small amounts of blood-streaked sputum for the past 2 weeks, but had coughed up approximately “a cup” of bright red blood a day prior to his referral to emergency department. While still in the emergency, he had an episode of large volume hemoptysis, estimated to be approximately 200-250cc of fresh blood. The patient had a past history of TB 6 years back, for which he had taken a complete course of ATT for 6 months.\nThe patient underwent computed tomographic bronchial angiography (CTBA) to identify the cause of hemoptysis. The CTBA showed approximately 45 mm × 35 mm × 32 mm sized contrast filled outpouching seen arising from the left internal mammary artery (LIMA) in relation to one of the pocket of empyema located anteriorly in the paramidline location [Figure and ]. In addition, multiple other loculated pockets of empyema were also seen. Multiple coalescing centrilobular nodules were seen scattered in bilateral lungs [], suggestive of reactivation.\nPatient became hemodynamically unstable with falling blood pressure and went into shock. The decision was taken for angioembolization of the pseudoaneurysm. The LIMA was selectively cannulated, which showed contrast filled outpouching [] with faint abnormal blush. Three multiple curled soft platinum coils (2.0-2, 3.0-3 and 3.0-3) were deployed and the check angiogram showed no residual pseudoaneurysm [].\nHemoptysis stopped post-procedure; however, the patient went into refractory shock. The patient was given crystalloids (in the form of normal saline) and whole blood. As the patient was not responding to the intravenous fluid resuscitation, he was started on vasoactive agents also (noradrenaline and dopamine). However, he could not be revived and died 4 h post-embolization. | [[15.0, 'year']] | M | {'14760484': 1, '3893696': 1, '11733152': 1, '12932188': 1, '15290563': 1, '19438800': 1, '16252143': 1, '11452057': 1, '32685069': 1, '20965895': 1, '16227490': 1, '24339495': 2} | {} |
164,442 | 3841695-1 | 24,339,496 | noncomm/PMC003xxxxxx/PMC3841695.xml | An unusual masquerade of community acquired pneumonia: Left-side unilateral pulmonary edema | A 76-year-old man, a known case of dilated cardiomyopathy, presented to the Emergency Department with severe breathlessness and cough productive of blood stained sputum of 2 days duration. His compliance with diet and medication was poor.\nAt admission, he was orthopnic, had an RR of 40 bpm, BP of 140/100 mmHg, HR of 110/min, and body temperature of 37.2°C. His neck veins were full, and there was pedal edema. Respiratory system examination revealed impaired percussion note and fine crackles in the entire left hemithorax. Cardiac auscultation revealed S3 gallop and a high-pitched, holosystolic murmur at apex radiating to the left axilla.\nLaboratory investigations revealed a TLC of 14000/μL with 75% neutrophils. Chest radiograph showed left-sided airspace disease with cardiomegaly [] and electrocardiogram showed LBBB. His creatinine 1.4 mg/dL, sodium 140 mEq/L, potassium 4.0 mEq/L, B-natriuretic peptide 1200 pg/mL, creatine kinase isoenzyme MB 6.1 ng/mL, and troponin I 0.14 ng/mL.\nDifferential diagnosis of pneumonia versus UPE was kept. He was started on oxygen, diuretics, low molecular weight heparin, GTN infusion, anti-platelets, statins, intravenous antibiotics (cefepime and azithromycin), and non-invasive mechanical ventilation. Echocardiography done revealed a reduced global left-ventricular ejection fraction (LVEF 35%), and a large eccentric mitral regurgitation jet reaching the left pulmonary veins. His serial CRP and PCT were low. His cultures (sputum and blood) did not grow any organism, and therefore antibiotic were discontinued on day 4. With decongestive therapy, there was significant clinico-radiological improvement. Repeat chest radiography done after 48 h of admission showed significant resolution of the unilateral opacities []. The patient was discharged uneventfully on day 5 of hospitalization, and presently he is on a regular follow-up with the Cardiology Department. | [[76.0, 'year']] | M | {'20805429': 1, '11292212': 1, '22244564': 1, '16103546': 1, '12910856': 1, '18036943': 1, '15201653': 1, '17157714': 1, '16520136': 1, '12135127': 1, '16635722': 1, '15323396': 1, '11788208': 1, '20640211': 2, '19479097': 1, '11766552': 1, '24339496': 2} | {'2894493-1': 1, '2894493-2': 1, '2894493-3': 1} |
164,443 | 3841696-1 | 24,339,497 | noncomm/PMC003xxxxxx/PMC3841696.xml | Pulmonary cryptococcosis: An unusual presentation | A 33-year-old male bank employee presented to our outpatient department with a 4 month history of dry cough, and breathlessness on exertion associated with wheeze. He was a nonsmoker and teetotaller. There was no history of high risk behavior, but he had a history of exposure to pigeons in his house for the past 1 year. He had a history of being treated with empirical antituberculous therapy for an exudative pleural effusion 2 years ago. For his current symptoms, he had been initially treated by his local physician with antibiotics and inhaled bronchodilators, but his symptoms persisted. At presentation, he had no neurological symptoms.\nPhysical examination revealed decreased breath sounds on the whole left hemithorax. Vital signs were stable. Initial investigations such as total leukocyte count, differential count, and renal and liver function tests were within normal limits. A chest X-ray [] revealed a left upper zone, mid zone, lower zone air space consolidation; and an elevated hemidiaphragm possibly due to collapse of the left lower lobe. A computerized tomography (CT) scan of the chest [] showed a mass lesion in the left main bronchus (LMB), causing complete collapse of left upper lobe and partial collapse of left lower lobe with consolidation with no mediastinal lymph adenopathy and no peripheral lung nodules.\nFiberoptic bronchoscopy [] performed under local anesthesia revealed a white polypoid endobronchial mass lesion in LMB causing complete occlusion. Bronchial washings showed no evidence of TB or fungal infection. However, bronchial biopsy of the lesion showed yeasts consistent with Cryptococcus [] and subsequent cultures grew Cryptococcus. The cryptococcal antigen was not tested in our patient as the clinical suspicion was very low. Moreover the value of serological tests in the diagnosis of this condition is doubtful. The patient was then evaluated for his immune status. Test for human immunodeficiency virus (HIV) by ELISA technique was negative. His total lymphocyte count, CD4 and CD8 counts, and immunoglobulin levels were normal. The patient was initiated on intravenous amphotericin B (0.7 mg/kg daily) and fluconazole (1,200 mg per day). A repeat chest X-ray [] after 10 days of therapy showed significant resolution of the lesion and his symptoms had improved. Intravenous amphotericin was stopped and he was discharged home on oral fluconozole 1,200 mg per day. After a month of oral fluconozole (1,200 mg per day), he was switched over to maintenance dose of oral fluconozole 400 mg per day. He remained well with good improvement in symptoms and chest X-ray findings. CT scan chest and bronchoscopy have not been repeated in our patient as he was not keen on having either of them. Further, his remarkable clinical improvement made us agree with him on this management decision. | [[33.0, 'year']] | M | {'16471118': 1, '30719369': 2, '6609567': 1, '16864987': 1, '5078941': 1, '9797753': 1, '15742861': 1, '7235394': 1, '7777885': 1, '30302308': 1, '20047480': 1, '8726953': 1, '20592924': 1, '4583538': 1, '17443047': 1, '22337198': 1, '27704021': 1, '24339497': 2} | {'6334315-1': 1} |
164,444 | 3841697-1 | 24,339,498 | noncomm/PMC003xxxxxx/PMC3841697.xml | Cystic lung disease in tuberculosis: An unusual presentation | A13-year-old female patient presented with the complaints of fever for 1 month duration and shortness of breath for 10 days. She also complained of decreased appetite and significant loss of weight for the same duration. On examination, patient's pulse rate was 130 beats/min, blood pressure was 100/70 mmHg, respiratory rate was 48/min. On auscultation chest revealed bilateral crepitations. Examination of the other systems was unremarkable. Arterial blood gas (ABG) analysis showed paO2:42 mmHg, pCO2:44 mmHg, HCO3:27.1 mmol/L, pH 7.406. Chest X-ray showed bilateral diffuse reticular shadows. A contrast enhanced computed tomography thorax [Figures and ] showed multiple thin walled cysts seen in both the lungs (left > right; upper lobe > lower lobe); diffuse ground glass opacities and centrilobular nodules in both lung fields.\nPatient was intubated and ventilated in view of respiratory failure and impending respiratory arrest In the Intensive Care Unit bronchoscopy was performed through the endotracheal tube and washings taken. Transbronchial lung biopsy was performed and sent for histopathological examination, which showed granulomatous inflammation consistent with tuberculosis. Bronchial washings sent for Mycobacterium tuberculosis culture was positive.\nPatient was treated with antitubercular regimen (Isoniazid, Rifampicin, Pyrazinamide and Ethambutol) with steroids (1 mg/kg). The fever subsided and the patient could be weaned off the ventilator within 10 days of starting the above treatment. Patient was discharged after 1 week. At the time of discharge ABG showed paO2:73 mmHg, paCO2:28.5 mmHg, pH:7.446. Steroids were continued for 1 month after which it was tapered gradually over 1 month. Anti-tubercular drugs were continued for 6 months. At the end of treatment, ABG showed paO2:95 mmHg, paCO2:39 mmHg, pH:7.39. Repeat high resolution computed tomography thorax [Figures amd ] showed a reduction in the number and size of cysts in both the lung fields with decrease in diffuse lung opacities and nodular lesions. | [[13.0, 'year']] | F | {'10972868': 1, '30799368': 1, '22347931': 1, '27185999': 2, '26752829': 1, '18195376': 1, '11045687': 1, '33816198': 1, '24339498': 2} | {'4857571-1': 1} |
164,445 | 3841698-1 | 24,339,499 | noncomm/PMC003xxxxxx/PMC3841698.xml | Pleural effusion presenting as mediastinal widening | A 55-year-old female presented with low grade fever, dry cough and chest discomfort. There was no history of chest pain. She was having psoriasis since 15 years. Patient was on azathioprine 50 mg since 1½ years. She developed diabetes mellitus 6 months back and her blood sugar levels were under control. She had toothache (left side molar area) due to periodontal infection associated with discharge of pus from the cheek since 15 days. Pus culture showed Staphylococcus aureus. Patient was given injection ampicillin, gentamycin and metronidazole. Her total leukocyte count was 20,400 with 88% neutrophils.\nShe visited us for chest discomfort and dry cough with chest radiographic abnormality of mediastinal widening []. To explore the cause of mediastinal shadow, contrast enhanced computed tomography (CECT) thorax was carried out and it showed two large loculated pleural effusions (mean Hounsfield unit of 8) along left anterior and left posterolateral chest wall []. Larger collection was of size 9 cm × 8 cm. Both collections had communication with each other and the fluid accumulated medially.\nIntercostal drain was inserted in left 5th intercostal space in midaxillary line. About 800 ml of pus was drained. Pus culture was sterile and negative for acid fast bacilli. Patient was continued on same antibiotics. Chest radiograph improved gradually []. Ultrasound chest showed the collection of less than 50 ml fluid. Intercostal tube drain was removed and patient discharged in a stable condition. | [[55.0, 'year']] | F | {'16034263': 1, '16337509': 1, '9340065': 1, '2357135': 1, '15332792': 1, '3164054': 1, '8754967': 1, '20860508': 1, '30263991': 1, '24339499': 2} | {} |
164,446 | 3841699-1 | 24,339,500 | noncomm/PMC003xxxxxx/PMC3841699.xml | Fruiting bodies of Aspergillus: An unusual finding in histopathology | A 62-year-old female patient who was an agriculturist presented to us in a critically ill-condition and had complaints of cough and hemoptysis since 3 months and also had respiratory distress at presentation. A chest X-ray was performed, which showed a left sided hilar mass. A computed tomography scan of the thorax revealed a moderately enhancing soft-tissue density lesion measuring 6 cm × 4.9 cm × 4 cm. in the left hilar region extending to apicoposterior segment of left upper lobe. A bronchoscopy was performed, which revealed a mass lesion in the left main bronchus. With a clinical and radiological diagnosis of lung carcinoma, a biopsy was carried out.\nThe specimen obtained for histopathological examination consisted of greywhite, friable soft-tissue aggregate measuring 0.5 cm × 0.5 cm. Examination of Hand E stained sections revealed mainly necrotic tissue and clusters of tumor cells with crush artefact []. Amidst the necrotic material were seen branching septate hyphae of Aspergillus. Apart from hyphal forms, many fruiting bodies of Aspergillus were also seen []. A methenamine silver stain was carried out, which highlighted the fungi []. On immunohistochemistry, the tumor cells were positive for cytokeratin and synaptophysin. A diagnosis of small cell carcinoma of lung with co-existent Aspergillosis was made. Our patient was then lost to follow-up and hence culture and species identification could not be carried out. | [[62.0, 'year']] | F | {'28920192': 1, '23248489': 2, '25379399': 1, '8028079': 1, '4200814': 1, '16200896': 1, '24778470': 1, '26535103': 2, '22084428': 1, '18763205': 1, '10194462': 1, '19365982': 1, '21762198': 1, '23101010': 2, '26894041': 2, '12742315': 1, '24339500': 2} | {'4757915-1': 1, '4628811-1': 1, '3475467-1': 1, '3519232-1': 1} |
164,447 | 3841700-1 | 24,339,501 | noncomm/PMC003xxxxxx/PMC3841700.xml | A case of spontaneous pneumothorax following radiation therapy for non-small cell lung cancer | A 64-year-old male with 50-pack-year of smoking history and moderately severe chronic obstructive lung disease (COPD-FEV1 54%) was recently diagnosed with right lower lobe non-small cell lung cancer (NSCLC Stage IIB T3N0M0-Squamous Cell). On the computerized tomographic scan, the lower lobe pulmonary mass was associated with significant post-obstructive atelectasis suggesting endobronchial location [Figures and ]. This lung mass was deemed inoperable due to close proximity to the carina. It was decided to start patient on intensity-modulated radiation therapy (IMRT) with a planned total dose of 6660 cGy over 37 cycles. Right after the 12th cycle of his treatment, patient developed sudden shortness of breath and right-sided chest pain. He was tachypneic but normotensive. Physical exam showed hyper resonant right chest with absent breath sounds and left sided tracheal deviation concerning for pneumothorax. No jugular venous distention was noted. An arterial blood gas analysis showed hemoglobin oxygen saturation of 96%, partial pressure of oxygen (PaO2) at 80 mmHg, partial pressure of carbon dioxide (PaCO2) at 40 mmHg, and pH 7.36. Chest radiograph and computerized tomographic scan confirmed the presence of large right-sided pneumothorax involving around 50 percent of right lung field with some left mediastinal shift [Figures and ]. A small bore 14-French pigtail catheter was inserted into right pleural cavity resulting in complete resolution of the pneumothorax and re-expansion of the lung []. Air leakage stopped in the pleural pigtail catheter drain setup within 48 hours and the catheter was removed. Patient refused pleurodesis for recurrence prevention. | [[64.0, 'year']] | M | {'1028401': 1, '2298622': 1, '7940440': 1, '27190612': 1, '6835175': 1, '29344194': 1, '34287252': 1, '17409880': 1, '10682772': 1, '19714435': 1, '4053713': 1, '20803975': 1, '9530037': 1, '11845936': 1, '11171742': 1, '4832494': 1, '24339501': 2} | {} |
164,448 | 3841701-1 | 24,339,502 | noncomm/PMC003xxxxxx/PMC3841701.xml | Rifampicin induced adrenal crisis in an uncommon setting | A 46-year-old nondiabetic and nonhypertensive female patient presented initially with complaint of central chest pain for 3 months which was insidious in onset, no particular aggravating and relieving factors. She also had weight loss, anorexia, and fatigue for the same duration. A computed tomography (CT) of thorax showed mediastinal lymphadenopathy with no parenchymal involvement. Transbronchial needle aspiration (TBNA) from the mediastinal lymphnodes revealed granulomatuos inflammation. Bronchial washings’ analysis was negative for acid fast bacilli (AFB) stain and culture. A Mantoux test was strongly positive. Based on these investigations, the patient was started on four drug antitubercular therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol). Ten days after starting of antitubercular therapy, patient presented to the emergency department with complaint of increased chest pain and vomiting. On examination, patient was fully conscious with blood pressure of 70/50 mmHg. Adrenal insufficiency was suspected and serum cortisol was sent which was low. A corticotrophin test showed adequate response indicating secondary adrenal insufficiency due to hypothalamopituitary axis (HPA) failure.[] A CT abdomen done revealed normal adrenals, suggesting involvement of HPA as a cause of adrenal insufficiency. On further enquiry, the patient gave a history of significant postpartum bleeding around 17 years back with difficult lactation in the last childbirth. In the last 2 years she had also noticed gradual loss of axillary and pubic hair and her periods had stopped since last 3 years. Hormone assay revealed low luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone, thyroid stimulating hormone (TSH) []. Magnetic resonance imaging (MRI) of brain revealed empty sella turcica with nonvisualization of pituitary gland [Figures and ]. A diagnosis of postpartum hypopituitarism (Sheehan syndrome) was made based on the above history and investigation findings. Patient was put on steroids (intravenous hydrocortisone followed by oral prednisolone) to which she responded. The chest pain and vomiting abated and hypotension was reversed. She subsequently recovered completely. Steroids and antitubercular drugs were continued. | [[46.0, 'year']] | F | {'7982772': 1, '32307006': 1, '6247603': 1, '13171425': 1, '20550784': 1, '11572546': 1, '12426284': 1, '24339502': 2} | {} |
164,449 | 3841921-1 | 24,340,230 | noncomm/PMC003xxxxxx/PMC3841921.xml | An unusual case of pediatric bow hunter's stroke | A 16-year-old male presented with right-sided numbness, dysphagia, and right peripheral vision loss after working out during football practice. In the emergency room (ER) his right-sided visual field defect persisted, with anomia and alexia. He stated that he had experienced intermittent episodes and discreet events over the past year including weakness, numbness, and vision loss.\nHe had a computerized tomography scan of the head, which revealed areas of hypodensity in the left temporoparietal region suggestive of stroke. This finding was confirmed by magnetic resonance imaging, which revealed multiple strokes of different ages. Specifically, he had an acute stroke in the left temporoparietal region, along with subacute strokes in the right thalamus, spanning the corpus callosum and left cerebellum. The patient was then admitted to the pediatric intensive care unit (PICU) for observation and further workup. A cerebral angiogram revealed a focal dissection of the distal right VA with a small nonocclusive thrombus proximal to the dissection. The only suspicious event from the patient's history was a wrestling incident in the locker rooms a few days before the onset of stroke. He was followed by neurology and hematology/oncology, and had workups to rule out vasculitis, metabolic, hypercoagulable, and cardiac embolic sources, all of which were negative. Anticoagulation with enoxaparin was then initiated, and the patient was discharged home with instructions to avoid weight lifting and contact sports.\nApproximately 3 months after his initial presentation and completing his 3-month course of anticoagulation with therapeutic enoxaparin, the patient experienced new transient neurological symptoms of headache, blurred vision, and confusion. Incidentally, he began weightlifting a week prior to the onset of his new symptoms. Magnetic resonance imaging of the brain revealed a subacute stroke in the left medial cerebellum, and a new area of encephalomalacia, suspicious for a stroke, in the parietal region near the vertex that occurred after his initial hospitalization. The patient was then admitted for further evaluation.\nA dynamic cerebral angiogram was performed and revealed that the patient had a Bow Hunter's type phenomenon, with dynamic occlusion of the right VA in the chin up position looking to the left [].\nA dynamic computerized tomography angiogram performed with the patient's head in rotated position showed a near complete occlusion of the V3 segment of the right VA resulting from an anomalous spur emanating from his right occipital condyle that pinched off his VA between the C1 ring and this condylar spur []. This was determined to be the etiology of the dissection. Therefore, the patient was managed by neck immobilization via a cervical collar, and we initiated aspirin 81 mg and coumadin with an INR goal of 2-3. At this time, the plan was to allow the dissection flap to heal and then bring the patient back for elective surgical decompression of the condylar spur.\nHowever, 2 weeks after the treatment modality of immobilization and pharmacotherapy, the patient presented with a transient ischemic attack. He reported right hemibody numbness and tingling. His INR at that point was subtherapeutic, first at 1.8 then at 1.6. A magnetic resonance imaging and magnetic resonance angiography of the head and neck revealed persistent narrowing of the V3 segment of the VA to 50%, with new strokes noted in the occipital lobe, right cerebellum, and a thrombus in the left P2-3 segment of the left posterior cerebral artery.\nSince the patient had further thrombotic episodes due to the dissection, he was admitted and placed on 325 mg aspirin, clopidrogrel (300 mg load followed by 75 mg daily), and a heparin infusion. After a thorough discussion of all treatment options, including stenting of the artery, surgery to drill off the spur, or continued medical therapy, the decision was made to proceed with coil embolization/sacrifice of the right VA so as to prevent further thromboembolic events as well as to avoid the future need for surgical decompression of the anomalous occipital condyle process. The right VA was sacrificed with coil embolization and trapping of a 4 mm thrombus over the dissected segment []. The patient tolerated the procedure without complication and was subsequently discharged home.\nDuring his initial postoperative clinic visit, one week status-post right VA sacrifice, his cervical collar was discontinued. During his 5 week postoperative clinic visit, he reported no further episodes of seizures, paresthesias, headache, or neck pain. He was doing well on aspirin 81 mg with a plan to continue antiplatelet therapy indefinitely\nThree months status-post right VA sacrifice, the patient had a baseline right homonymous hemianopsia and a mild nystagmus, especially with right lateral gaze, but was otherwise doing well and denied any symptoms. He had increased his level of activity and started weightlifting but was not cleared for contact sports. | [[16.0, 'year']] | M | {'20881570': 1, '12451196': 1, '32983299': 1, '19729536': 1, '29018650': 1, '28503618': 2, '9402591': 1, '732978': 1, '31511914': 1, '6018539': 1, '22206692': 1, '21099720': 1, '27053329': 1, '19838975': 1, '26301025': 1, '20959996': 1, '19772401': 1, '21789571': 1, '18787197': 1, '12461405': 1, '9120624': 1, '32715110': 1, '18469685': 1, '27610119': 1, '24340230': 2} | {'5417278-1': 1} |
164,450 | 3841922-1 | 24,340,226 | noncomm/PMC003xxxxxx/PMC3841922.xml | Ruptured mycotic cerebral aneurysm development from pseudoocclusion due to septic embolism | A 14-year-old girl with no major past medical history was sent to the emergency department for evaluation after her primary care doctor found a new heart murmur on physical examination in the setting of a 2-week history of fevers, myalgias, fatigue, and shortness of breath. She was admitted to the hospital for treatment of subacute endocarditis and was found to have blood cultures positive for nontypeable Hemophilus influenzae. Mitral valve vegetations were confirmed on transesophageal echocardiography. The patient's history was remarkable for a recent orthodontic appliance adjustment 1 month prior to admission.\nNeurosurgical involvement began after the patient was found to have a right middle cerebral artery (MCA) territory infarct on computed tomographic (CT) imaging with symptoms starting 1 day earlier consisting of a left-sided hemiparesis and facial asymmetry. After removal of the patient's orthodontic appliance, magnetic resonance (MR) imaging and MR angiography of the brain confirmed completed infarction of approximately one-half of the right MCA territory due to a focal pseudoocclusion (high-grade stenosis causing near occlusion) in the distal M1 at the MCA bifurcation []. Endovascular revascularization was felt to be a poor option due to the >24-hour duration of symptoms prior to neurosurgical involvement, completed nature of the infarction, and large volume of MCA territory involved []. Because endovascular revascularization would not be pursued, in conjunction with the high-quality noninvasive imaging findings and the need to minimize pediatric exposure to ionizing radiation, diagnostic cerebral angiography was not pursued. A trial of heparin was initiated instead because the patient still had preserved speech, implying at-risk MCA territory. However, the heparin infusion was halted due to early signs of hemorrhagic transformation in the ischemic infarct. Subsequently, a decompressive craniectomy was performed due to increasing mass effect from the progression of stroke causing increased lethargy and left-sided hemiplegia [Figures and ]. After decompression, the patient's examination improved such that she was fluent with an age-appropriate level of consciousness and had moderate left-sided hemiparesis; her facial asymmetry persisted.\nOn postoperative day 3 after the decompressive craniectomy, 5 days after original presentation and MR angiography documenting the M1 pseudoocclusion, the patient became acutely comatose with right-sided mydriasis. CT angiography of the head revealed a ruptured 19 × 16 mm mycotic aneurysm arising from the M1 occlusion site, associated with a large intracerebral hemorrhage and midline shift [Figures –]. While the operating room was being prepared for a hematoma evacuation, the patient was taken to the endovascular suite for emergent coil embolization. Given completion of the M1 occlusion, extension of the MCA infarction, and rapid growth of the pseudoaneurysm, both parent vessel and pseudoaneurysm were rapidly coiled to complete obliteration [Figures –]. From the endovascular suite, the patient was taken directly to the operating room for hematoma evacuation []. After emergency interventions were completed, pupil function was restored and standard intracranial pressure management ensued. Ultimately, she was discharged home with intact speech, cognitive function appropriate for age, and residual left hemiparesis. | [[14.0, 'year']] | F | {'10549930': 1, '8316194': 1, '2234359': 1, '16264027': 1, '19322683': 1, '19838745': 1, '17067923': 1, '11354404': 1, '15864599': 1, '15883063': 1, '1595103': 1, '20837863': 1, '31892631': 1, '6548001': 1, '11025635': 1, '4740154': 1, '12879875': 1, '12383359': 1, '11383721': 1, '17360002': 1, '24340226': 2} | {} |
164,451 | 3841936-1 | 24,340,232 | noncomm/PMC003xxxxxx/PMC3841936.xml | Spontaneous spinal epidural hematoma and spinal cord infarction following orthotopic liver transplantation: Case report and review of the literature | A 65-year-old female with hepatitis C-related cirrhosis and HCC presented for OLT. The patient previously underwent treatment for HCC with multiple transarterial chemoembolizations, radiofrequency ablation, and laparoscopic hepatic wedge resection for masses in the right lobe of the liver. Her past history was significant for hypertension and uterine cancer requiring total abdominal hysterectomy with bilateral salpingo-oopherectomy. Prior to transplantation, the patient was neurologically intact.\nWhen a suitable donor organ became available, the patient was taken to the operating room for OLT using conventional techniques and veno-venous bypass. Surgery was complicated, however, by donor liver edema after reperfusion. Secondary to edema and with inability to obtain adequate hemostasis, the abdomen was packed and temporarily closed. Posttransplant Doppler ultrasound was performed and ruled out inferior vena cava (IVC) outflow obstruction. The patient was resuscitated in the intensive care unit and then taken back to the operating room the following day. Approximately 1 L of hematoma was evacuated from the abdomen after which careful inspection showed excellent hemostasis. The abdomen was then closed in standard fashion. The patient was extubated. She did have a fluctuating coagulopathy and thrombocytopenia (INR 1.7 and platelets 21,000 on posttransplant day one); this is not abnormal for patients postliver transplantation.\nOn posttransplant day 5 she developed respiratory distress and subsequently suffered a cardiac arrest with pulseless electrical activity. Cardiopulmonary resuscitation (CPR) was administered with eventual conversion to ventricular fibrillation, which was then treated with electrical defibrillation using 300 J. Following the cardiac arrest, the patient required reintubation and suffered from aspiration pneumonitis. Hypotension required the administration of vasopressive medications. Left lower extremity edema prompted a Doppler ultrasound that showed an occlusive deep venous thrombosis (DVT). This warranted the placement of a retrievable IVC filter, during which a nonocclusive thrombus in the infrarenal IVC was noted.\nWhen the patient's mental status improved on posttransplant day 10, it became clear that she was plegic in both lower extremities. Magnetic resonance imaging (MRI) of the cervical, thoracic, and lumbar spine [] demonstrated epidural hematoma located dorsally at the foramen magnum, and both ventrally and dorsally from C7 to T6. The hematoma was hyperintense on both T1- and T2-weighted sequences, consistent with extracellular methemoglobin (late subacute hemorrhage, >7 days). In the lower thoracic spine there was marked spinal cord edema consistent with infarction characterized by an increased T2 signal from T8-T12.\nDue to the age of the hematoma, the plegic deficit and presence of spinal cord infarction, and her life-threatening continued coagulopathy, the patient was not considered a candidate for surgery (e.g., decompressive laminectomy for evacuation of the hematoma). She did, however, receive an 8-day course of intravenous methylprednisolone as part of the routine posttransplant immunosuppresion. Although the patient slowly recovered (tracheostomy for prolonged ventilator-dependent respiratory failure with subsequent weaning from the ventilator), she remained plegic in both lower extremities 6 months posttransplantation. | [[65.0, 'year']] | F | {'9335475': 1, '29423296': 1, '19929346': 1, '21790886': 1, '8757000': 1, '8875479': 1, '8911174': 1, '9760981': 1, '7191526': 1, '7782824': 1, '27843682': 2, '21513425': 1, '13170854': 1, '17652921': 1, '9002576': 1, '24340232': 2} | {'5054634-1': 1} |
164,452 | 3841942-1 | 24,340,239 | noncomm/PMC003xxxxxx/PMC3841942.xml | A blunt needle (Epimed®) does not eliminate the risk of vascular penetration during transforaminal epidural injection | A 59-year-old female presented with chronic lumbar radiculopathy attributed to L5-S1 foraminal stenosis documented by magnetic resonance imaging (MRI) []. She underwent a TFESI at the L5-S1 level. Negative aspiration was confirmed, and a 0.5 ml of 1% lidocaine was administered as a test dose; there were no neurological changes. Next, a 22-gauge blunt curved Epimed® needle was slowly advanced into the foramen. Despite negative aspiration, the spread of contrast under live fluoroscopy was clearly consistent with an intravascular injection []. The needle was, therefore, slightly withdrawn and repositioned until contrast spread along the nerve root and epidural canal (epidurogram). There was neither vascular uptake nor intrathecal spread, and aspiration revealed neither blood nor cerebrospinal fluid []. Next, 80 mg of methylprednisolone acetate with 3 ml of lidocaine 0.5% was injected, and the needle was removed with a flash of 1% lidocaine. She tolerated the procedure well without apparent complications. | [[59.0, 'year']] | F | {'20171936': 1, '12749976': 1, '10707395': 1, '14588291': 1, '12544950': 1, '17197337': 1, '17147672': 1, '15706327': 1, '10943753': 1, '24340239': 2} | {} |
164,453 | 3841957-1 | 24,339,689 | noncomm/PMC003xxxxxx/PMC3841957.xml | Bilateral Proliferative Retinopathy as the Initial Presentation of Chronic Myeloid Leukemia | In January 2011 a 48-year-old Caucasian male presented to the Eye Casualty Department, Hospital de Santo António-Centro Hospitalar do Porto, Porto, with a 1 1 day history of acute visual loss and floaters in his left eye (LE). The patient also complained of a 1 week history of blurred vision in the right eye (RE). He had been diagnosed with hypertension and dyslipidemia in 2009 and he was medicated with candesartan/hydrochlorothiazide 16mg/12.5mg once per day (qd) and simvastatin 20mg qd. His past ocular history was unremarkable. Both his parents had hypertension and dyslipidemia, without major ocular complications; besides this the remaining family history was unremarkable. In the last appointment (March 2010) his best corrected visual acuity (BCVA) was 20/20 with a myopia correction of 1D in both eyes (BE). When asked specifically about other symptoms, he stated he did note some fatigue over the last 3 months but it was not severe enough to seek medical attention as it disappeared with rest. He denied any history of radiation treatment, injury, weight loss, fever, rash, bone pain, abdominal discomfort, left upper quadrant pain or night sweats. On presentation, his BCVA was 20/50 in the RE and 20/200 in the LE with no improvement with pinhole. On slit-lamp examination, the anterior segment had no abnormalities with an intraocular pressure of 14mmHg (Goldmann Applanation Tonometry) in BE. Gonioscopy was unremarkable. No relative afferent pupillary defect was observed; ocular movements were preserved in all fields of gaze. Dilated fundus examination showed the presence of multiple vascular abnormalities in the posterior pole and in all four quadrants of the peripheral retina in BE, including, dilated and tortuous veins, widely scattered dot-blot and flame-shaped retinal hemorrhages, microaneurysms, multiple sea fan peripheral retinal neovascularisations with arteriovenous anastomosis, and vitreous hemorrhage more evident in the LE []. Fluorescein angiography showed some degree of blockage due to the vitreous hemorrhage and the retinal hemorrhages in BE. Fluorescein angiography also showed widely scattered microaneurysms, marked areas of peripheral retinal non-perfusion due to capillary dropout, arteriovenous anastomosis, and peripheral retinal neovascularisations with a sea fan configuration but without evidence of vasculitis [Figures and ]. A diagnosis of bilateral proliferative retinopathy was made and an initial systemic evaluation was performed. The blood pressure was 124/78 mmHg. Several laboratory test results were within normal limits, including : 0 the fasting glucose and hemoglobin A1c; lipid profile; reactive protein C activity; erythrocyte sedimentation rate; homocysteine level; serum protein S, protein C, and antithrombin III. Coagulation parameters were also normal. Factor II mutation, factor V Leiden mutation, anti-cardiolipin antibodies, and lupus anticoagulant antibodies were negative. Hemoglobin electrophoresis and serum protein electrophoresis showed no abnormalities. Complete blood count and peripheral blood smear evaluation revealed hyperleukocytosis (248×103 cells/mm3; reference value, 4.5-11.0×103 cells/mm3), thrombocytosis (684×103/mm3; reference value, 150-450×103/mm3), normochromic normocytic anemia (10.8g/dL; reference value, 13.0-18.0g/dl), hyperuricemia and elevated serum levels of lactate dehydrogenase; the white blood cell differential count indicated an increased number of circulating mature and immature granulocytes, with the presence of blasts (1%) and a basophilia of 5%. Renal and hepatic functions were normal.\nBased on the ocular findings and hematological abnormalities, the patient was referred to a hematologist for further management. The physical examination revealed a palpable splenomegaly 10cm below the left costal margin and mild signs of anemia. Bone marrow aspiration and biopsy were performed. The bone marrow was hypercellular with an elevated myeloid-to-erythroid ratio and increased number of megakaryocytes but without fibrosis; the blast percentage was 4%. The morphologic findings combined with the cytogenetic analysis showing the reciprocal chromosomal translocation t(9;22) were diagnostic of CML. The patient was started on hydroxyurea (2g twice a day), allopurinol (300mg qd) and imatinib mesylate (400mg qd) which brought about a reduction in his white cell and platelets counts over a period of 5 weeks. Subsequently, hydroxyurea and allopurinol were discontinued but imatinib 400mg qd was maintained. The patient achieved complete cytogenetic remission 6 months after initiation of therapy, and after 9 months of therapy he had undetectable levels of BCR-ABL.\nBilateral scatter panretinal photocoagulation (PRP) of the peripheral avascular retina was performed in several sessions. A vitrectomy with peripheral proliferative membrane peeling and endolaser was also performed in the LE as the persistent vitreous hemorrhage did not allow the laser photocoagulation to be performed. The vitreous hemorrhage in the RE gradually cleared over a period of 3 months. Following treatment the proliferative retinopathy completely regressed in BE. The patient has been stable for the last 10 months and his BCVA is 20/25 in BE at the most recent visit.\nThe patient is being monitored closely by his oncologist and by his ophthalmologist. The patient will continue imatinib treatment for the foreseeable future. | [[48.0, 'year']] | M | {'15291801': 1, '15824241': 1, '19884523': 1, '30911698': 1, '15271393': 1, '8866143': 1, '26628310': 1, '32110213': 2, '17218931': 1, '11185681': 1, '32510022': 2, '27437258': 1, '14134405': 1, '21422402': 1, '18827185': 1, '12614770': 1, '29283147': 2, '30451209': 2, '31755450': 1, '24339689': 2} | {'7265268-1': 1, '5778555-1': 1, '6256890-1': 1, '7036576-1': 1, '7036576-2': 1} |
164,454 | 3841958-1 | 24,339,690 | noncomm/PMC003xxxxxx/PMC3841958.xml | Inverted Autologous Internal Limiting Membrane for Management of Optic Disc Pit with Macular Detachment | A 41-year-old female presented with a history of decreased vision in her left eye for 1 year. The best correctable visual acuity in that eye was 6/60. Anterior segment examination showed cortical cataractous changes. The intraocular pressure (IOP) was 16 mmHg. The left fundus showed an optic disc pit along-with a large macular detachment []. Ocular coherence tomography (OCT - Stratus III, Carl Zeiss, Dublin, USA) of the macula was performed, which confirmed the clinical finding [Figures and ]. The right eye was normal.\nThe patient was counseled on the available treatments. Then, we discussed the new technique which we were going to adopt for her surgery. The patient was also informed about the use of brilliant blue dye to stain the ILM during surgery. The patient signed an informed consent which contained all the details of the proposed surgical.\nThe patient underwent combined phacoemulsification and in-the-bag implantation of intraocular lens (+23.00 Diopter, Acrysof IQ, Alcon Laboratories, Tx, USA) and pars plana vitrectomy (PPV) combined with peeling of ILM. PPV was carried out with a 23-G sutureless technique. After initial core vitrectomy, triamcinolone assisted posterior hyaloid removal was performed. The ILM was stained with brilliant blue stain (Fluoron GmbH, Magirus-Deutz).\nThe stained ILM between the temporal vascular arcades was peeled in a manner that it was removed as a single sheet keeping the part adjacent to the superotemporal edge of optic disc still attached in a pedicle like fashion, as used in skin graft surgery [Figures and ]. Then, the peeled ILM flap was inverted with 23-G ILM-forceps and reflected over the optic disc [Figures and . Fluid-air exchange was then carried out keeping the silicone tipped back-flush cannula just medial to the free edge of the inverted flap thus preventing the displacement of the inverted ILM from the optic disc. Finally, intravitreal air was exchanged with non-expansile concentration (14%) of octafluoropropane (C3F8). At the end surgery, the patient was discharged with instruction to lie face down for 1 week, postoperatively.\nThe patient was examined on the first postoperative day, at 7 days, 2 weeks, monthly intervals for the next 3 months; and then at 3-month intervals. Examinations at every visit included visual acuity, anterior segment assessment, measurement of IOP, and clinical evaluation of the posterior segment. OCT examination of the optic nerve and macula were performed once the gas bubble cleared the macular area when the patient was sitting.\nThe macular detachment regressed completely at 1 month [Figures and ]. Postoperatively, the best corrected visual acuity improved to 6/24 at one month and to 6/12 at 3 months, which was maintained out to10 months (last visit to date). Although it was clinically difficult to assess the newly relocated ILM, the postoperative OCT examination confirmed coverage of optic pit by the inverted ILM []. | [[41.0, 'year']] | F | {'20844688': 2, '27847606': 1, '20195057': 1, '31920283': 2, '32606575': 1, '21638030': 1, '28512423': 2, '32824838': 1, '20234982': 1, '17638827': 1, '18654607': 1, '13753957': 1, '19787620': 1, '19384802': 1, '28405756': 1, '34085023': 2, '28574004': 2, '22131786': 2, '24339690': 2} | {'5565901-1': 1, '2934724-1': 1, '5422833-1': 1, '6938193-1': 1, '6938193-2': 1, '3223716-1': 1, '8081078-1': 1, '8081078-2': 1} |
164,455 | 3841959-1 | 24,339,691 | noncomm/PMC003xxxxxx/PMC3841959.xml | Long Term Result of Intravitreal Bevacizumab in a Patient Newly Transformed to Proliferative Macular Telangiectasia Type 2 | A 47-year-old female was admitted to our clinic with a complaint of decreased vision in the right and left eye (OU) in December 2009. She was in excellent health. On baseline examination, monocular best corrected visual acuity (BCVA) was 20/25 in both eyes. Biomicroscopic anterior segment examination was normal, and intraocular pressure was within normal limits OU. Biomicroscopic fundus examination revealed macular hole like images OU. FA, showed a horse shoe shaped hyperfluorescence on the temporal fovea OU []. Optical coherence tomography (OCT) showed an internal limiting membrane (ILM) drape OU []. The central retinal thickness (CRT) was 198 microns and 210 microns, in the right and left eyes respectively. Based on the clinical and imaging findings the patient was diagnosed with MacTel type 2 and advised to present for examinations every 2 months. Four months later, the patient complained of decreased vision in the left eye (OS). On the examination, BCVA was 20/100 OS, and fundus examination revealed a grey reflex representing a SRN beneath the fovea. FA showed a subfoveal classic choroidal neovascularization (CNV) associated with leakage OU []. OCT showed a high reflective area located subfoveally, and associated with intraretinal and subretinal fluid collection, and the CRT was 318 microns OS []. The patient was diagnosed with proliferative MacTel type 2 OS, and underwent 3 consecutive monthly 1.25 mg IVB injections. After these injections, BCVA increased to 20/25, and both clinical and angiographic features showed significant improvement with minimal leakage on FA and absence of intra- or sub-retinal fluid on OCT examination. The CRT was 258 microns []. Follow-up examinations were scheduled monthly and treatment regimen of IVB injections as clinically required was planned. Retreatment criteria were determined as; loss of visual acuity of ≥1 line, and detection of any amount of intra- or subretinal fluid on OCT. At month 12, OCT showed subretinal fluid with a CRT of 259 microns OS. BCVA remained stable at 20/25 OS. The patient underwent another IVB injection OS. At month 24, the BCVA decreased to 20/63, and FA showed active leakage around the CNV OS. After the fifth IVB injection, BCVA improved to 20/40 OS. At month 29 as BCVA decreased to 20/126 and OCT showed subretinal fluid, a sixth IVB injection was administered. At month 30, visual acuity improved to 20/40, and OCT revealed a hyperreflective CNV scar located subfoveally, with a CRT of 198 microns OS []. No adverse events were detected due to IVB injections during follow up. The right eye remained stable with a visual acuity of 20/25 for 30 months, and did not show any signs of proliferative MacTel type 2. | [[47.0, 'year']] | F | {'17345090': 1, '16606869': 1, '20844678': 1, '16462869': 1, '30788805': 1, '8414413': 1, '27500120': 1, '11879135': 1, '18637105': 1, '21610563': 1, '19503767': 1, '24339691': 2} | {} |
164,456 | 3841960-1 | 24,339,692 | noncomm/PMC003xxxxxx/PMC3841960.xml | Recurrent Central Serous Chorioretinopathy with Dexamethasone Eye Drop used Nasally for Rhinitis | A 35-year-old male, optometrist by profession, visited our hospital with complaint of seeing a dark circle in front of his right eye with onset three days prior to presentation. Patient was a non-smoker, non-alcoholic, non-hypertensive, was not on any medication and followed a healthy life style. Vision was 6/18 in the right eye with best corrected visual acuity (BCVA) of 6/6 with +2.0 D sphere. Anterior segment and intraocular pressure were normal. Fundus examination showed a bleb like elevation of retina. Fundus fluorescein angiography (FFA) showed ink blot leakage []. Coherence tomography (OCT) is shown in . The patient was diagnosed with CSC. The patient was prescribed 0.5% carboxymethylcellulose eye drops thrice a day and asked to return for follow up every two weeks. CSC completely resolved, clinically and on OCT, within seven weeks []. Four weeks later the patient had a recurrence that again resolved spontaneously over eight weeks. In all, patient had three additional episodes of CSC in the same eye over the next year []. Each time patient denied any form of corticosteroid use. After detailed questioning, he admitted, that he used dexamethasone eye drops, nasally for five to seven days before each episodes. This suggests the strong correlation between steroids given by any route and pathogenesis of CSC. This is also first case ever of confirmed CSC due to nasal intake of steroid drops. | [[35.0, 'year']] | M | {'12359603': 1, '15019370': 1, '8363466': 1, '16049541': 1, '31049263': 1, '16680921': 1, '16033370': 1, '22024860': 1, '15136332': 1, '9331207': 1, '11157885': 1, '24339692': 2} | {} |
164,457 | 3841961-1 | 24,339,693 | noncomm/PMC003xxxxxx/PMC3841961.xml | Trichilemmal Cyst of the Bulbar Conjunctiva: A Rare Presentation | A 55-year-old female from South India of Dravidian race presented with a history of gradually progressive, painless swelling in the left bulbar conjunctiva adjacent to the nasal limbus of 3 years duration. It was not associated with redness, discharge or blurring of vision. There was no history of trauma or history of any surgery performed in the past. There was no significant family history. On clinical examination, there was a nodular mass adjacent to the nasal limbus of left eye measuring 5 mm × 5 mm, fixed to the underlying tissue, non-tender, lying within the pterygium [Figures and ]. The transillumination test was negative. Examination of the rest of the anterior and posterior segment was unremarkable. The right eye was unremarkable. A fold of subconjunctival tissue extending from the swelling to the caruncle was observed during wide excision biopsy of the lesion. The specimen was sent for histopathological examination.\nHistopathology indicated the presence of sebaceous material.\nMicroscopic examination showed a cyst lined by stratified squamous epithelium with the absence of granular cell layer, focal basal cell hyperplasia, and flakes of keratin within the cyst [Figures –]. A diagnosis of a conjunctival trichilemmal cyst was made based on the histopathological findings. | [[55.0, 'year']] | F | {'15002107': 1, '23238396': 1, '16234696': 1, '17760602': 1, '22606489': 2, '20164755': 1, '1360441': 1, '17524785': 1, '31309066': 2, '14510806': 1, '19617807': 1, '24339693': 2} | {'6620810-1': 1, '3350258-1': 1} |
164,458 | 3841962-1 | 24,339,694 | noncomm/PMC003xxxxxx/PMC3841962.xml | Visual Hallucinations (Charles Bonnet Syndrome) Associated with Neurosarcoidosis | A 46-year-old African American female presented in March 2010 with a 1-year history of bilateral progressive vision loss accompanied by right facial paresthesia in the V2 distribution, a right seventh-nerve palsy, eye pain, and photophobia. Over the next several weeks, the patient developed lucid visual hallucinations consisting mostly of an unfamiliar little girl. The images did not speak to the patient nor did she attempt to interact with the patient. The patient recognized that the hallucinations were not real and she was not disturbed or frightened by them. The hallucinations were not accompanied by any delusions, paranoid ideation, mental status changes, seizure activity or change in the level of consciousness. Past medical history was significant for a colonoscopy in 1990. The patient was not on any medications and denied the use of hallucinogens (i.e., anti-psychotics, barbiturates, sedatives, illicit drugs). The patient had been treated with topical antibiotic drops for her eye pain without relief. She had no prior psychiatric history.\nOn neuro-ophthalmic examination in March 2010, the patient was awake, oriented, and alert, but continued to complain of visual hallucinations. Best corrected visual acuity was 20/200 in both eyes. Pupils were 4.0 mm in the dark and 2.0 mm in the light with a left relative afferent pupillary defect and light-near dissociation in both eyes External examination revealed right partial peripheral facial nerve palsy. Motility and intraocular pressure exams were normal. Slit lamp bio-microscopy was normal without uveitis or granuloma formation. Dilated funduscopic examination showed bilateral optic nerve atrophy with temporal pallor in both eyes. Automated (Humphrey 24-2) visual fields revealed a cecocentral defect in the right eye and a central defect with superior arcuate nerve fiber layer defects in the left eye. Optical coherence tomography of the optic discs showed diffuse nerve fiber layer loss measuring 57 microns in the right eye and 70 microns in the left eye on the global indices.\nAngiotensin-converting enzyme levels were markedly elevated (<200 ug/L). A cranial magnetic resonance imaging study showed enhancement of both optic nerves [], both oculomotor nerves, the left V2 branch of the trigeminal nerve, and the right facial nerve as well as right cavernous sinus meningeal enhancement extending anteriorly and inferiorly into the pterygopalatine fossa, the orbital apex and the infratemporal fossa with minimal involvement of the occipital cortex. A full-body positron emission tomography scan and chest computed tomography scan revealed mediastinal lymphadenopathy as well as multifocal areas of hypermetabolic activity involving the head, neck, chest, abdomen, and pelvis with no evidence of occipital cortex involvement. Cerebrospinal fluid was significant for inflammatory pleocytosis (19 WBC's mm[], elevated protein, normal glucose). Mediastinal lymph node biopsy showed non-caseasting granulomas consistent with the diagnosis of sarcoidosis. The patient was started on 50 mg of prednisone daily for 3 months that was subsequently tapered to a maintenance dose of 5 mg.\nThe patient's visual hallucinations had completely resolved by September 2010. At last follow-up in April 2011, best visual acuity had improved to 20/25 bilaterally and the central visual field defects improved bilaterally with some residual mild nerve fiber layer defects and optic atrophy in both eyes. There was complete resolution of the patient's peripheral nerve palsy. | [[46.0, 'year']] | F | {'16794440': 1, '19349864': 1, '31769759': 1, '8565336': 1, '22687320': 1, '26593141': 1, '20736834': 1, '24339694': 2} | {} |
164,459 | 3842150-1 | 24,286,007 | noncomm/PMC003xxxxxx/PMC3842150.xml | The variable course of women with X-linked Alport Syndrome | A 25-year-old white female presented in 2006 at age 19 with nephrotic syndrome. Her serum creatinine (SCr) was 0.9 mg/dL (79.6 μmol/L) with an estimated glomerular filtration rate (eGFR) [] of 74 mL/min/1.73 m2, serum albumin (SAlb) was 2.9 g/dL (29 g/L) and a urinalysis had 4+ protein and large blood by dipstick. A 24-h urine protein was 6.4 g/day. She had no history of gross hematuria, hearing difficulty or visual changes. Family history was negative for proteinuria, renal failure or AS, but was positive for microscopic hematuria in her maternal grandmother and aunt. A kidney biopsy was performed for the evaluation of nephrotic syndrome and microscopic hematuria.\nLight microscopy (LM) contained six glomeruli, one of which was globally sclerotic. The remaining glomeruli had preserved architecture with delicate basement membranes, patent glomerular capillaries and normal mesangial matrix and cellularity (Figure A). Tubular atrophy and interstitial fibrosis involved 5% of the cortex, and interstitial foams cells (Figure B) affected 10–15% of the cortex. IF demonstrated weak mesangial staining for IgM (trace–1+) and C3 (trace). The tissue was stained with antibodies to the alpha 1, 3 and 5 chains of type IV collagen. This revealed 1–2+ segmental/mosaic staining of the GBM with the alpha 3 chain of type IV collagen (Figure ). Staining for the alpha 5 chain of type IV collagen also showed 1+ segmental/mosaic staining of the GBM (Figure ). There was no staining of the dTBM for either the alpha 3 or the alpha 5 chains of type IV collagen. Electron microscopy (EM) demonstrated diffusely thinned GBMs, measuring 124 nm in average thickness (Figure ), but there was no lamellation or splitting. Segmental foot process effacement involved 50% of the total glomerular capillary surface area.\nHeterozygous XLAS was diagnosed based on the ultrastructural findings and the segmental/mosaic IF staining of the GBM and Bowman's capsule and the lack of staining of the dTBM for the alpha 3 and alpha 5 chains of type IV collagen.\nAn angiotensin-converting enzyme inhibitor (ACEi) was started after the biopsy. In 2012, her SCr rose to 1.6 mg/dL (141.4 μmol/L) (eGFR—38 mL/min/1.73 m2), and she remained nephrotic (urine protein creatinine ratio 3.7 g/g) with microscopic hematuria. Additionally, she developed progressive high-tone hearing loss and now requires hearing aids. | [[25.0, 'year']] | F | {'22237748': 1, '19854849': 1, '4028523': 1, '12969134': 1, '7398144': 1, '20773074': 1, '14133841': 1, '30883042': 1, '4750912': 1, '14514738': 1, '22166847': 1, '21614513': 1, '2195878': 1, '14871398': 1, '5763827': 1, '9697665': 1, '27402170': 1, '9563792': 1, '8914010': 1, '20386926': 1, '17657099': 1, '20573260': 1, '7706490': 1, '1404298': 1, '23349312': 1, '16908915': 1, '17400558': 1, '24286007': 2} | {'3842150-2': 2} |
164,460 | 3842150-2 | 24,286,007 | noncomm/PMC003xxxxxx/PMC3842150.xml | The variable course of women with X-linked Alport Syndrome | A 36-year-old white female presented in 1990 at age 14 with microscopic hematuria and nonnephrotic proteinuria, and had a normal SCr of 0.8 mg/dL (70.7 μmol/L) (eGFR—98 mL/min/1.73 m2). A kidney biopsy demonstrated TBMN, but there was no other evidence of AS. Her urinalysis findings persisted, but her kidney function remained normal so no further work-up was pursued. The family history was negative for AS, TBMN, microscopic hematuria, proteinuria or renal disease. In 2007, she had proteinuria of 500 mg/day which by 2008 had progressed to 4 g/day with a SAlb of 3.6 g/dL (36 g/L) and a SCr of 0.8 mg/dL (70.7 μmol/L) (eGFR—84 mL/min/1.73 m2), and the urinalysis continued to demonstrate microscopic hematuria. A serological evaluation (rheumatoid factor, C3 and C4 levels, myeloperoxidase and proteinase 3 anti-neutrophil cytoplasmic antibody, hepatitis B surface antigen, hepatitis C antibody, HIV, anti-nuclear antibody, anti-Smith antibodies and anti-ribonucleoprotein antibodies) was negative. She had no history of gross hematuria, hearing difficulty or visual changes. She underwent a second kidney biopsy in 2008 for the evaluation of nephrotic-range proteinuria and microscopic hematuria.\nThe biopsy contained eight glomeruli by LM and two were globally sclerotic. The remaining six glomeruli appeared normal. Small foci of tubular atrophy and interstitial fibrosis affected 10% of the total cortex. IF demonstrated segmental/mosaic staining of the GBM and Bowman's capsule with the alpha 3 and alpha 5 chains of type IV collagen. There was no staining of the dTBM for either the alpha 3 or alpha 5 chains of type IV collagen. EM demonstrated variable thinning and thickening of the GBMs, averaging 265 (range 157–427) nm with no splitting or lamellation. Foot process effacement was focal.\nHeterozygous XLAS was diagnosed based on the ultrastructural findings and the segmental/mosaic IF staining of the GBM and Bowman's capsule and the lack of staining of the dTBM for the alpha 3 and alpha 5 chains of type IV collagen.\nShe was placed on an ACEi. Nonetheless, in 2012, her SCr had risen to 1.1 mg/dL (97.2 μmol/L) (eGFR—54 mL/min/1.73 m2), she remained nephrotic with proteinuria of 4–6 g/day and continued to have microscopic hematuria. Additionally, formal hearing test demonstrated high-frequency hearing loss and an ophthalmologic evaluation showed anterior lenticonus. | [[36.0, 'year']] | F | {'22237748': 1, '19854849': 1, '4028523': 1, '12969134': 1, '7398144': 1, '20773074': 1, '14133841': 1, '30883042': 1, '4750912': 1, '14514738': 1, '22166847': 1, '21614513': 1, '2195878': 1, '14871398': 1, '5763827': 1, '9697665': 1, '27402170': 1, '9563792': 1, '8914010': 1, '20386926': 1, '17657099': 1, '20573260': 1, '7706490': 1, '1404298': 1, '23349312': 1, '16908915': 1, '17400558': 1, '24286007': 2} | {'3842150-1': 2} |
164,461 | 3842151-1 | 24,286,006 | noncomm/PMC003xxxxxx/PMC3842151.xml | Secondary amyloidosis in a patient carrying mutations in the familial Mediterranean fever (FMF) and tumour necrosis factor receptor-1 syndrome (TRAPS) genes | A 21-year-old Romanian woman at the 35th week of gestation was admitted due to acute left upper quadrant abdominal pain for 3 days, associated with nausea and vomiting.\nShe had been healthy until the age of 20 when she underwent appendectomy for acute appendicitis and contracted hepatitis C virus infection. During pregnancy, blood pressure was normal and total weight gain was 6 kg. Mild oedema in the lower limbs was present before pregnancy, but it worsened during the first trimester. Due to her socioeconomic status, the patient did not receive any prenatal care.\nUpon admission, blood pressure was 100/60 mmHg, pulse rate 90 beats/min and respiratory rate 28/min. There was no fever. Physical examination revealed mild abdominal distention and hypoactive bowel sounds. Moderate pitting oedema was present in the lower limbs. Lung, heart and neurological examinations were within normal limits. She was placed on parenteral nutrition and bowel rest, but her clinical condition worsened and the patient developed an inability to pass flatus. A Caesarean delivery was immediately performed and a premature child was delivered. A few days after delivery, abdominal pain, nausea and vomiting resolved spontaneously.\nTable summarizes the laboratory examination performed after delivery. Proteinuria 3.6 g/24 h was noted, serum creatinine was 53 µmol/L (0.6 mg/dL) and urea 7.1 mmol/L (20 mg/dL). Haemoglobin was 78 g/L (7.8 g/dL), white blood cells 20 × 109/L (19.700/µL) with 94% of neutrophils and platelets 738 × 109/L (738.000/µL). C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were 150 mg/L and 90 mm/h, respectively; fibrinogen was normal. Serum protein was 33 g/L (3.3 gr/dL) and albumin 16 g/L (1.6 g/dL). No monoclonal band was present in serum protein electrophoresis. Autoimmune and coagulation parameters were normal, as well as thyroid and liver function tests. Hepatitis B virus infection markers were negative, and apart from a slight increase in hepatitis C virus antibody titre, no signs of active hepatitis were detected. The SAA protein level was high (591.28 ng/mL). Abdominal ultrasonography showed hyperechogenic cortex. Echocardiography revealed only mild mitral regurgitation. Electromyography detected initial signs of lower-limb sensory neuropathy. While abdominal fat pad aspirate was negative for amyloidosis, kidney biopsy revealed a diffuse glomerular deposition of amorphous hyaline material that stained weakly with periodic acid Shiff's and bound Congo red and thioflavine T (Figure ). Vascular and tubular deposits were also present. Rectal biopsy was performed as well, showing the presence of A protein and the absence of immunoglobulin light chains. Molecular genetic screening tests for secondary (AA) amyloidosis were performed. A blood sample was obtained from the patient after her informed consent and genomic DNA was extracted from peripheral blood lymphocytes. The entire coding regions and intron–exon junctions, which are important in order to identify variants affecting mRNA splicing, were amplified and screened for mutation in Apo A-I, TNFRS1A and MEFV genes by the Sanger sequencing method to identify the causing mutation. Reference sequences were obtained from NCBI RefSeq and all sequences were compared with these sequences. The standard nomenclature recommended by HGVS was used to number nucleotides and name mutations or variants. Two different mutations were identified by sequencing analysis. The first involved a copy of the gene of the FMF (MEFV) and it was c2082G>A, p.M694I on the short arm of chromosome 16. The second involved a copy of the tumour necrosis factor receptor-1 gene (TNFRSF1A), and it was c.362G>A, p.R92Q on the short arm of chromosome 12 (Figure ). The diagnosis of AA amyloidosis was then confirmed. The Apo A-I gene did not present any mutations. | [[21.0, 'year']] | F | {'12077709': 1, '16508982': 1, '12209523': 1, '19479871': 1, '16234278': 1, '16284730': 1, '15643295': 1, '22714396': 1, '19302049': 1, '7156325': 1, '18163488': 1, '17554117': 1, '13130484': 1, '32684647': 1, '23031807': 1, '11464238': 1, '10914855': 1, '20177433': 1, '11085810': 1, '11132099': 1, '11443543': 1, '22884554': 1, '24286006': 2} | {} |
164,462 | 3842215-1 | 24,294,001 | noncomm/PMC003xxxxxx/PMC3842215.xml | Duloxetine in panic disorder with somatic gastric pain | GV, a 29-year-old Caucasian woman suffering from panic disorder with agoraphobia, was referred to our clinic for recurrent gastroenteric panic symptoms. She had a negative family history for mental illness and had no past history of substance use/abuse. The patient’s psychiatric history dated back to 8 years previously when, at the age of 21 years, she presented with somatic panic symptoms, ie, tachycardia, chest tightness, heartburn, and panic attacks. On her first outpatient visit to the gastroenterology clinic at the age of 26 years, she presented with recurrent heartburn, but tested negative for hiatal hernia, Helicobacter pylori, and esophagogastric reflux. At that time, she was also experiencing isolated panic attacks characterized by palpitations (tachycardia), chest tightness, somatopsychic depersonalization, fear of dying, anticipatory anxiety, harm avoidance, and a fear of being alone. She was not given any psychopharmacologic treatment but was treated with triple gastric therapy comprising a proton pump inhibitor (esomeprazole), antacids (alginic acid and sodium bicarbonate), and an antidopaminergic gastrointestinal prokinetic agent (clebopride).\nAt the first outpatient visit, the patient presented primarily with somatic symptoms, including heartburn, chest tightness and pain, somatopsychic depersonalization, tachycardia, and fear of dying and anxiety in the context of asthenia and anergia. We assessed her symptomatology using the Structured Clinical Interview for Panic-Agoraphobic Spectrum lifetime version, and the score was 85 at the first visit. We initially prescribed citalopram 20 mg/day, but the patient reported sexual dysfunction (reduction/loss of libido and difficulty achieving orgasm), cognitive impairment, and fatigue. The patient reported improvement in her anxiety symptoms and panic attacks on a selective serotonin reuptake inhibitor, but not in her troublesome gastric somatic symptoms. We therefore decided to gradually reduce the dose of citalopram and introduced escitalopram 7 mg/day, but the patient continued to report loss of libido with no change in her gastric symptoms. We then prescribed duloxetine 30 mg/day, which was subsequently increased to 60 mg/day, with slow withdrawal of escitalopram. After 6 months of treatment, the patient showed complete remission of her gastric and panic-related symptoms, and all three gastric treatments were able to be discontinued. | [[29.0, 'year']] | F | {'17012978': 1, '8917132': 1, '21668963': 1, '22454807': 1, '20962541': 1, '16699602': 1, '11287057': 1, '20668442': 1, '12197851': 1, '21386950': 1, '21062615': 1, '19228176': 1, '15939839': 1, '21190637': 1, '19548294': 1, '16585471': 1, '32691294': 1, '24294001': 2} | {} |
164,463 | 3842706-1 | 24,350,077 | noncomm/PMC003xxxxxx/PMC3842706.xml | Mycobacterium Tuberculosis Infection within a Warthin Tumor: A Case Report and Literature Review | A 46-year-old male presented with a mass in the left parotid region of 6-month duration. The patient's history was only remarkable for a facial swelling, night sweats and a 38.5 C° fever. There were no other symptoms such as pain, facial paralysis, cough associated with this swelling. His past medical history was nonrevealing. There was no family history of tuberculosis. On physical examination, a 2 × 3-cm mobile, non-tender, mass with a smooth surface was palpated on left parotid tail. The physical examination was otherwise unremarkable. Routine laboratory tests, and a chest radiograph were normal. Ultrasound examination showed a well-defined, hypoechoic solid mass in the superficial lobe of the left parotid gland accompanied with the lymph node in same region. CT examination showed a well defined 30 mm in diameter tumor mass in the left superficial lobe of the parotid gland []. A superficial parotidectomy operation was performed under general anesthesia. The lymph nodes were also excised. The final pathological diagnosis of the parotidectomy specimen was reported as a Warthin tumor and epitheloid granulomas with caseification necrosis []. An intradermal test with purified protein derivative (PPD) was performed and it was 30 mm in enduration. Antituberculosis treatment with isoniazid, rifampicin, pyrazinamid and ethambutol was started for a 6-month duration. Two weeks after the antituberculosis treatment fever declined to normal values and night sweats decreased. | [[46.0, 'year']] | M | {'22540099': 1, '22614566': 1, '11881733': 1, '13651631': 1, '18302769': 2, '19434322': 1, '16303681': 1, '19098552': 1, '32049782': 2, '9764307': 1, '7467121': 1, '8486105': 1, '24350077': 2} | {'2267472-1': 1, '7035061-1': 1} |
164,464 | 3842707-1 | 24,350,078 | noncomm/PMC003xxxxxx/PMC3842707.xml | Leaking Heart: Ticking Time Bomb! | A 72-year old male with hypertension presented to emergency room with light headedness and hypotension. Initial blood pressure was 80/50 mmHg and heart rate was 70 beats/minute. Electrocardiogram revealed evidence of tall R waves in lead V1-2 []. Troponin I level was 11.9 ng/mL. An emergent echocardiogram revealed a large pericardial effusion with fibrinous material []. Patient denied any other complaints including chest pain or dyspnea and wished to be discharged home. He did mention that he had an episode of chest pain 1 week earlier that resolved spontaneously and he did not seek medical care. Based on electrocardiogram and echocardiogram findings, we suspected patient suffered a posterior myocardial infarction which was complicated by contained free wall rupture and pericardial effusion. Based on the high index of suspicion, patient was taken for emergent coronary angiography which revealed 100% circumflex occlusion and right heart catheterization was consistent with tamponade physiology. Left ventriculogram showed an ejection fraction of 40% with staining of postero-basal wall suggestive of possible cardiac rupture. Patient underwent emergent percutaneous coronary intervention to the left circumflex along with placement of an intraaortic balloon pump, and emergent pericardiocentesis with removal of 50cc of hemorrhagic fluid. This led to hemodynamic stabilization. Limited pericardiocentesis was done to prevent dislodgement of the clot which may be tamponading the ruptured site. Patient was then taken to operating room immediately. Intraoperative a large amount of hemorrhagic fluid with clot was removed. The infarcted posterior myocardium showed necrosis and hemorrhage with multiple puncture sites leaking/oozing blood. A large patch was created with combination of Bio Glue and patient's own pericardium. This was glued onto the posterior wall and then sewn with a running 5-0 Prolene reinforced with multiple pledgeted 5-0 Prolene circumferentially around the posterior wall in the area of the circumflex distribution with care taken to avoid the circumflex artery itself. This appeared to completely stop all the bleeding. Post-operatively, patient did well in the intensive care unit for three days. However, on the fourth day patient suddenly developed pulseless electrical activity due to repeat free wall rupture and died. | [[72.0, 'year']] | M | {'31793256': 2, '27398201': 1, '2338333': 1, '2648779': 1, '8626938': 1, '4015910': 1, '7737750': 1, '3052010': 1, '20078707': 1, '8607710': 1, '10881802': 1, '2980052': 1, '24350078': 2} | {'6894036-1': 1} |
164,465 | 3842708-1 | 24,350,079 | noncomm/PMC003xxxxxx/PMC3842708.xml | Bilateral Putaminal Hemorrhages: Serious Complication of Methanol Intoxication | A 56-year-old man with history of episodic alcohol abuse and rectal adenocarcinoma status post-surgery and neoadjuvant chemoradiation therapy presented to emergency department with altered mental status. On admission, he was comatose with dilated pupils and minimal reaction to light. Fundus examination showed optic disc edema without evidence of retinal hemorrhage. Arterial Blood Gas (ABG) revealed severe metabolic acidosis; pH 6.89, pCO2 13, pO2 178, HCO3 < 3. Blood tests also demonstrated anion gap and osmolal gap. Head computed tomography (CT) showed new hypodense lesions in basal ganglia bilaterally and old small vessel ischemia changes in periventricular matter [].\nEmergent hemodialysis (HD) and treatment with intravenous fomepizole were initiated. Serum methanol level, obtained after hemodialysis, came back significantly elevated. Ophthalmologist was consulted for visual defect and diagnosed the patient with legal blindness without other focal neurological deficit prior to discharge. Type of alcohol, consumed by the patient, was still unknown. Unfortunately, patient developed confusion and lethargy 2 weeks after discharge. New CT of head without contrast demonstrated new hyperdensities in putaminal area compatible with the diagnosis of putaminal hemorrhages []. | [[56.0, 'year']] | M | {'11562866': 1, '21715637': 1, '22883652': 1, '22257634': 1, '22810212': 1, '26722590': 1, '24350079': 2} | {} |
164,466 | 3842730-1 | 24,347,896 | noncomm/PMC003xxxxxx/PMC3842730.xml | Comparative outcome of revascularization in bilateral, non-vital, immature maxillary anterior teeth supplemented with or without platelet rich plasma: A case series | A healthy 10-year-old boy was referred for evaluation and management of his broken upper anterior teeth, subsequent to a fall 3-year prior. Root canal therapy was initiated, but not completed by a general dental practitioner. Intraoral examination revealed Ellis class III fracture and a well-defined, localized swelling in relation to both the upper central incisors. Radiographic examination showed immature open apices with thin dentinal walls in relation to both the teeth []. Based on clinical and radiographic examination, a diagnosis of acute periapical abscess in relation to both the central incisor was established. Taking into consideration the stage of root development, the maturation of the dentinal walls and the wide-open apices, revascularization procedure with and without PRP was planned. The risks, complications and possible outcome of this treatment were explained and parental informed consent was obtained.\nTeeth were isolated under rubber dam and re-accessed with a round diamond and an endo-Z bur (Dentsply Maillefer, Tulsa, OK). Purulent discharge was observed in both the teeth. The canals were copiously irrigated with normal saline. Working length was established with a paper point (Dentsply Maillefer, Tulsa, OK) and confirmed radiographically by placing a large file in the canal. Minimal mechanical instrumentation with an International Organization for Standardization number 60H-file (Dentsply Maillefer, Tulsa, OK) and irrigation with 20 mL 2.5% sodium hypochlorite (NaOCl, Cmident, India) was performed. The canal was dried with paper points and an inter-appointment medication of triple antibiotic paste (as per the protocol mentioned by Hoshino et al. 1996) was applied with a sterile number 30 hand lentulo spiral (Dentsply Maillefer, Tulsa, OK). Teeth were temporarily restored with intermediate restorative material (Caulk Dentsply, Milford, DE). This was the chemo-mechanical and disinfection protocol followed for all cases. However, in cases of weeping canals, another inter-appointment dressing was given until the tooth was symptom-free and the canal was dry. Patients were recalled after 4-week. Teeth were re-accessed under rubber dam and revascularization with and without PRP were randomly induced in upper left and right central incisors respectively [].\nLocal anesthetic solution without adrenaline (LOX 2% Neon Lab, India) was infiltrated around the apices of both the central incisors. A sterile endodontic file with a rubber stopper set at 2 mm beyond the established working length was taken. With sharp, fine strokes, the file was pushed past the confines of the canal into the periapical tissue. When frank bleeding was evident, a dry cotton pellet was inserted 3-4 mm into the canal and held there for 5-7 min to allow blood clot formation in the apical third. This revascularization protocol was followed for both the teeth.\nPRP preparation was carried out in a simple, table top laboratory centrifugation machine (Remi model no. — R–8C, India). A total volume of 8.5 mL of whole blood was drawn by venipuncture of antecubital vein. It was then collected in a 10-mL sterile glass tube coated with an anticoagulant (acid citrate dextrose). Whole blood was initially centrifuged (soft spin at 2400 rpm for 10 min) to separate PRP and platelet-poor plasma (PPP) portions from the red blood cell fraction. PRP and PPP portions were again centrifuged (hard spin at 3600 rpm for 15 min) to separate the PRP from the PPP.\nIntra-canal bleeding was induced as described above. Freshly prepared PRP, soaked on a 1 mm2 × 1 mm2 sterile collagen sponge (Metrogene, Septodont, France) was introduced into the root canal of maxillary left central incisor with cotton pliers and carried to the middle third with a size 30 finger plugger (Sybronendo, CA, USA). Access openings were restored with resin modified glass ionomer cement (Photac-Fill, 3MESPE, Minnesota). Standardized intraoral periapical baseline and subsequent follow-up radiographs at 6 and 12 months were taken with a Rinn positioning device (Dentsply, Elgin, IL). | [[10.0, 'year']] | M | {'98608': 1, '32765197': 1, '28567136': 1, '32647469': 1, '21419310': 1, '25110649': 2, '18634921': 1, '33623248': 2, '19410097': 1, '33238625': 1, '27857762': 1, '11087820': 1, '28092093': 1, '30364277': 1, '29563446': 1, '18565373': 1, '21238815': 1, '25125845': 1, '275441': 1, '20171379': 1, '19912384': 1, '9133465': 1, '31803727': 1, '11585146': 1, '5264906': 1, '30546220': 2, '21207794': 1, '5216747': 1, '1067526': 1, '6579180': 1, '34095133': 1, '16805357': 1, '34815932': 1, '24347896': 2} | {'3842730-2': 2, '3842730-3': 2, '6249949-1': 1, '4125589-1': 1, '7883779-1': 1, '7883779-2': 1, '7883779-3': 1, '7883779-4': 1} |
164,467 | 3842730-2 | 24,347,896 | noncomm/PMC003xxxxxx/PMC3842730.xml | Comparative outcome of revascularization in bilateral, non-vital, immature maxillary anterior teeth supplemented with or without platelet rich plasma: A case series | A healthy 23-year-old man was referred with the complaint of lingering pain in upper front teeth for the past 1 week. Patient had a history of trauma 15-year ago, for which no treatment was sought. Intraoral examination revealed discolored both upper central incisors and a sinus tract on palatal aspect of upper left lateral incisor. Radiographic examination revealed well-defined, bilateral periapical radiolucency involving both upper centrals and upper left lateral incisor []. Both the central incisors had open apices and thin lateral dentinal walls. Based on clinical and radiographic examination, a diagnosis of pulpal necrosis with chronic apical abscess in relation to all three teeth was established. Upper left lateral incisor was managed by conventional endodontic therapy. Revascularization procedure with and without PRP was randomly induced in upper left and right central incisors respectively []. Final esthetic rehabilitation was carried out with porcelain fused to metal crowns. | [[23.0, 'year']] | M | {'98608': 1, '32765197': 1, '28567136': 1, '32647469': 1, '21419310': 1, '25110649': 2, '18634921': 1, '33623248': 2, '19410097': 1, '33238625': 1, '27857762': 1, '11087820': 1, '28092093': 1, '30364277': 1, '29563446': 1, '18565373': 1, '21238815': 1, '25125845': 1, '275441': 1, '20171379': 1, '19912384': 1, '9133465': 1, '31803727': 1, '11585146': 1, '5264906': 1, '30546220': 2, '21207794': 1, '5216747': 1, '1067526': 1, '6579180': 1, '34095133': 1, '16805357': 1, '34815932': 1, '24347896': 2} | {'3842730-1': 2, '3842730-3': 2, '6249949-1': 1, '4125589-1': 1, '7883779-1': 1, '7883779-2': 1, '7883779-3': 1, '7883779-4': 1} |
164,468 | 3842730-3 | 24,347,896 | noncomm/PMC003xxxxxx/PMC3842730.xml | Comparative outcome of revascularization in bilateral, non-vital, immature maxillary anterior teeth supplemented with or without platelet rich plasma: A case series | A healthy, 13-year-old girl was referred with the chief complain of dull, continuous pain for past 3 months in her upper front teeth. Intraoral soft-tissue and radiographic examination revealed a well-defined, localized swelling and a bilateral periapical radiolucency involving upper central incisors. Both teeth had open apices and thin lateral dentinal walls []. Based on clinical and radiographic examination, a diagnosis of chronic abscess in relation to both the teeth was established []. After the infection control revascularization, with and without PRP was randomly induced in upper left and right central incisors respectively. | [[13.0, 'year']] | F | {'98608': 1, '32765197': 1, '28567136': 1, '32647469': 1, '21419310': 1, '25110649': 2, '18634921': 1, '33623248': 2, '19410097': 1, '33238625': 1, '27857762': 1, '11087820': 1, '28092093': 1, '30364277': 1, '29563446': 1, '18565373': 1, '21238815': 1, '25125845': 1, '275441': 1, '20171379': 1, '19912384': 1, '9133465': 1, '31803727': 1, '11585146': 1, '5264906': 1, '30546220': 2, '21207794': 1, '5216747': 1, '1067526': 1, '6579180': 1, '34095133': 1, '16805357': 1, '34815932': 1, '24347896': 2} | {'3842730-1': 2, '3842730-2': 2, '6249949-1': 1, '4125589-1': 1, '7883779-1': 1, '7883779-2': 1, '7883779-3': 1, '7883779-4': 1} |
164,469 | 3842731-1 | 24,347,897 | noncomm/PMC003xxxxxx/PMC3842731.xml | Management of a large periapical lesion using Biodentine™ as retrograde restoration with eighteen months evident follow up | A healthy 24-year-old male patient was reported to the Department of Conservative Dentistry and Endodontics with a chief complaint of broken, discolored tooth and swelling in the previously traumatized maxillary anterior region. The patient gave a history of fall and broken tooth 2 years ago. Medical history was noncontributory and clinical examination revealed a soft, fluctuant, and nontender swelling in the anterior region with fractured and discolored maxillary right central incisor []. Radiographic examination revealed well-defined radiolucency involving the coronally fractured and discolored maxillary right central incisor and lateral incisor.\nBoth the teeth presented a negative response to pulp testing and endodontic treatment for both the incisors were scheduled. The endodontic treatment procedures were conducted under magnification (loops × 2.5, Carl Zeiss, Germany). After teeth isolation the access cavities were prepared followed by shaping and cleaning and placement of intracanal medicament of calcium hydroxide (RC Cal, Prime Dental Products, India), which was renewed every 15 days for 3 months. Radiographic examination at 3 months proved no traits of healing and hence a periapical surgery was scheduled.\nThe teeth were then obturated using cold lateral condensation []. Raising a double vertical trapezoidal flap, a periapical surgery was performed and periapical pathosis was enucleated []. Maxillary right central and lateral incisors were apically resected 3 mm from the apex and retrograde cavity was prepared using ultrasonic tip. Biodentine™ was placed as retrograde restorative material of 3 mm thickness. The placement of the retrograde filling material was confirmed using a radiograph [] and the sutures were placed. Biopsy of enucleated lesion was sent for histopathologytests.\nThe patient was recalled after a week for suture removal. The patient was kept under symptomatic and radiographic observation for the purpose of postoperative evaluation of healing of the periapical intervention in intervals of 1, 3, 6, 12, and 18 months. Biopsy report confirmed the periapical pathology to be a periapical cyst. Periodic radiographic evaluation of the area of intervention showed progressive healing and 18 months follow-up X-ray showed complete bone formation and tooth was asymptomatic [Figures -]. The patient refused for an orthodontic treatment for correcting his misaligned teeth so the tooth was restored by an esthetic composite class IV restoration []. | [[24.0, 'year']] | M | {'21217952': 1, '24944453': 1, '26229383': 1, '21777256': 1, '23956530': 1, '12657145': 1, '2132213': 1, '22368341': 2, '2094761': 1, '29372451': 1, '26180420': 1, '28571302': 1, '5273692': 1, '25025034': 1, '7641616': 1, '29628640': 1, '28969295': 1, '25506153': 2, '24347897': 2} | {'3284020-1': 1, '3284020-2': 1, '4252939-1': 1} |
164,470 | 3842732-1 | 24,347,898 | noncomm/PMC003xxxxxx/PMC3842732.xml | Endodontic management of a four rooted retained primary maxillary second molar | An 18-year-old male patient reported to the Department of Conservative Dentistry and Endodontics with the complaint of pain in the left upper posterior region of the mouth since 1 week. Intraoral clinical examination of the patient revealed the presence of retained primary second molar in first and second quadrant of the oral cavity and absence of maxillary second premolars; however, there was no retained primary tooth in the mandibular arch. Remaining teeth except third molars were present in the oral cavity in their usual anatomic position. The left side primary second molar was deeply carious. The primary tooth had similar cusp-fossa relationship alike adjacent permanent teeth and infraocclusion was not clearly visible. Patient had Angle's Class I molar relationship. Furthermore, there was the absence of any obvious crowding or spacing in the permanent dentition. Radiographic examination of the left primary second molar showed the presence of deep caries involving pulp space. Furthermore, the presence of extra root in the primary left second molar and congenital absence of the second premolar tooth bud was noted, also occlusal height of primary tooth was at similar level as compared to adjacent permanent teeth in intraoral periapical radiograph []. Patient was recommended following treatment options: (1) Extraction of primary tooth followed by space closure using either crown and bridge placement or implant placement. (2) Extraction of primary tooth followed by orthodontic space closure. (3) Root canal treatment for the same tooth alike permanent tooth and follow-up. Also, in third treatment option patient was informed about the possibility of root resorption or ankylosis leading to tooth loss, which again had to be treated with implant or prosthodontic crown or bridge or orthodontic treatment. Patient insisted on saving the tooth rather than immediate extraction; hence, root canal treatment was planned. After, obtaining patient's consent root canal treatment was initiated under local anesthesia and strict rubber dam isolation. Adequate access preparation revealed four root canal orifices. Working length was measured using electronic apex locator (Root ZX™, Morrita, Tokyo, Japan) and radiographic technique using Ingle's method. Working length radiograph confirmed the presence of four separate roots and canals []. Biomechanical preparation was done using NiTi rotary endodontic instruments (Protaper™, Dentsply, New Delhi, India) in a crown down manner. 17% ethylenediaminetetraacetic acid (EDTA) and urea peroxide paste (Glyde™, Dentsply, New Delhi, India) was used as canal lubricant along with 3% sodium hypochlorite as irrigating solution. Apical canal size was prepared until size F3 for all the canals. After complete instrumentation, all canals were flushed with 17% EDTA solution to remove the smear layer followed by final flush with 5% sodium hypochlorite solution. Later on canals were completely dried using absorbent paper points (Dentsply, New Delhi, India) and all the root canals were obturated using resin based sealer (AH Plus™, New Delhi, India) and Gutta-percha points (Protaper Gutta Percha™, Dentsply, New Delhi, India) [] and the access was restored with dental composite (Ceramax Mono™, Dentsply, New Delhi, India). Post-treatment radiograph showed adequate obturation [] and the patient was asymptomatic. | [[18.0, 'year']] | M | {'22557822': 2, '20483015': 1, '14760900': 1, '10920556': 1, '20123588': 1, '30697399': 2, '22629056': 2, '5234030': 1, '19212522': 1, '9927930': 1, '6573352': 1, '21260925': 1, '25125856': 2, '5234026': 1, '14666074': 1, '14719741': 1, '24347898': 2} | {'6343985-1': 1, '3339018-1': 1, '3354789-1': 1, '4127702-1': 1} |
164,471 | 3842733-1 | 24,347,899 | noncomm/PMC003xxxxxx/PMC3842733.xml | Role of mineral trioxide aggregate in management of external root resorption | A 22-year-old male patient reported to the department of endodontic, with the chief complaint of pain with the lower right back region of tooth. He gave history of discontinued root canal treatment with same tooth []. There was no relevant medical history.\nOn clinical examination of tooth #46, tooth was temporarily restored, tender to vertical percussion and there was no mobility seen. Intraoral periapical radiographic examination of tooth #46 revealed extensive apical root resorption on both the roots, associated with diffused periapical radiolucency some bone loss.\nTaking into consideration the extent and the severity of the resorption, it was planned for orthograde MTA obturation of the canal space to arrest the resorption.\nThe existing access cavity was modified and working length of the tooth was determined with help of apex locator, Propex-II (Dentsply). Canals were cleaned and shaped with the help protaper rotary (Dentsply, Tulsa dental specialities, Ballaigues, Switzerland) up to F2, irrigating with copious amount of 3% of sodium hypochlorite, (Vishal dentocare Pvt. Ltd., Ahmedabad, Gujarat, India). This was followed by irrigation with normal saline to remove any remnants of hypochlorite, latter canals were dried with absorbents points and calcium hydroxide (R C Cal, Prime Dental products, Kalher, Thane) as an intracanal medicament was placed in canals followed by a temporary restorations for 1 week.\nAfter 1 week, temporary restorations were removed, canals were cleaned and dried. MTA, pro-Root MTA (Dentsply, Tulsa Switzerland) was manipulated according to manufacture instructions. Both the distal and mesial canals were obturated with MTA, material was placed in the canals with amalgam carrier and was condensed vertically with hand pluggers. After completion of obturation orifices were sealed, followed by postendodontic restoration [].\nThe patient was recalled after 6 [] and 24 [] months for clinical and radiograph follow up. Clinical examination of tooth #46 was functional without sensitivity to percussion or palpation. Tooth showed normal physiologic mobility and no periodontal pockets on probing. Intraoral periapical radiograph showed regression in the size of periapical radiolucency with sign of osseous repair and no further progression of ERR []. | [[22.0, 'year']] | M | {'19482173': 1, '12848710': 1, '18570985': 1, '17429181': 1, '14977307': 1, '19840502': 1, '23304567': 2, '20171353': 1, '21129158': 1, '24944454': 1, '24347899': 2} | {'3530227-1': 1} |
164,472 | 3842734-1 | 24,347,900 | noncomm/PMC003xxxxxx/PMC3842734.xml | An unusual occurrence of bilaterally geminated mandibular second premolars resulting in premolar molarization: A case report | A 27-year-old, healthy male was reported with the chief complaint of pain in the lower left back tooth region for the past 1 week. Following a clinical examination, molar resembling second premolar tooth were seen in the left mandibular region. A thorough clinical examination confirms the presence of molar resembling second premolar tooth also in the right quadrant due to gemination. This molar resembling second premolar tooth gives the impression of four molars [] in both the quadrant. The involved teeth had normal morphology; crowns and roots were significantly developed but smaller in size. The length of the root was normal relative to its crown. The root apex was completely developed. The panoramic radiograph [] reveals the presence of single root and single root canal in both the involved mandibular second premolar teeth. | [[27.0, 'year']] | M | {'26861010': 1, '9477888': 1, '3475662': 1, '11398389': 1, '26078889': 2, '3856006': 1, '24895584': 1, '10456607': 1, '5675897': 1, '7608374': 1, '2393359': 1, '2333217': 1, '10815574': 1, '24347900': 2} | {'4452850-1': 1} |
164,473 | 3843024-1 | 24,302,955 | noncomm/PMC003xxxxxx/PMC3843024.xml | Myasthenia Gravis, Schizophrenia, and Colorectal Cancer in A Patient: Long-Term Follow-Up with Medication Complexity | Ms A, a 46-year-old woman, diagnosed as disorganized type schizophrenia when she was 20 years old in 1985, was frequently hospitalized to the psychiatric ward and showed poor response to medication. At age 35, she was hospitalized for pneumonia and acute respiratory distress syndrome (ARDS), and at 38, she was hospitalized 2 times for dyspnea associated with pneumonia.\nAt 39, her fourth ARDS occurred after infectious symptoms of the upper respiratory track. Based on clinical symptoms, such as repetitive respiratory failure, ptosis, and dysphonia, MG was suspected and diagnosis was confirmed by tensilon tests, as well as detecting antibodies for acetylcholinesterase. In order to exclude MG with thymoma, mediastinal computerized tomography (CT) was taken and there were no sign of thymoma. Respiratory failure was improved by administrating pyridostigmine and immunosuppressants after plasmapheresis, and afterwards, Ms A was transferred to a chronic mental hospital.\nAt 42, respiratory failure recurred. Despite additional 15 mg of prednisolone, symptom was aggravated and she was transferred to the department of psychiatry, Kyung Hee University Hospital (KHUH). After maintaining the additional dosage, respiratory symptom was relieved and she was transferred back to the chronic mental hospital.\nIn January, 2011, respiratory failure symptoms recurred, and the patient was hospitalized at the intensive care unit of KHUH. Along with the administration of additional 10 mg of prednisolone, plasmapheresis and high dosage steroid pulse therapy were carried out and dyspneic symptom was stabilized. Aripiprazole 15 mg, paliperidone 6 mg and quetiapine 1200 mg was being administrated for psychiatric symptom control from the transferred hospital. However, in order to avoid potential drug interactions, only quetiapine 1200 mg was administrated through the nasogastric tube. Afterwards, psychotic symptoms aggravated. As persecutory and somatic delusions, as well as insomnia continued, the patient was moved to the psychiatric ward and haloperidol was added up to 10 mg. After increasing the dosage of haloperidol, lower extremity tremor, which seemed to be one of the symptoms of extrapyramidal syndrome (EPS), was observed, and procyclidine, an anticholinergic, was added. Three weeks later, the patient showed respiratory distress, with particular aggravation during night time. This was thought to be caused by exacerbation of myasthenia gravis due to administration of anticholinergics. Then, anticholinergics were stopped. Afterwards, dyspnea, somatic and persecutory delusions got worse at night and had trouble falling asleep. The patient's symptoms were suspected to be exacerbation of schizophrenia or sleep disorder due to respiratory muscle fatigue from MG. While the patient complained of insomnia, arterial blood gas analysis was tested and showed normal results. Chest X-rays were filmed because of frequent respiratory infections and atelectasis history and mild atelectasis was seen at the left lower lobe of the lung. Therapy with spirometer was considered, but postponed concerning respiratory muscle fatigue. MG exacerbation was suspected as ptosis and hoarseness symptoms worsened, and maintenance therapy with 10 mg prednisolone was carried out without dose reduction. For aggravated symptoms of schizophrenia, such as day time emotional fluctuation and aggravated persecutory delusions, haloperidol was increased to 20 mg and chlorpromazine 50 mg was added for sleep control. Overall symptoms improved after 130 days of hospitalization and Ms A was discharged.\nFour months after discharge, in order to evaluate severe anemia, she was transferred to KHUH and underwent a colonoscopy. Biopsy specimen was diagnosed as colorectal cancer. After surgical resection in the colon, she was hospitalized to the psychiatric ward for 2 weeks, and afterwards, Ms A was discharged to a chronic mental hospital. | [[46.0, 'year']] | F | {'17245324': 1, '16513876': 1, '8248922': 1, '9046891': 1, '20149832': 1, '15033152': 1, '19087469': 1, '9285246': 1, '15330399': 1, '21180568': 1, '21810731': 1, '1543353': 1, '24302955': 2} | {} |
164,474 | 3843025-1 | 24,302,956 | noncomm/PMC003xxxxxx/PMC3843025.xml | Impulsive Behavior and Recurrent Major Depression Associated with Dandy-Walker Variant | A 33-year-old man presented depression, aggressiveness, and impulsivity in his visit to the authors' hospital and was thus compulsorily admitted. He had a two-year depressive episode, was diagnosed as having major depressive disorder a year earlier, and has been on medication irregularly. He had a history of three-time admission to a psychiatric unit in the previous 12 months. His initial admission was a year earlier, after attempting suicide by ingesting pesticide. One day before admission, he presented verbal abuse and aggression. He had no family history of psychiatric disorder, including depression. The patient had two-year, withdrawn university education and he had had various jobs but never managed to keep any of them for more than two months. There was no evidence of substance use and head trauma in the history of the patient.\nBrain MRI () disclosed an enlarged cisterna magna, hypoplasia of the cerebellar vermis, and dilated ventricles, indicating Dandy-Walker variant. Intelligence testing (K-WISC) confirmed a normal range of intelligence (IQ: 94; latent IQ: 105). The result of the psychological testing showed that the patient had aggressive perceptions of other people, and that he had poor impulse control ability. The patient was anticipated to be sensitive to trivial external stimuli, to easily become angry, and to be aggressive. Beck Depression Inventory (BDI) and Hamilton Depression Scale (HAM-D) tests were performed the day after his admission, and the patient obtained 23/63 and 28/50 scores, respectively.\nMirtazapine treatment was started at a dose of 7.5 mg/day and the dose was increased to 45 mg/day on the fifth day, for the patient's depression. Valproate treatment was started at a dose of 450 mg/day for the patient's aggressiveness and lack of impulse control, and the dose was increased to 1500 mg/day on the 12th day of the patient's confinement. About a week after the initiation of valproate treatment, the patient's aggressiveness and uncontrolled impulsive behavior were slightly alleviated. Quetiapine was added for further treatment of his aggression. Quetiapine was added at a dose of 100 mg/day on the 12th day of confinement, and the dose was increased to 800 mg/day on the 20th day. The BDI score decreased from 23 to 9, and the HAM-D score went down from 28 to 10 after three months of treatment. The patient still presented some uncontrolled impulse and aggression, although these had improved much in the three months. | [[33.0, 'year']] | M | {'21253417': 2, '33615095': 1, '14504962': 1, '10379520': 1, '33192350': 1, '15377747': 1, '11368032': 1, '17478081': 1, '21887198': 2, '21983277': 1, '8790444': 1, '31133834': 1, '25976218': 1, '18662866': 1, '27493822': 2, '12153822': 1, '1953406': 1, '15827586': 1, '18372312': 1, '24302956': 2} | {'3022320-1': 1, '3162782-1': 1, '4963583-1': 1} |
164,475 | 3843038-1 | 24,303,362 | noncomm/PMC003xxxxxx/PMC3843038.xml | Endodontic treatment of maxillary lateral incisors with anatomical variations | A 26-year-old male in good health was referred to the endodontic clinic of Kyungpook National University Dental Hospital for root canal treatment of the maxillary right lateral incisor. The root canal treatment had been initiated by a general dentist, who opted for a referral after observing its unusual root canal morphology. Clinical examination revealed a sinus tract labially to the lateral incisor and swelling at this level. There was tenderness to palpation and percussion. Radiographically, a diffuse radiolucent area was noticed at the apices of roots of the maxillary right lateral incisor (). The sinus tract was traced with a gutta-percha cone to tooth #12 that showed a second root surrounded by a radiolucent area. The pulpal diagnosis was previous endodontic treatment and the periapical diagnosis was chronic apical abscess with sinus. There appeared to be two roots that had distinct root canal space.\nA rubber dam was applied, and temporary sealing material was removed. The principle canal was found easily but the second canal was not negotiated. At the following visit, because the second canal was not negotiated again while the patient had labial swelling with fever and pain, incision and drainage was performed at the labial swollen area (). At the third visit, the second canal was negotiated with ultrasonic instruments under an operating microscope. The second canal was located at the corresponding part of palatogingival groove in the pulpal chamber of the tooth. After removing dentin carefully with an ultrasonic device, an orifice was detected by using a size 10 stainless steel K-file (Mani, Tochigi, Japan). Both canals were cleaned and shaped with stainless steel K-files using the step-back technique. Radiograph revealed a narrow second canal, which was prepared with 2 mm increments per each size of file (.025 taper).\nAfter preparation, the root canals were irrigated with 17% ethylenediaminetetraacetic acid (EDTA) followed by 5% sodium hypochlorite solution and dried with sterile paper points. The root canals were obturated with gutta-percha using cold lateral compaction technique with an epoxy resin sealer (AH Plus, Dentsply De Trey GmbH, Konstanz, Germany) (). After verifying that the root canal filling was complete with a radiograph, the crown was restored with a composite resin (Gradia PA2, GC, Alsip, IL, USA). At six month examination, the tooth was asymptomatic and there was no radiolucency around the root apex (). | [[26.0, 'year']] | M | {'22050710': 1, '4500261': 1, '10530214': 1, '11210263': 1, '13484205': 1, '28119787': 2, '17697108': 1, '7673821': 1, '25469361': 2, '23633825': 2, '9257019': 1, '22794206': 1, '25984479': 2, '11108527': 1, '15167464': 1, '30083218': 2, '13613719': 1, '24790927': 2, '25984480': 2, '9594762': 1, '6595621': 1, '24303362': 2} | {'3843038-2': 2, '3843038-3': 2, '4247845-1': 1, '4432260-1': 1, '3636845-1': 1, '3978104-1': 1, '5227125-1': 1, '4432261-1': 1, '6064016-1': 1} |
164,476 | 3843038-2 | 24,303,362 | noncomm/PMC003xxxxxx/PMC3843038.xml | Endodontic treatment of maxillary lateral incisors with anatomical variations | A 12-year-old male was referred from the Department of Pediatric Dentistry for root canal treatment of the maxillary left lateral incisor. Upon clinical examination, the upper left lateral incisor showed mild tenderness to percussion and palpation. The tooth did not respond to electric and thermal pulp sensibility test while the adjacent teeth responded within normal limits. The periapical radiograph suggested two root canals in a bulbous root and a diffuse apical lesion (). From the clinical and radiographic findings, the maxillary lateral incisor was diagnosed as pulp necrosis and chronic apical abscess without sinus, for which root canal treatment was planned.\nAn access opening was made after rubber dam isolation. The main canal was wider and C-shaped. Another narrower canal was seen running towards palate under an operating microscope (). Along the dentinal map, the second canal was detected easily by extending the access cavity palatally. Working lengths were determined with an apex locator (Root ZX, Morita, Tokyo, Japan) and confirmed radiographically. Under copious irrigation with 5% sodium hypochlorite and 17% EDTA, the root canals were cleaned and shaped up to a size 35 with stainless steel K-files using the step-back technique and the circumferential filing technique. Obturation of the root canal was performed by cold lateral compaction of gutta-percha using an epoxy resin sealer (AH Plus) (). The access cavity was restored with composite resin (Filtek Z350 XT, 3M ESPE, St. Paul, MN, USA) and a postoperative radiograph was taken. The tooth was asymptomatic and the periapical lesion resolved over the subsequent six months (). | [[12.0, 'year']] | M | {'22050710': 1, '4500261': 1, '10530214': 1, '11210263': 1, '13484205': 1, '28119787': 2, '17697108': 1, '7673821': 1, '25469361': 2, '23633825': 2, '9257019': 1, '22794206': 1, '25984479': 2, '11108527': 1, '15167464': 1, '30083218': 2, '13613719': 1, '24790927': 2, '25984480': 2, '9594762': 1, '6595621': 1, '24303362': 2} | {'3843038-1': 2, '3843038-3': 2, '4247845-1': 1, '4432260-1': 1, '3636845-1': 1, '3978104-1': 1, '5227125-1': 1, '4432261-1': 1, '6064016-1': 1} |
164,477 | 3843038-3 | 24,303,362 | noncomm/PMC003xxxxxx/PMC3843038.xml | Endodontic treatment of maxillary lateral incisors with anatomical variations | A 17-year-old male patient was referred for endodontic treatment of his upper left lateral incisor. Two years earlier, he had received root canal treatment for a severe pain in the same region. He reported swelling, pain and discharge of pus at the mucosal area in the lateral incisor for one week. His medical history was noncontributory. An intraoral examination revealed a sinus tract on the labial gingiva associated with the lateral incisor. The tooth was sensitive to percussion and palpation. A periapical radiograph demonstrated a diffuse radiolucency at the apex of the lateral incisor (). The pulp diagnosis was previous endodontic treatment, and the periapical diagnosis was periapical abscess with sinus.\nAn access opening was made after removal of the prosthesis and rubber dam isolation. Old gutta-percha was removed from the first and second canals with a size 25 stainless steel H-file (Mani). The canals were irrigated with 5% sodium hypochlorite. At the following visit, the third canal running into the second canal was negotiated under the operating microscope (). To ascertain the location of the fourth canal, a cone-beam computerized tomography (CBCT, Mercuray, Hitachi, Tokyo, Japan) was taken. The fourth canal was negotiated by cutting the overlying dentin of the expected site with a pointed tip of an ultrasonic device under the microscope, considering the locations of the first and the second canals in CBCT axial section images (). The orifice of the fourth canal was located on the mesiopalatal side at the external wall of the prepared tooth (). All canals were cleaned and shaped using K-files with the step-back technique and copious irrigation with 5% sodium hypochlorite solution. The root canals were obturated by cold lateral compaction of gutta-percha using an epoxy resin sealer (AH Plus, ). The access cavity was restored with composite resin (Filtek Z350 XT) and a post-obturation radiograph was taken. The patient returned for review four months later at which time he remained symptomless. On inspection, neither swelling nor sinus tract was seen. The tooth was not tender to percussion or palpation (). | [[17.0, 'year']] | M | {'22050710': 1, '4500261': 1, '10530214': 1, '11210263': 1, '13484205': 1, '28119787': 2, '17697108': 1, '7673821': 1, '25469361': 2, '23633825': 2, '9257019': 1, '22794206': 1, '25984479': 2, '11108527': 1, '15167464': 1, '30083218': 2, '13613719': 1, '24790927': 2, '25984480': 2, '9594762': 1, '6595621': 1, '24303362': 2} | {'3843038-1': 2, '3843038-2': 2, '4247845-1': 1, '4432260-1': 1, '3636845-1': 1, '3978104-1': 1, '5227125-1': 1, '4432261-1': 1, '6064016-1': 1} |
164,478 | 3843039-1 | 24,303,363 | noncomm/PMC003xxxxxx/PMC3843039.xml | Conservative approach of a symptomatic carious immature permanent tooth using a tricalcium silicate cement (Biodentine): a case report | A 12 year-old girl presented at the emergency dental clinic, Hospices Civils de Lyon, Lyon, France, for an acute, spontaneous and lasting referred pain in the right posterior mandibular quadrant. Clinical and radiographic examinations revealed extensive occlusal caries invading the pulp on the second right lower premolar, an immature permanent tooth with incomplete root formation (). The diagnosis was acute pulpitis (#45).\nAfter taking the informed consent of her parents due to the young age of the patient, a conservative pulpal treatment option was adopted in order to allow for further root formation and to preserve the growing potential of the root and the healing potential of the pulp. Accordingly, #45 was anesthetized by a peri-apical injection with 1.5 mL of a 2% articaine and 1/200,000 epinephrine solution (Primacaine Adrenaline 1/200,000, Acteon Pierre Rolland, Merignac, France) and isolated under rubber-dam.\nFollowing caries removal, a partial pulpotomy was performed using a round low-speed carbide bur (H1.204.021, Komet France, Paris, France) under constant irrigation until a normal bleeding was obtained (). The hemostasis was obtained by irrigation with saline solution and application of sterile cotton pellets. Biodentine was processed according to the manufacturer's instruction by mixing a single-unit powder part (tricalcium silicate-dicalcium silicate-zircon dioxide) and 5 drops of a single-unit liquid part (calcium chloride-distilled water) for 30 seconds (). displays the immediate post treatment X-ray which shows the pulp capping material located at the roof of the pulp chamber. Direct pulp capping was performed with a 2 mm-thickness layer of the tricalcium silicate cement (Biodentine). The tooth #45 was restored with conventional glass ionomer cement (Fuji IX extra, GC Corp., Tokyo, Japan) and checked for centric occlusion. At a postoperative phone call the following day, the patient reported complete cessation of the painful episode within 12 hours after completion of the treatment. At seven day follow-up, a clinical examination found responses to thermal pulpal tests within normal limits for a non-inflammatory pulp (hot and cold were discriminated and the response did not exceed the stimulus duration). At a three months recall, a clinical examination showed a normal pulpal sensitivity. There were no clinical or radiographic signs of root resorption or apical periodontitis. A radiograph showed morpho-differentiation of a dentin bridge immediately under the tricalcium silicate cement. (). Root formation had occurred and a thickening of the root dentin walls was noted. At 6 month recall, the bevel-shaped ends of the dentin at 3 months appeared to change to thicker round-shaped root-dentin walls. | [[12.0, 'year']] | F | {'17036703': 1, '12657149': 1, '29234957': 1, '22188368': 1, '24790925': 2, '16764130': 1, '20113774': 1, '20171353': 1, '25110649': 2, '19549154': 1, '16739540': 1, '29372451': 1, '17956562': 1, '26097752': 2, '28969295': 1, '21895969': 1, '18155482': 1, '22983409': 1, '21535021': 1, '16948659': 1, '21600643': 1, '20728209': 1, '19134040': 1, '21353694': 1, '23429542': 1, '20003930': 1, '22411260': 1, '29059236': 1, '25025034': 1, '17180780': 1, '22431145': 1, '22436906': 1, '25657533': 2, '33884264': 1, '27471534': 1, '21777256': 1, '19335509': 1, '18615987': 1, '17586038': 1, '22251035': 1, '24303363': 2} | {'4313486-1': 1, '4313486-2': 1, '4313486-3': 1, '4313486-4': 1, '4449924-1': 1, '4125589-1': 1, '3978102-1': 1} |
164,479 | 3843323-1 | 24,347,845 | noncomm/PMC003xxxxxx/PMC3843323.xml | MRI brain in monohalomethane toxic encephalopathy: A case report | A 29-year-old female, working in a pharmaceutical company, presented with sudden-onset diplopia, slurred speech, imbalance while walking, and behavioral changes which had developed over a period of 2-3 days. She reported to have headache for 2 weeks. On examination, she had cerebellar signs, bilateral extensor plantar reflexes, and bilateral VI nerve palsy. After ruling out other possibilities clinically, the clinician raised the possibility of probable toxic encephalopathy. A detailed personal and occupational history was obtained. Occupational history revealed that the pharmaceutical company used MI as a chemical intermediate. There was increase in its production in last 2 months probably leading her to sudden exposure of excessive amounts of MI before she presented. In view of the rapid onset of neuropsychiatric symptoms, acute MI toxic encephalopathy was suspected and MRI brain was advised.\nMRI brain was done at our center. T2-weighted and fluid-attenuated inversion recovery (FLAIR) images revealed bilateral symmetrical hyperintense signal in peri-third ventricular thalami [], peri-aqueductal region [], dorsal pons in the region of superior colliculus [], medial leminiscus and abducens nuclei [], and dorsal medulla and inferior olivary nuclei []. Bilateral symmetrical hyperintense signal was also noted in dentate nuclei []. Dentate nuclei lesions had target appearance; they were extremely bright in the center on T2-weighted images and were surrounded by a rim of ill-defined mild hyperintensity.\nAll these lesions were hypointense on T1-weighted images []. No restriction of diffusion was noted on diffusion-weighted images (DWI) []. Mild cortical and cerebellar atrophy was evident. However, the basal ganglia appeared normal. No evidence of altered signal was noted in the corpus callosum. No contrast was administered and MR spectroscopy was not performed.\nBased on the clinical profile, possibility of MI toxic encephalopathy was considered and other differentials with similar MRI features were excluded. Patient was advised follow-up MRI after avoiding exposure to MI.\nRepeat MRI brain was done after 4 months which showed complete resolution of the above-mentioned findings [], confirming the diagnosis. | [[29.0, 'year']] | F | {'16219836': 1, '21329723': 1, '1488088': 1, '15898088': 1, '10588115': 1, '11498799': 1, '11808354': 1, '20550674': 2, '15824365': 1, '18575299': 1, '17885234': 1, '8914723': 1, '1119768': 1, '24347845': 2} | {'2902496-1': 1} |
164,480 | 3843324-1 | 24,347,846 | noncomm/PMC003xxxxxx/PMC3843324.xml | Call-Fleming syndrome | A 30-year-old Indian male presented with acute onset of orbito-frontal throbbing headache, which the patient described as the worst pain in his life. There was no photophobia or nausea associated. The pain was not relieved with positional change or on taking medications (acetaminophen). He had no similar history prior to this. On examination, his vitals were found to be stable. He did not have any neurological deficits.\nMagnetic resonance imaging (MRI) brain was done which demonstrated hyperintensity involving right precentral and superior frontal sulci on the fluid-attenuated inversion recovery (FLAIR) axial sequence []. Rest of the cisterns and sylvian fissures were normal. There were no altered parenchymal intensities, areas of restricted diffusion, or parenchymal hemorrhage.\nFurther, a magnetic resonance angiogram (MRA) was done which showed multiple areas of vasospasm involving the supraclinoid segment of internal carotid artery (ICA), M1 segment of middle cerebral artery, A1 segment of anterior cerebral artery on the right side [], and the A1 segment of anterior cerebral artery on the left side. These findings were reconfirmed with cerebral angiogram under digital subtraction angiography (DSA) [Figures and ].\nThe laboratory investigations including CSF analysis were found to be inconclusive. Based on the imaging findings, a provisional diagnosis of RCVS was put forth and the patient was put on Nimodipine 30 mg, 3 times daily. The follow-up MRI which was taken 8 weeks later showed complete resolution of the above-mentioned findings []. This confirmed the diagnosis of RCVS.\nOn a detailed history taking and evaluation, the patient was found to have no other co-morbidities and was not on any medications. Hence, the final diagnosis of Call–Fleming syndrome was made. | [[30.0, 'year']] | M | {'17200220': 1, '18077478': 1, '22074635': 2, '3418381': 1, '21140058': 1, '20884866': 1, '21675454': 1, '24347846': 2} | {'3260136-1': 1} |
164,481 | 3843325-1 | 24,347,847 | noncomm/PMC003xxxxxx/PMC3843325.xml | Cavernous hemangioma located at the foramen of Monro: Radiopathological correlation | A 29 year-old female patient presented with non-throbbing intermittent headache for a month before admission. The pain aggravated in the last 2 days. The patient also complained of projectile vomiting in the last 2 days. There was no history of fever, seizures, associated memory disturbance, or altered consciousness. On physical examination, no neurological deficit was found. Magnetic resonance image (MRI) brain revealed a relatively well-delineated lobulated lesion in the anterosuperior aspect of the third ventricular roof, centered in the region of foramen of Monro. On T1-weighted images (T1WI), the lesion was isointense with few small hyperintense hemorrhagic foci within [], and on T2-weighted images (T2WI), the lesion appeared heterogeneous with a peripheral rim of marked hypointensity []. Cystic areas and fluid-fluid levels were seen within the lesion. The lesion showed mild heterogeneous enhancement on post-contrast imaging []. Susceptibility-weighted images revealed marked blooming confirming the hemorrhagic nature of the lesion []. The lesion was causing mass effect in the form of moderate dilatation of bilateral lateral ventricles with periventricular T2W hyperintensities suggesting obstructive hydrocephalus with transependymal ooze. An incidental note was also made of a tubular vascular enhancing structure with branching pattern in the left cerebellum representing developmental venous anomaly [].\nEndoscopic transventricular excision of the vascular malformation and septostomy of septum pellucidum was done. Intraoperatively, the mass was seen to be located in the third ventricle, causing obstruction at the foramen of Monro, and showed xanthochromic appearance. Complete excision of the lesion was done and histological examination revealed mulberry-like cluster of dilated thin-walled capillaries without any intervening neural tissue and surrounding hemosiderin, suggesting cavernous hemangioma []. | [[29.0, 'year']] | F | {'23091674': 2, '15808709': 1, '10069603': 1, '15916846': 1, '27812456': 2, '29199381': 1, '24347847': 2} | {'5073084-1': 1, '3467373-1': 1} |
164,482 | 3843326-1 | 24,347,848 | noncomm/PMC003xxxxxx/PMC3843326.xml | Herniation of spinal cord into nerve root avulsion pseudomeningocele: A rare cause of delayed progressive neurological deficit | A 40-year-old male patient presented with history of progressive weakness of the right lower limb. Four years back, he had sustained injuries in a road traffic accident and was admitted with head trauma. He had profound weakness of the right upper limb. Clinically, brachial plexus injury was suspected and nerve conduction studies suggested involvement of right C5–D 1 nerve roots. Patient recovered from his head injuries and was left with residual right monoplegia. Four years later, the patient developed progressive weakness of the right lower limb and started walking with a limp. On examination, there was wasting and weakness of the right upper limb muscles. Mild wasting of the right thigh and calf muscles was noted. The power in the right hip and knee flexors was Grade 4/5 Medical Research Council (MRC). The power in dorsiflexor and plantarflexors of ankle was Grade 4/5 MRC. The right knee and ankle jerks were exaggerated and right plantar reflex was extensor. There was no sensory loss in either lower limbs or left upper limb. Clinically, myelopathy was suspected and MRI of the cervical spine was suggested. MRI of the patient was done on Magnetom Avanto 1.5 T MRI (Siemens, Erlangen, Germany). Axial, sagittal, and coronal T1- and T2-weighted images of the cervical spine were acquired, which revealed the presence of lateral pseudomeningoceles at C7–D1and D1–D2 levels []. Dedicated 3-D SPACE sequence and oblique coronal inversion recovery sequence of the right brachial plexus were also acquired. There was lateral herniation of a knuckle of cord into the pseudomeningocele at D1–D2 neural foramen [Figures and ]. Reconstruction of data set in any specified plane and superior spatial resolution of the 3-D sequence resulted in better appreciation of dura, dural defect, and the cord herniation.\nDue to progressive neurological deficit, a decision to treat the patient surgically was made. Through a posterior approach, laminectomies were performed at D1 and D2 levels. Herniation of the cord was seen into the pseudomeningocele through a dural defect. The herniated cord was reduced and the dural defect repaired. After surgery, there was slight improvement in the right lower limb power. | [[40.0, 'year']] | M | {'9726479': 1, '32181298': 1, '3113210': 1, '9156027': 1, '19350043': 1, '4730343': 1, '624977': 1, '7815118': 1, '17228230': 1, '14563149': 1, '25422647': 1, '18349454': 1, '17987326': 1, '24347848': 2} | {} |
164,483 | 3843327-1 | 24,347,849 | noncomm/PMC003xxxxxx/PMC3843327.xml | Pseudoaneurysm of internal carotid artery after carotid body tumor excision | A 35-year-old male patient presented with swelling in the left side of the neck. USG and magnetic resonance imaging (MRI) revealed a well-marginated mass lesion measuring 3.8 cm × 2.8 cm at the left carotid bifurcation [] splaying the proximal internal and external carotid arteries, with circumferential area of contact with ICA of 180°-270°, consistent with the imaging diagnosis of Shamblin stage 2 CBT. Subadventitial excision of CBT was done after retraction of the carotids. No special technique was used to visualize the tumor and the excision was simple. Proximal and distal control of the internal, external, and common carotid arteries was done over vascular loops and the vessel loops were used to retract the external and internal carotid artery bifurcation. There were no arterial or nerve injuries. No preoperative embolization was planned. The postoperative course was uneventful and the patient was given intraoperative heparin based on body weight. No neurological deficits were observed at recovery or in the immediate postoperative period. The patient developed right-sided dense hemiplegia on the morning of the first postoperative day, with a score of 29/48 according to the Scandinavian Stroke scale.[] Plain computed tomography (CT) of the brain [] revealed a recent infarct involving the left capsuloganglionic region and corona radiata (middle cerebral artery territory). Color Doppler of the carotid arteries [] revealed partial thrombosis of the left ICA with approximately 50% reduction in vessel lumen and hypoechoic hematoma around the proximal ICA, consistent with a diagnosis of postoperative dissection. Patient was managed conservatively with low molecular weight (LMW) heparin. In view of ICA thrombus, oral warfarin was started and LMW heparin was stopped after 5 days. Two weeks later, a follow-up carotid Doppler study [] showed a pseudoaneurysm measuring 2.3 cm × 1.5 cm in the medial aspect of proximal left ICA with a central patent lumen of size 10 mm × 8 mm and a mural thrombus around it. Neck of the pseudoaneurysm measured 2 mm. ICA thrombus had significantly resolved with good distal flow. Carotid angiography done on the 17th postoperative day [] showed a pseudoaneurysm measuring 2.3 cm × 1.8 cm, medial to the proximal left ICA filling through a small neck of 2 mm []. Intimal irregularity was noted in the lateral wall of the left ICA, suggesting arterial injury/dissection. The neck of the pseudoaneurysm was very narrow, so a 0.018-inch guide wire could not be negotiated and attempts to close the pseudoaneurysm were not successful. Microcatheters and stent grafts were not available in our hospital, as it was a primitive hospital set-up. Non-invasive methods were avoided in this patient because he developed stroke on the first postoperative day, mandating anticoagulation. In view of the ICA pseudoaneurysm and no significant intraluminal thrombus in ICA on angiogram, he was started on oral antiplatelets (aspirin) on the 18th postoperative day and oral anticoagulant was stopped after 2 days. But the pseudoaneurysm had spontaneously thrombosed with no demonstrable flow into the aneurysm in follow-up Doppler done after a week of stopping anticoagulants. There was minimal hypoechoic intimal thickening and irregularity of the proximal ICA with no significant lumen narrowing, thrombus, or false lumen. The patient was continued on oral antiplatelets for 6 months, and is on regular follow-up for 5 years. His neurological weakness has improved significantly with regular physiotherapy. | [[35.0, 'year']] | M | {'20732785': 1, '10954281': 1, '26862461': 2, '7563403': 1, '15897427': 1, '3901425': 1, '33425309': 1, '9418195': 1, '26029351': 1, '18417602': 1, '22953119': 2, '11574979': 1, '24347849': 2} | {'3420369-1': 1, '3420369-2': 1, '4722514-1': 1} |
164,484 | 3843329-1 | 24,347,851 | noncomm/PMC003xxxxxx/PMC3843329.xml | Role of dual-energy contrast-enhanced digital mammography as a problem-solving tool in dense breasts: A case report | A 55 year-old lady who complained of occasional heaviness in the left chest was referred to us from cardiac OPD. As she required no active cardiologic intervention, a screening mammogram was undertaken as a part of routine health check-up. There was no family history of any breast or gynecological malignancy and no prior breast imaging had been undertaken. Digital mammograms in both craniocaudal [] and mediolateral [] views were taken on a GE Senographe Essential and viewed on an IDI work station. Both breasts were extremely dense (>90%) with no definite area of mass lesion being noted. Few prominent left axillary lymph nodes were noted. Benign scattered calcifications were noted bilaterally with no evidence of microcalcifications. Clinically, both breasts had an irregular lumpy feel on palpation. On USG, a suspicious hypoechoic area was noted within the dense glandular tissue of left breast with evidence of intralesional vascularity. Two enlarged left axillary nodes were noted measuring 2.5-2.7 cm each, with preserved hilar architecture. Screening of right breast appeared unremarkable. In view of dense mammogram and suspicious USG findings, the patient underwent a dual-energy CEDM. Baseline renal function of the patient was evaluated prior to contrast injection. Institutional review board approval and informed patient consent was obtained. Approximately 70 ml (at 1.5 ml/kg) of non-ionic contrast medium (Iomeron 350 mg/ml) was loaded into a Liebel-Flarsheim pressure injector. The rate was set at 3 ml/sec. The right (contralateral) antecubital vein was punctured and connected to the injector. A stopwatch on the console set at 0 sec was started simultaneously with initiation of contrast injection. The radiographer had a time gap of approximately 90 sec after cessation of contrast injection for positioning the patient for the right craniocaudal (RCC) view. This was taken at the 2nd minute. The left craniocaudal (LCC), right mediolateral (RMLO) and left mediolateral (LMLO) views were taken at 3rd, 4th, and 5th minute since start of the contrast, respectively. All images were acquired well within the 7-min cut-off as recommended by the manufacturer and as noted in various clinical studies.[] Approximately 10 daN compression was applied for each exposure. All views were obtained using dual energy where the low-energy exposure was acquired using a Mo/Rh target/filter combination with tube voltages (kVp) ranging from 26 to 30 kVp. The high-energy images were acquired using Mo/Cu target/filter combination and with tube voltages in the range of 45-49 kVp. Within approximately 5 sec, a recombination algorithm, using the low-energy, high-energy X-ray spectra and the thickness of compressed breast produced dual-energy subtracted images which highlighted the iodine-enhanced areas. A small enhancing nodule was noted in the right breast centrally while a mass-like enhancement was noted in left breast lower inner quadrant in the respective CC views []. While the right breast lesion was no longer visualized, the left lesion was only subtly imaged in the respective MLO views, suggesting a probable rapid washout []. The enhancing left breast mass corresponded to the suspicious area noted on USG, while the focal nodular enhancement on the right corresponded to an isoechoic lesion which was completely missed on the initial scan. Both lesions were biopsied under ultrasound guidance in the same sitting. Histopathological evaluation revealed the right breast nodule to be a grade 1 and the left breast mass to be a grade 3 invasive ductal carcinoma. The patient preferred to pursue metastatic work-up and further treatment at her hometown. | [[55.0, 'year']] | F | {'12888621': 1, '7563205': 1, '15973130': 1, '33252334': 1, '20839001': 1, '7752271': 1, '18086762': 1, '22697607': 1, '18024435': 1, '12881585': 1, '17056886': 1, '20929881': 1, '16775176': 1, '23220903': 1, '14695385': 1, '24347851': 2} | {} |
164,485 | 3843331-1 | 24,347,853 | noncomm/PMC003xxxxxx/PMC3843331.xml | CT imaging findings and endovascular management of isolated spontaneous dissecting aneurysm of celiac artery | A 45-year-old man presented to our emergency department with sudden onset of sharp epigastric pain. He gave history of hospital admission elsewhere, 6 months back for similar complaint. Upper gastrointestinal (GI) endoscopy performed at that time revealed peptic ulcer, and since then, he had been on antacids. His medical history was also remarkable except for uncontrolled hypertension. At presentation, his blood pressure was 180/100 mm Hg. Routine blood tests and basic metabolic profile including liver, cardiac enzymes, and serum amylase/lipase levels were normal. Emergency ultrasound performed on him did not reveal any significant abnormality. So, a biphasic contrast-enhanced CT of the abdomen was performed on a GE Light Speed Discovery 750 HD, 64-slice scanner, using oral contrast and 80 ml of non-ionic iodinated contrast material 350 mg I/ml, injected at the rate of 3 ml/s. Arterial phase images of the upper abdomen were obtained using smart prep technique followed by portal venous phase acquisition of whole abdomen at 50 s from the start of contrast injection.\nThe CT study revealed celiac artery aneurysm of 1.4 cm, approximately 0.8 cm from its origin with focal dissection as evidenced by true lumen and thrombosed false lumen. The caliber of the true lumen was severely compromised [Figures and ]. Distal propagation of the dissection and mural thrombus into the ostia-proximal hepatic and splenic arteries was seen which were occluded. The left gastric artery was originating from the celiac axis, proximal to the dissecting aneurysm and was normal. Replaced left hepatic artery from left gastric artery was seen as a normal variant. Fat infiltration was seen surrounding the celiac axis and proximal hepatic and splenic arteries []. This finding is a sign of dissection acuity and indicates predisposition toward progressive extension of dissection into adjacent vessels. The abdominal aorta and its other major branches were normal with no stenosis or aneurysm or dissection. There was no evidence of organ or bowel infarction. Subsequent Digital subtraction angiogram performed with therapeutic intent confirmed the CT findings []. Also, superior mesenteric artery injection showed retrograde filling of the hepatic and splenic arteries via the anterior, posterior pancreaticoduodenal arcades and the gastroduodenal artery [].\nSevere abdominal pain present in spite of good collateral flow indicates dissection to be the cause of pain, rather than intestinal ischemia. Also, in view of peri-celiac fat infiltration on CT and the complicating aneurysm with inherent potential risk of rupture, it was decided to treat him either with endovascular stent grafting or coil embolization. Stent grafting can be done if there is good landing zone of 2 cm on either side of the aneurysm. In our case, stent graft would have compromised the flow through the left gastric artery originating just proximal to the aneurysm. Also, in view of the good collateral flow to the hepatic and splenic arteries from superior mesenteric artery, it was decided to occlude the aneurysm distal to left gastric origin to prevent rebleed. Transarterial embolization was performed and the aneurysm was packed with detachable micro coils (Covidien, Ireland). Post coil embolization angiogram [] showed that the parent artery was obliterated except for its proximal portion with left gastric origin and that the intrahepatic branches were supplied through collateral pathways and the replaced left hepatic artery. His initial pain subsided gradually, and he was symptom free during discharge. | [[45.0, 'year']] | M | {'19540708': 1, '27489674': 1, '25049002': 1, '30344811': 2, '15387350': 1, '11769152': 1, '33781323': 1, '22091295': 2, '7572520': 1, '18502087': 1, '19909685': 1, '21764241': 1, '23466182': 1, '22470724': 1, '17515339': 1, '23255765': 1, '22096724': 1, '23109773': 1, '15235239': 2, '10917586': 1, '24347853': 2} | {'2698142-1': 1, '2698142-2': 1, '6188032-1': 1, '3214384-1': 1} |
164,486 | 3843332-1 | 24,347,854 | noncomm/PMC003xxxxxx/PMC3843332.xml | Extrahepatic biliary atresia with choledochal cyst: Prenatal MRI predicted and post natally confirmed: A case report | A 25-year-old primigravida presented to our hospital at 22nd week of gestation for target scan Targetted imaging for fetal anomalies (TIFFA). Fetal biometric parameters were normal. Liquor was adequate. Anatomical survey revealed a longitudinally oval, avascular anechoic cyst measuring 14 × 9 mm in the right upper abdomen, separate from duodenum, showing continuity with hepatic hilum superiorly without identifiable gall bladder (GB). No other abnormalities were detected. Presumptive diagnosis of CDC was made.\nFetal MRI was performed 2 weeks later on 1.5T Essenza (Siemens, Erlangen, Germany) to investigate the correct anatomical location of the cyst and its relationship with adjacent organs to assist with prognostication and treatment planning for the perinatal period.\nT2-weighted Half-Fourier acquisition single-shot turbo spin-echo (HASTE, TR/TE 900/86 ms, 4-mm slice thickness) sequences were obtained in the axial, coronal, and sagittal planes with respect to the fetus. Sequences were monitored in real time and manipulated to determine optimal imaging planes during the scan, as fetal orientation is unpredictable and often changes during acquisitions. In addition to the standard orthogonal planes, oblique planes were acquired for demonstrating the relationship to surrounding structures.\nMRI showed a 14 × 9 mm ellipsoid [] homogenous cystic lesion at liver hilum hyperintense on T2W images. Axial images revealed the cyst posterior to the duodenum []. The cyst was longitudinally oval, coursing posteroinferiorly from hepatic hilum appreciated on sagittal images []. Intrahepatic ducts were not dilated; CBD was not visualized. Coronal images revealed hyperintense cord-like structure above the cyst, showing communication with it []. The normal morphology of fetal GB was not visualized in the inferior surface of liver in right upper quadrant. The spleen was normal. Inferior vena cava (IVC) showed normal course. Liver showed normal signal intensity and contour.\nThe imaging characteristics on USG and MRI are presented in .\nFollow-up using serial USG scans in pregnancy revealed static size of the cyst with persistent ghost GB. Interval growth was normal till term.\nA female infant weighing 2.9 kg was delivered by cesarean section at 39 weeks.\nPostnatal USG, on day 3 after a 4-h fast, revealed liver extending beyond subcostal margin; echotexture was homogenous with normal surface contour. Intrahepatic ducts were not dilated. There was an echogenic area anterior to the portal vein at porta and measured 3.2 mm []. A well-defined, longitudinally oval anechoic cyst was present at the hilum ~14 × 9 mm. The cyst size, echogenicity, and morphology were the same as seen in prenatal imaging []. Maximum width and length of GB was 11 × 2 mm, with irregular, compressed lumen s/o ghost GB []. Hepatic artery was prominent, running parallel to the right portal vein, and measured 1.7 mm. Main portal vein (MPV) diameter was obtained at the same level, which measured 3 mm. The ratio of HA/MPV diameter was >0.5 (>0.45 increase) []. Hepatic subcapsular flow appeared subjectively increased. Spleen measured 3.8 cm. No varices were present. No free fluid was noted.\nThe imaging characteristics at porta are presented in .\nLiver function tests (LFT) revealed increased γ-glutamyl transferase (831 U/L), elevated alkaline phosphatase (698 U/L), conjugated hyperbilirubinemia (2.8 mg/dL), and normal serum glutamate pyruvate transaminase (SGPT) 10 U/L, serum glutamate oxaloacetate transaminase (SGOT) 29 U/L, albumin, and International Normalised Ratio [(INR). Hepatobiliary scintigraphy was performed on day 24 which showed prompt and good uptake by the liver and absent tracer excretion into the intestines in 24-h delayed images. GB and extrahepatic ducts were not visualized [].\nA diagnosis of extrahepatic cystic biliary atresia (CBA) was made based on imaging.\nThe child was explored with on day 31. Operative findings included firm brownish liver, fibrotic porta inclusive of non-visualized right/left hepatic duct, common hepatic duct, and proximal CBD []. GB was small and did not have a lumen. A cystic structure was seen at the site of terminal part of CBD. The cyst was going behind the duodenum and ending blindly. No communication was seen with the pancreatic duct. Corresponding schematic representation is shown in and was classified as type 3 BA according to Japanese classification system.\nExcision of fibrotic hilar structures including cyst en masse with a Kasai's portoenterostomy was performed with ~30 cm of Roux-en-Y jejunal loop. Histopathologic examination confirmed the diagnosis of BA. Bilirubin returned to 1 mg by the 11th postoperative day. The child is aged 2 months now and doing well. | [[25.0, 'year']] | F | {'10796915': 1, '33201318': 1, '11666059': 1, '9574750': 1, '16124073': 1, '11702847': 1, '22644679': 1, '21482505': 1, '18955804': 1, '16979949': 1, '12149700': 1, '24347854': 2} | {} |
164,487 | 3843333-1 | 24,347,855 | noncomm/PMC003xxxxxx/PMC3843333.xml | Herlyn–Werner–Wunderlich syndrome presenting with infertility: Role of MRI in diagnosis | A 22-year-old female, cohabiting with her husband for last 3 years, was evaluated for primary infertility in a private hospital. She attained menarche at the age of 13 years and had a normal menstrual history with no complaints of excessive dysmenorrhoea, dyspareunia, or vaginal discharge. Routine hematological laboratory tests were normal. An abdominal USG and computed tomography (CT) were performed, which revealed absent left kidney, a bicornuate uterus, bilateral cystic adnexal lesions, and left hydrosalpinx. She was taken up for laparotomy and underwent left ovarian cystectomy and adhesiolysis. Histopathology from the left adnexal lesion showed endometriotic cysts and aspirated pelvic fluid showed hemosiderin-laden macrophages. Postoperatively, she was kept on medical management for endometriosis.\nShe did not resume her menses for 3 months post-surgery and urine pregnancy test was negative, following which she was referred to our institute for further evaluation. MRI examination of the pelvis was performed to assess the current status of endometriosis. MRI revealed two separate uterine cavities, cervices, and vaginas, suggestive of uterus didelphys [Figures -]. The right uterine cavity, cervix, and vagina were normal. The left uterine cavity and cervical canal were dilated and filled with fluid which was hyperintense on both T1W and T2W MRI [Figures and ] with few T2-hypointense areas [] suggesting blood products. Left hemivagina was dilated [Figures , , and ] with blood products within, implicating the presence of an obstructing left vaginal septum. Multiloculated left adnexal cystic lesions with blood products were seen suggestive of endometriotic cysts []. In addition, a tubular structure was noted in left adnexal location extending laterally from left uterine cornu with hemorrhagic fluid within, indicative of left hematosalpinx. Right ovary was normal. In addition, there was absent left kidney [] with loculated hemorrhagic fluid collections in bilateral paracolic gutters, suggestive of peritoneal endometriosis [].\nHence, a diagnosis of uterus didelphys with left hematometra, hematosalpinx, hematocolpos, and left hemivaginal obstruction with adnexal and peritoneal endometriosis was made. Considering that she also had absent left kidney, a final diagnosis of HWWS or obstructed hemivagina ipsilateral renal anomaly (OHVIRA) syndrome was made. Since the patient had already undergone recent laparotomy, no further surgery was immediately performed. She has been kept on short-term conservative management with oral contraceptives to suppress menstruation and laparoscopic vaginal septal excision has been planned after 3 months. | [[22.0, 'year']] | F | {'30285830': 2, '9663283': 1, '10869793': 1, '9207807': 1, '31523565': 2, '22470758': 1, '31391743': 1, '22405336': 2, '22421561': 1, '16418966': 1, '456629': 1, '22348499': 1, '9798876': 1, '27857474': 1, '10438409': 1, '30319221': 1, '28191231': 1, '18625502': 1, '16677898': 1, '32269958': 2, '24347855': 2} | {'3314562-1': 1, '3314562-2': 1, '3314562-3': 1, '7137359-1': 1, '6171225-1': 1, '6741396-1': 1} |
164,488 | 3843336-1 | 24,347,858 | noncomm/PMC003xxxxxx/PMC3843336.xml | Rare complications of cesarean scar | A 38-year-old gravida 3, para 2 with history of in vitro fertilization and a positive pregnancy test was admitted with vaginal spotting. The patient had undergone cesarean delivery 5 years ago. TAS revealed anteverted uterus with a 38-mm gestational sac, 5-mm yolk sac, and a live embryo with crown–rump length 13.3 mm corresponding to 7 weeks and 6 days in the lower uterine cavity at the scar site. TVS showed an empty endometrial cavity and endocervical canal. The gestational sac was implanted in the anterior myometrium with myometrial thinning (maximum thickness 5.2 mm) between the gestational sac and the urinary bladder [Figure and ]. The hypoechoic cesarean scar (CS) was visualized adjacent to the gestational sac. On Color Doppler USG, mild increased peritrophoblastic flow was seen around the sac. MRI confirmed the presence of a gestational sac in the lower uterine segment at the scar site, with very thin (4 mm) myometrium between the gestational sac and the urinary bladder. The endometrial cavity and endocervical canal were empty and were displaced by the gestational sac posteriorly []. However, no bladder invasion was seen. The medical termination was then performed with fetal intracardiac potassium chloride injection under USG guidance. | [[38.0, 'year']] | F | {'33370250': 1, '9806299': 1, '15572961': 1, '17624346': 1, '15027012': 1, '8591641': 1, '28050453': 1, '7714169': 1, '9754109': 1, '22567509': 2, '24347858': 2} | {'3843336-2': 2, '3335479-1': 1} |
164,489 | 3843336-2 | 24,347,858 | noncomm/PMC003xxxxxx/PMC3843336.xml | Rare complications of cesarean scar | A 32-year-old gravida 3, para 2 with a previous lower segment cesarean section (LSCS) 3 years back had an elective LSCS at 40 weeks. She had no existing medical or antenatal problems. LSCS was done. A healthy baby was delivered, but she had severe pain in the lower abdomen for next 4 days along with spotting. TAS showed 10.2 × 5.3 × 6.2 cm hypoechoic collection along the anterior aspect of uterus. However, limited evaluation was possible due to abdominal tenderness and pain on probe compression. TVS was performed and it showed a large heterogeneously hypoechoic collection anterior to the uterus, which was communicating with the endometrial cavity with myometrial defect in the region of the CS []. MRI was done to confirm CSD. MRI showed a 10.5 × 8 × 6.6 cm hematoma appearing as heterogeneously hyperintense on T1-weighted image (T1WI) and T2-weighted image (T2WI), anterior to uterus [Figure and ]. This hematoma was communicating with the endometrial cavity through a defect in the anterior wall of myometrium in the region of CS. Mild free fluid was seen in the peritoneal cavity [Figures and ]. The patient was started on antibiotics and managed conservatively. Under USG guidance, a 10-French pigtail catheter was inserted into the collection which yielded thick hemorrhagic blood. Regular flushing and reaspiration was done. The hematoma resolved and the patient's clinical condition improved with antibiotics. On follow-up after 6 months, there was almost complete resolution of the hematoma and the CS had healed. | [[32.0, 'year']] | F | {'33370250': 1, '9806299': 1, '15572961': 1, '17624346': 1, '15027012': 1, '8591641': 1, '28050453': 1, '7714169': 1, '9754109': 1, '22567509': 2, '24347858': 2} | {'3843336-1': 2, '3335479-1': 1} |
164,490 | 3843337-1 | 24,347,859 | noncomm/PMC003xxxxxx/PMC3843337.xml | Increased fetal endocardial echogenicity mimicking endocardial fibroelastosis following maternal organophosphorus poisoning and its complete regression in utero | A 23-year-old primigravida at 20 weeks of gestation was hospitalized, following suicidal attempt by ingestion of organophosphorus pesticide (carbofuran). She was treated with antidote, corticosteroid steroid, and supportive measures. Following recovery after 2 weeks, she was referred for a targeted scan for anomalies at 22 weeks of gestation.\nAll fetal routine biometric parameters were normal on routine scanning. Fetal echocardiography showed normal cardiac situs, size, and axis. Both ventricular and interventricular septal endocardial surfaces showed diffuse hyperechoic thickening []. The interventricular septum was pearly white []. This pearly white lining was extending along the crux and atrioventricular valves []. These changes were more involving the left ventricle and the mitral valve. The abnormally curved mitral leaflets had rolled tips []. There was mild degree incompetence of the mitral valve. The proximal outflow tracts, mainly up to the semilunar valves, were also brighter with normal crossing, dimensions, and flow []. The aortic and pulmonary artery valves showed no evidence of stenosis or incompetence. Pulsed Doppler study (cursor directed through the left ventricle along the junction of the anterior leaflet of the mitral valve and left ventricular outflow tract) showed E/A ratios of mitral and tricuspid valves below the 2.5th percentile (0.41 and 0.45, respectively) for this period of gestation.[] The E/A ratio of the atrioventricular valves is calculated by dividing the peak velocity of “E” wave (due to early diastolic filling of the ventricle) by the peak velocity of the “A” wave (due to late diastolic filling of the ventricle from atrial contraction).\nThe myocardial performance index (MPI), otherwise known as Tei index (TI), for the left ventricle was more (0.71)[] than the normal value expected at this gestational age (average value at this age is 6). There were no significant Doppler spectral changes of the inferior vena cava (such as reversal of A wave in the inferior vena cava or hepatic veins) or umbilical vein (biphasic rather than triphasic spectral pattern and umbilical venous pulsations) to suggest impending cardiac failure. The routine serum immunological studies for maternal viral infections were normal.\nReassessment at 26 weeks of gestation showed non-progressive echocardiographic abnormalities and mild mitral incompetence as before. The endocardial thickening and hyperechogenicity were persisting and the ventricular wall thickness was normal. Follow-up echocardiography at 36 weeks of gestation showed normal fetal cardiac chambers and outflow tracts. The endocardial thickening and hyperechogenicity had completely regressed by this time. The myocardial contractions and ventricular fractional shortening were normal. The atrioventricular valves showed no stenosis or incompetence now. The fetal growth parameters and biophysical score were normal. She delivered a normal male baby by term with normal echocardiographic features. | [[23.0, 'year']] | F | {'15846168': 1, '21046540': 1, '11118755': 1, '22759646': 1, '12528158': 1, '7788496': 1, '13031402': 1, '7990167': 1, '24347859': 2} | {} |
164,491 | 3843340-1 | 24,347,862 | noncomm/PMC003xxxxxx/PMC3843340.xml | Unilateral sternocostoclavicular hyperostosis in a patient with ankylosing spondylitis: A case report with color Doppler ultrasonogram findings | A 42-year-old male attended our Rheumatology outpatient clinic with a history of swelling and mild pain of right SCJ for about eight months. There was no history of trauma or fever. The patient had been diagnosed to have ankylosing spondylitis since ten years with predominantly axial involvement. Clinical examination revealed a warm, hard and tender swelling over right SCJ. No skin lesions such as acne or pustulosis palmaris et plantaris were observed. Ankylosing spondylitis disease activity was fairly controlled (Bath ankylosing spondylitis disease activity index: 2.5.[] Radiograph of sternoclavicular joint did not detect any abnormality. Ultrasonography (USG) and doppler examination revealed calcifications around the joint with periarticular hypervascularity [Figures and ]. Doppler spectral analysis revealed low-resistance flow []. All the features were compared with normal left SCJ. CT scan showed calcifications around the right sternoclavicular joint and adjacent right first rib []. A diagnosis of right SCCH was made from clinical and imaging features. The patient was treated with non-steroidal anti-inflammatory agent and advised rest, physiotherapy and follow-up. | [[42.0, 'year']] | M | {'1616334': 1, '118719': 1, '2789434': 1, '12610490': 1, '23206619': 1, '20191525': 1, '31647009': 2, '22870470': 1, '26110174': 1, '3940368': 1, '11317030': 1, '1471317': 1, '24347862': 2} | {'6806564-1': 1} |
164,492 | 3843640-1 | 24,379,674 | noncomm/PMC003xxxxxx/PMC3843640.xml | Adjunctive enteral phenobarbital for adult status epilepticus: a brief report | A 76-year-old man with history of diabetes and hypertension was admitted because of pneumonia and received ceftazidime and clindamycin. During admission, the patient developed acute right hemiparesis. An acute cerebellar infarction was found at the right cerebellar hemisphere, along the posterior cerebellar artery. He also developed hospital-acquired pneumonia from Acinetobacter baumannii. The patient was referred to the university hospital with Glasgow Coma Scale (GCS) score of E4VTM6 (E = eye opening; V = verbal response; M = motor response). One week later, he became comatose, had dilated pupils (4 mm, with reaction to light), with eye deviation to left side and horizontal nystagmus. The CT scan of the brain showed right cerebellar infarction with hemorrhagic transformation and also left cerebellar infarction. At day 60 of admission, he had alteration of consciousness related to hypoglycemia (plasma glucose 22 mg/dL). He also had generalized tonic-clonic seizures for 30 minutes and was treated with 50% glucose and four times with 10 mg IV diazepam. The seizures were persistent despite his plasma glucose returning to 128 mg/dL, and he did not respond to 750 mg of IV phenytoin (two doses) or 1,200 mg of IV sodium valproate. An EEG showed persistent generalized spikes, and waves were found in both cerebral hemispheres, compatible with CSE. He was successfully treated with 960 mg PB via NG tube feeding. The IV phenytoin and sodium valproate were discontinued. His maintenance therapy was 180 mg/day of PB enterally. He developed uncontrolled sepsis and a second episode of GTCSE 26 days later and was successfully treated with 960 mg PB via NG tube feeding again. Even though the seizures were controlled, the patient had cardiac arrest and 3 hours later died, from uncontrolled sepsis. | [[76.0, 'year']] | M | {'12823581': 1, '19943867': 1, '21987289': 1, '15329080': 1, '8531974': 1, '22528274': 1, '20050893': 1, '29922905': 1, '17784539': 1, '22326977': 1, '16376283': 1, '20564764': 1, '23205961': 1, '20724088': 1, '24379674': 2} | {'3843640-2': 2, '3843640-3': 2, '3843640-4': 2, '3843640-5': 2, '3843640-6': 2} |
164,493 | 3843640-2 | 24,379,674 | noncomm/PMC003xxxxxx/PMC3843640.xml | Adjunctive enteral phenobarbital for adult status epilepticus: a brief report | A 53-year-old male without prior comorbidity was admitted due to acute extensive anterior wall ST elevated myocardial infarction with cardiac arrest. He had three cardiac arrests with successful cardiopulmonary resuscitation (CPR) for 8, 2, and 2 minutes. The patient was comatose and developed acute kidney injury, hyperphosphatemia, mild hepatitis, and ventricular tachycardia after the CPR. He was given IV amiodarone and an intra-aortic balloon pump. The patient had a GTCSE from hypoxic ischemic encephalopathy. His SE was not controlled after treatment with IV diazepam (10 mg, four times) or IV sodium valproate (1,200 mg, twice). An EEG showed persistent epileptic discharge, which was found starting at the left temporal area and secondary to both cerebral hemispheres. The seizures were successfully controlled with 960 mg PB via NG tube feeding. The PB level was 32.51 μg/mL (10–40 μg/mL), and the free form of sodium valproate was 32.51 μg/mL (5–10 μg/mL) 48 hours later. He was free of seizures with the maintenance dose of PB of 180 mg per day and returned home completely recovered. | [[53.0, 'year']] | M | {'12823581': 1, '19943867': 1, '21987289': 1, '15329080': 1, '8531974': 1, '22528274': 1, '20050893': 1, '29922905': 1, '17784539': 1, '22326977': 1, '16376283': 1, '20564764': 1, '23205961': 1, '20724088': 1, '24379674': 2} | {'3843640-1': 2, '3843640-3': 2, '3843640-4': 2, '3843640-5': 2, '3843640-6': 2} |
164,494 | 3843640-3 | 24,379,674 | noncomm/PMC003xxxxxx/PMC3843640.xml | Adjunctive enteral phenobarbital for adult status epilepticus: a brief report | A 35-year-old, previously healthy male was admitted due to a history of headaches and alteration of consciousness for 4 days. His CSF revealed 6 cells/mm3 of red blood cells and white blood cells. An MRI brain scan was compatible with herpes encephalitis. The patient received 750 mg IV of acyclovir every 8 hours. During hospitalization, he had GTCSE and received endotracheal intubation, 1,200 mg sodium valproate, and 1,000 mg IV phenytoin. The seizures were uncontrolled, and an EEG showed persistent generalized sharp waves followed by slow waves, in both cerebral hemispheres. He was given 900 mg PB by NG tube, and the SE was partially controlled. The seizures were recurrent but successfully treated with reloading of 900 mg of PB, IV phenytoin, and IV propofol. The PB level was 255.55 μg/mL (10–40 μg/mL), the free sodium valproate level was 12.21 μg/mL (50–100 μg/mL), and the free phenytoin level was 0.75 μg/mL (10–20 μg/mL) at day 3 after admission. A follow-up MRI showed evidence of encephalitis at the left limbic system and insular lobe of the left temporal lobe, and diffuse meningitis with evidence of basal arachnoiditis. After 23 days of admission, the patient was still comatose and was referred to a community hospital as per request from his relatives. | [[35.0, 'year']] | M | {'12823581': 1, '19943867': 1, '21987289': 1, '15329080': 1, '8531974': 1, '22528274': 1, '20050893': 1, '29922905': 1, '17784539': 1, '22326977': 1, '16376283': 1, '20564764': 1, '23205961': 1, '20724088': 1, '24379674': 2} | {'3843640-1': 2, '3843640-2': 2, '3843640-4': 2, '3843640-5': 2, '3843640-6': 2} |
164,495 | 3843640-4 | 24,379,674 | noncomm/PMC003xxxxxx/PMC3843640.xml | Adjunctive enteral phenobarbital for adult status epilepticus: a brief report | A 57-year-old male patient with history of diffuse systemic sclerosis, hypothyroidism, and myositis was admitted with an acute fever with seizures for 1 day. A CT scan of the brain showed normal findings with no white blood cells in his CSF. He received piperacillin/tazobactam and 1,000 mg oral levetiracetam per day, and the seizures were controlled. During the admission, he had bronchial secretion obstruction with hypoxemia and severe metabolic acidosis, and cardiac arrest. After a successful CPR, he was comatose and developed GTCSE. An EEG showed persistent epileptic discharges in the right temporal area, compatible with SE. The seizures were uncontrolled after 5 mg IV midazolam and an IV fentanyl infusion, at 5 mL/hour. Finally, 900 mg PB, via NG tube feeding, was prescribed, with successful seizure control. He was given a maintenance dose of 180 mg PB. The PB level was 31.61 μg/mL (10–40 μg/mL) at 4 hours after PB administration. A repeat CT brain scan showed posterior reversible encephalopathy syndrome. The patient completely recovered. | [[57.0, 'year']] | M | {'12823581': 1, '19943867': 1, '21987289': 1, '15329080': 1, '8531974': 1, '22528274': 1, '20050893': 1, '29922905': 1, '17784539': 1, '22326977': 1, '16376283': 1, '20564764': 1, '23205961': 1, '20724088': 1, '24379674': 2} | {'3843640-1': 2, '3843640-2': 2, '3843640-3': 2, '3843640-5': 2, '3843640-6': 2} |
164,496 | 3843640-5 | 24,379,674 | noncomm/PMC003xxxxxx/PMC3843640.xml | Adjunctive enteral phenobarbital for adult status epilepticus: a brief report | A 27-year-old female with carcinoma of the tongue stage T2N1M0, who was post-wide excision and radiotherapy, was admitted because of pneumonia. On the second day of admission, the patient had cardiac arrest from upper airway obstruction, resulting in hypoxic ischemic encephalopathy. Four days later, the patient developed tonic downward nystagmus in both eyes. An EEG revealed persistent epileptic discharge in the right temporal lobe. The diagnosis of NCSE was made, but this was not successfully controlled by 10 mg IV diazepam or 1,200 mg of IV sodium valproate. The seizures were controlled after a loading of 900 mg PB via NG tube feeding. The PB level at 7 hours after PB administration was 43.98 μg/mL (10–40 μg/mL). She received 180 mg of PB as a maintenance dose. She developed seizures again at day 12 after admission and was treated with oral topiramate. Her final status was bedridden. | [[27.0, 'year']] | F | {'12823581': 1, '19943867': 1, '21987289': 1, '15329080': 1, '8531974': 1, '22528274': 1, '20050893': 1, '29922905': 1, '17784539': 1, '22326977': 1, '16376283': 1, '20564764': 1, '23205961': 1, '20724088': 1, '24379674': 2} | {'3843640-1': 2, '3843640-2': 2, '3843640-3': 2, '3843640-4': 2, '3843640-6': 2} |
164,497 | 3843640-6 | 24,379,674 | noncomm/PMC003xxxxxx/PMC3843640.xml | Adjunctive enteral phenobarbital for adult status epilepticus: a brief report | A female, aged 15 years, with systemic lupus erythematosus was admitted due to seizures and diagnosed with central nervous system (CNS) vasculitis. A CT scan of the brain was normal, and the CSF had a mild elevation of protein, at 50 mg/dL. She was given 1 gm of methyl prednisolone IV for 3 days. She also had urinary tract infection and an infected bedsore. Previously, her seizures were controlled by 300 mg of phenytoin orally. During the admission, she developed GTCSE, and her MRI of the brain showed venous infarction with hemorrhagic transformation. The SE was uncontrolled by the IV loading of 750 mg phenytoin, 100 mg of IV sodium valproate, and 300 mg of oral topiramate. An EEG showed persistent epileptiform discharges at both parietooccipital and parasagittal areas. She was intubated and treated successfully with a 720 mg PB NG tube feeding. The seizures were recurrent 22 hours later, whereupon a reloading of 720 mg of PB enterally was prescribed for eleven times, until the seizures were completely controlled both clinically and by EEG. The PB level was 86.48 μg/mL (10–40 μg/mL). The serological tests revealed positive anti-RO, anti-RNP, and lupus anticoagulant. She was finally diagnosed as having antiphospholipid syndrome and treated with enoxaparin and dexamethasone. The patient completely recovered. | [[15.0, 'year']] | F | {'12823581': 1, '19943867': 1, '21987289': 1, '15329080': 1, '8531974': 1, '22528274': 1, '20050893': 1, '29922905': 1, '17784539': 1, '22326977': 1, '16376283': 1, '20564764': 1, '23205961': 1, '20724088': 1, '24379674': 2} | {'3843640-1': 2, '3843640-2': 2, '3843640-3': 2, '3843640-4': 2, '3843640-5': 2} |
164,498 | 3843899-1 | 24,348,321 | noncomm/PMC003xxxxxx/PMC3843899.xml | Fusobacterium Liver Abscess | A 65-year-old man presented to the emergency department with fever, chills, nausea and abdominal pain. A week prior to this admission the patient had been worked up for hematuria, a computed tomography (CT) scan of the abdomen showing multiple rim-enhancing liver lesions. The differential diagnosis at that time included metastatic colon carcinoma, amebic abscess and bacterial abscess seeded from sigmoid diverticulitis. Five days prior to admission, the patient underwent colonoscopy with biopsies, which showed acute inflammation but no evidence of malignancy. On the day of admission, repeat CT scan showed interval increase in size of his rim-enhancing liver lesions (fig. ) as well as acute cecal diverticulitis, chronic pancreatitis and a large thrombus in the portal vein. Based on the interval increase in size of the liver lesions and the colonoscopy findings, an infectious etiology was favored and four drains were placed for presumed abscesses (confirmed with drainage of purulent fluid) and empiric treatment with ciprofloxacin and metronidazole was initiated. The patient was also started on heparin for his portal vein thrombosis 3 days after admission (transitioned to Lovenox twice daily 6 days after admission). On day four, the causative organism for the patient's abscesses remained unidentified and a liver biopsy was performed to re-evaluate for the possibility of neoplasia or an unusual organism.\nThe liver biopsy showed neutrophil-rich debris (fig. ), consistent with abscess, and liver parenchyma embedded in fibrous tissue and scattered mixed inflammation consistent with abscess wall; no peliosis or viropathic changes were appreciated. Immunohistochemical staining for CD34 and CD31 showed no evidence of a vascular neoplasm, and S100 was negative, arguing against a neural crest-derived tumor (not shown). No bacteria were identified on Gram stain (fig. ), and no fungal organisms were seen on periodic acid-Schiff diastase or Gomori methenamine-silver stains. Also, there were no mycobacterial organisms on an acid-fast bacilli-stained slide (not shown). Warthin-Starry (WS) stain, however, showed filamentous bacteria within the necrotic debris (fig. ) consistent with Fusobacterium infection []. A week after admission, detection of Fusobacterium sp. in cultures of the patient's hepatic abscess fluid confirmed the diagnosis of Fusobacterium liver abscess.\nIn the interval between the biopsy and identification of the causative organism, ciprofloxacin was empirically changed to ceftriaxone because of concern for Streptococcus milleri infection; the patient improved on the combination of ceftriaxone 1 g daily and metronidazole 500 mg three times daily, his drains were removed, and he was discharged 8 days after admission on antibiotics as described above. | [[65.0, 'year']] | M | {'21881280': 1, '30700472': 1, '12525925': 1, '28754755': 1, '15192164': 1, '28243433': 2, '31341838': 1, '28942408': 1, '11136750': 1, '4566907': 1, '34976461': 2, '21269389': 1, '10448489': 1, '29967887': 1, '23784917': 1, '15599753': 1, '22633566': 1, '24348321': 2} | {'5264547-1': 1, '8682949-1': 1} |
164,499 | 3843901-1 | 24,348,499 | noncomm/PMC003xxxxxx/PMC3843901.xml | Intravenous Thrombolysis in a Stroke Patient Receiving Rivaroxaban | An 83-year-old man with a history of nonvalvular atrial fibrillation, heart failure (NYHA class III), biventricular pacing, hypercholesterolemia, arterial hypertension and two previous strokes 4 months and 4 years before admission presented with acute right hemiparesis and dysarthria that lasted for 2 h. The patient was treated with rivaroxaban at a reduced dose of 15 mg once daily. The last intake of rivaroxaban was 21 h before symptom onset.\nOn admission, blood pressure was 114/76 mm Hg and the NIHSS score equaled 9. Blood tests showed an increased partial thromboplastin time (41.9 s; normal 23-36), a normal thrombin time (18.9 s; normal 14-21) and a slightly elevated international normalized ratio (INR: 1.41; normal 0.85-1.18). Rivaroxaban plasma concentration was below the detection limit, and anti-factor Xa activity (COATEST®; Chromogenix, Lexington, Mass., USA) was absent. Platelet count was normal, whereas renal function was impaired (creatinine 132 μmol/l, normal <103; creatinine clearance according to the Cockcroft-Gault formula 28.2 ml/min). Cranial CT and CT-angiography revealed no early signs of cerebral ischemia or ICH, and the large brain vessels were patent. Since anti-factor Xa activity was absent and the INR was <1.7 [], the patient received IVT with rtPA at 0.9 mg/kg (total dose 50 mg) 210 min after stroke onset. Shortly afterwards, the neurological status rapidly improved. On a follow-up blood examination, partial thromboplastin time (52.5 s) and INR (1.33) continued to be slightly elevated, while renal function was still impaired (creatinine clearance 27.8 ml/min). ICH could be ruled out by a follow-up cranial CT. Ultrasound examination of the cerebral vasculature was normal, as was echocardiography. Twenty-four hours after thrombolysis, creatinine clearance had increased above 30.0 ml/min, and treatment with dabigatran 110 mg twice daily was initiated. The NIHSS score at discharge was 1. | [[83.0, 'year']] | M | {'21830957': 1, '20881383': 1, '22402056': 1, '22133608': 1, '21505718': 1, '23370205': 1, '21288169': 1, '30813169': 2, '23018342': 1, '19225703': 1, '23669868': 1, '22632907': 1, '24348499': 2} | {'6408142-1': 1} |
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