The patient’s corrected visual acuity was 20/20 OU.

His pupils, intraocular pressures, motilities, and confrontational visual fields were normal in each eye.

Findings from the anterior slitlamp examination were normal in both eyes.

A dilated fundus examination of the right eye was unremarkable, but examination of the fundus of the left eye revealed a lesion in the temporal periphery.

Figure 1 shows a wide-field photograph and the results of ultrasonography of the lesion.Intraocular mass in the left eye of a man in his 40s.

A, Wide-field photograph of the fundus of the left eye.

B, Ultrasonographic image of the left eye demonstrating a large cyst in the temporal peripheral retina.


A scar resulting from the stab wound was clearly visible just below his left brow.

The pulsatile proptosis had a difference of 14 mm between his eyes.

His left eye had a palpable thrill, audible bruit, chemosis, dilated conjunctival blood vessels, and a swollen upper eyelid.His intraocular pressures (IOPs) measured 40 mm Hg in the left eye and 24 mm Hg in the right eye by Goldmann tonometry.

His visual acuity was 6/6 Snellen in both eyes with restricted elevation of his left eye.

Gonioscopy (Schaffer grading) revealed 360° open angles, grade 2 in the left eye and grade 3 in the right eye, with blood visible in the Schlemm canal in the left eye only.

His left disc was pathologically cupped with a cup-disc ratio of 0.8, and his right disc had a ratio of 0.5.

A computed tomographic scan revealed an enlarged left superior orbital fissure (SOF) (Figure 1A) and engorged orbital veins (Figure 1B).A, Enlarged left superior orbital fissure (arrowhead) shown on 3-dimensional computed tomography (CT).

His IOP did not reduce with maximum medical treatment, which included acetazolamide sodium, latanoprost, timolol maleate, brimonidine tartrate, and mannitol, 20%.


His medical history was significant for trisomy 21, with mild cognitive delay and baseline dysarthria, but no aphasia.

He had been self-sufficient with daily activities.

He was taking acetaminophen and 10 mg of oxycodone every 4 hours.

He was somnolent immediately following the procedure, and had not spoken since the day after the procedure.

Right-sided hand and face weakness developed 2 days after the procedure.

In the emergency department, his examination was significant for a temperature of 38.1°C and significant scrotal swelling and pain.

The neurologic examination was remarkable for somnolence, right hemineglect, right facial droop with right hand weakness, right patellar hyperreflexia, and mutism, although he attempted to use sign language.

His laboratory values showed a white blood cell count of 6.8 × 103/μL (to convert to  × 109/L, multiply by 0.001), platelet count of 248×103/µL (to convert to × 109/L, multiply by 1), hematocrit level of 30.9% (to convert to proportion of 1.0, multiply by 0.01), hemoglobin level of 10.2 g/dL (to convert to grams per liter, multiply by 1) with a normal differential, activated partial thromboplastin time of 40 seconds, fibrinogen level of 678 mg/dL (to convert to grams per liter, divide by 100), and normal urinalysis results.

The right face and hand weakness persisted, and he was unable to walk independently.

Magnetic resonance imaging of the brain was performed (Figure 1).


Physical examination revealed a mobile, nontender, 4-cm mass in the left side of the floor of mouth.

A contrast-enhanced computed tomographic scan of the neck showed a 3.8-cm cystic neck mass in the left floor of mouth (Figure, A).

An ultrasonography (US)-guided fine-needle aspiration (FNA) biopsy showed bland-appearing cuboidal to columnar epithelial cells arranged in clusters; no malignant cells were identified.

Repeated US-guided FNA biopsy showed a hypercellular specimen composed of numerous fragments of bland-appearing cuboidal and columnar epithelium and granular debris, which was eosinophilic in cell block sections and papillary structures with fibrovascular cores.

The hypercellularity was atypical, and a low-grade neoplasm could not be ruled out.

A core biopsy showed a well-differentiated papillary neoplasm with hyalinized fibrovascular cores and some degenerative changes (Figure, B-D).

Immunophenotypically, the neoplastic cells were negative for the markers TTF-1, PAX-8, estrogen receptor, and thyroglobulin.

Pathologic examination revealed a cystic, 2.5-cm encapsulated mass arising from a minor salivary gland.A, Computed tomographic image of the neck showing a mass in the left floor of mouth.

She underwent excision of the cystic floor of mouth mass and a level I neck dissection.

These results, with the morphologic characteristics, were most consistent with a low-grade salivary neoplasm.

At this point, the patient elected observation of the mass and a repeated biopsy.


On evaluation, the patient had a bulging, hyperemic left tympanic membrane, along with fullness of the postauricular, upper cervical region.

She was eventually transferred to our hospital after a computerized tomographic (CT) scan was performed showing potential clinically significant ear abnormalities.

A CT scan of the temporal bones with contrast was performed at our facility (Figure).A-C, Axial computed tomographic (CT) scans with contrast.

No focal neurologic deficits or meningeal signs were observed.


He was obese and had congestive heart failure and hypertension.

Biopsy of the soft tissue at the external ear canal (EEC) showed granulation tissue.

Findings from the otolaryngologic examination were otherwise unremarkable.

Advanced-stage mixed conductive and sensorineural hearing loss in the left ear were noted.

Computed tomography (CT) showed a soft-tissue mass in the mastoid and middle ear cavity extending to the EEC with no significant erosion of ossicles (Figure, A).

Histopathological examination revealed a polypoid lesion showing typical papillary architecture with central fibrovascular cores and dilated glandular structures, lined by a bland-looking single layer of high columnar/cuboidal epithelial cells (Figure, B).

The richly vascularized fibrotic stroma consisted of cholesterol clefts, foamy macrophages, lymphocytes, and eosinophils, reminiscent of inflammatory granulation tissue (Figure, C).

The epithelial cells were positive for cytokeratin-7 (CK7) (Figure, D), CK19, epithelial membrane antigen, and glial fibrillary acidic protein.

Ki-67 immunostain showed a proliferation index of less than 1%.A, Temporal bone at the level of external acoustic canal.

During modified radical mastoidectomy, the mastoid cavity was found to be full of edematous, fragile soft tissue with mucoid secretions.

No mitotic activity or necrosis was detected.

M indicates mastoid cavity; J, jugular bulb; C, carotid canal; E, external ear canal.

B, Papillary structures; original magnification ×20.

C, Papillary and dilated glandular structures; original magnification ×10.

D, Strong CK7 positivity; original magnification ×20.


Her parents stated that at the age of 3 years she sustained minor trauma to her nose while at a playground but that she had not experienced any major head trauma.

The patient had a history of frequent cough and congestion, seasonal allergies, monthly migraine headaches, and considerable nose congestion at night.

Her family history was otherwise normal and did not include any pattern of familial anosmia or delayed puberty.

She reported the ability to detect very strong odors but not subtle ones.

She was even unable to smell smoke at times.

Physical examination revealed a clinically significant hump on the dorsum of the nose consistent with minimal prior trauma, but no other abnormal findings.

The patient failed the Penn smell tests, correctly identifying only 3 of the 11 smells.

Flexible fiber-optic examination of the nose revealed no masses, polyps, or cysts.

A magnetic resonance image of the anterior skull base demonstrated absent olfactory sulci (OS) and bilateral olfactory grooves containing minimal tissue (Figure, A, yellow arrowheads).

She did not recall a history of recurrent sinusitis, snoring, or mouth breathing.

The Figure, B, depicts normal OS (pink arrowheads) and bulbs (yellow arrowheads) from a different patient for comparison.A, The anterior skull base of the study patient.


Despite several previous attempts at surgical resection, the drainage had persisted for 6 years.

Initial computed tomography (CT) identified infiltration of the subcutaneous tissues in the left side of the neck anterior to the strap muscle at the level of the larynx, without discrete abscess.

Computed tomography also showed a small tract that extended from the skin of the lateral side of the neck to the left strap muscles.

When the patient stated that he tasted contrast material, the infusion was terminated, and the patient was transferred to the CT service, where axial images of the neck were obtained and reformatted in multiple planes (Figure, B and C).A, Conventional fluoroscopic fistulogram of the neck.

B and C, Maximum-intensity projection reformatted computed tomographic (CT) images of the neck.

The patient was referred to radiology, where a 22-gauge intravenous access catheter was inserted into the draining puncta.

Isovue-300 was infused under conventional fluoroscopic guidance (Figure, A).


The patient denied history of prior abdominal or lower extremity surgery, trauma, or cardiovascular problems.

Review of systems and family history revealed nothing remarkable.

The pain was aching, relieved with rest, and primarily in her buttocks and thighs bilaterally.

Physical examination revealed normal sinus rhythm and normal blood pressure.

She had no abdominal tenderness and no palpable masses.

Femoral pulses were weakly palpable and symmetric, and pedal pulses were not palpable.

Laboratory findings were unremarkable except for an elevated erythrocyte sedimentation rate (ESR) (34 mm/h).

Noninvasive arterial flow studies demonstrated an ankle brachial index of 0.60 on the right and 0.62 on the left with biphasic waveforms in the femoral, popliteal, and tibial vessels.

Subsequent magnetic resonance angiography (MRA) of the chest, abdomen, and pelvis showed mild stenosis of bilateral subclavian arteries and an abnormal-appearing infrarenal aorta (Figure 1).Magnetic resonance angiography of the abdomen and pelvis.


He was hypotensive (blood pressure, 87/55 mm Hg) on arrival to the emergency department.

The patient’s condition was rapidly stabilized and computed tomography with contrast demonstrated a large (12.4 × 10.2-cm) right hepatic mass with heterogeneous enhancement on arterial phase and intrahepatic and intraperitoneal hemorrhage (Figure 1A).

Emergency angiography was performed by interventional radiology, demonstrating active contrast extravasation originating from the right hepatic artery.

Embolization was performed with Gelfoam and microparticles, resulting in hemodynamic stability and a quick recovery.

Delayed liver resection was subsequently performed (Figure 1B).A, Large hepatic mass seen on computed tomography, with evidence of intrahepatic and intraperitoneal hemorrhage.

B, Pathologic specimen after delayed surgical treatment of the underlying mass.


He presented with progressive inguinal lymphadenopathy and a leukocytosis of 144 000/µL with 97% lymphocytes (intermediate modified Rai stage).

Bone marrow cytogenetics and fluorescence in situ hybridization demonstrated 11q and 13q deletions.

A next-generation sequencing (NGS) panel was ordered on peripheral blood to evaluate for potentially targetable genomic alterations (Table).CARD11 mutation is associated with ibrutinib resistance, therefore ibrutinib should not be used.CARD11 mutation is found only in a subclonal population and thus ibrutinib should be avoided.The significance of the amino acid exchange in CARD11 is a variant of unknown significance, so treatment with ibrutinib may be considered.The significance of the amino acid exchange in CARD11 is a variant of unknown significance, so treatment with ibrutinib should not be considered.

He received fludarabine, cyclophosphamide, and rituximab, achieving a complete remission.

He received bendamustine plus rituximab, with resolution of lymphadenopathy and lymphocytosis.

Six months later, he experienced disease recurrence.

Prolonged cytopenias precluded continuation of therapy, and lymphadenopathy and lymphocytosis again recurred.


He had been diagnosed with the metabolic syndrome many years previously but has not seen his physician in years.

He reported no current use of medications.

On examination, he had a body mass index of 30.6 and a blood pressure of 160/102 mm Hg.


She has had fewer than 6 menstrual cycles per year since menarche at 13 years of age.

The gynecologist referred the patient to an endocrinologist.The patient reported having oily skin, acne, and excessive facial hair growth since menarche.

She had recently gained 20 lb (9 kg) and has had a difficult time losing weight despite increasing her physical activity.On examination, the patient’s body mass index was 28 (calculated as weight in kilograms divided by height in meters squared), and she had excessive coarse dark hair on the chin and abdomen (upper and lower; Ferriman-Gallwey score of 9) and acne on the face and back.

Her gynecologist considered the possibility of polycystic ovary syndrome (PCOS) and obtained laboratory measurements for thyrotropin, prolactin, follicle-stimulating hormone, and luteinizing hormone but questioned the diagnosis of PCOS because of a normal luteinizing hormone-to-follicle-stimulating hormone ratio (Table 1).

Laboratory results from her gynecological visit were reviewed and additional tests were obtained.The elevated testosterone level is consistent with polycystic ovary syndrome (PCOS).The normal fasting glucose level excludes abnormal glucose tolerance.The normal leuteinizing hormone-to-follicle-stimulating hormone ratio excludes PCOS.The diagnosis of PCOS requires documentation of polycystic ovaries by ultrasonography.

Her last menstrual cycle was 9 months ago, and at that time, she sought gynecologic evaluation.


Six months ago he had a myocardial infarction complicated by heart failure with an ejection fraction of 35%.

His medications were lisinopril, metoprolol succinate, insulin, and furosemide.

Two days ago he noticed generalized weakness, which had worsened over the last 24 hours.

Physical examination showed resolving cellulitis on the right leg.

Other than symmetrical 3/5 strength in the upper and lower extremities, his neurologic examination results were normal.

An electrocardiogram was unchanged from 2 months ago.

Laboratory results are shown in the Table.

One week ago, he was diagnosed with cellulitis of the right leg and prescribed a 7-day course of trimethoprim-sulfamethoxazole.


She was taking folic acid and intramuscular cyanocobalamin supplements owing to deficiencies attributed to a dietary cause.

This was associated with enlargement of the tongue over the past 3 months, leading to difficulty with mastication.

She also reported numbness with no associated weakness of her distal lower limbs for 3 months.

This restricted her mobility to the extent that she required diapers.

This was accompanied by macroglossia, glossitis, and a hemorrhagic erosion on the hard palate (Figure, B).

On examination, there were circinate purpuric patches with erosions on the natal cleft, buttocks, inguinal creases, and vulva (Figure, A).

Hemorrhagic flaccid bullae were observed on the posterior perineum.

There were purpuric macules periorbitally and on the lips, inframammary folds, forearms, and thighs.

Laboratory findings revealed a platelet count of 171 × 103/μL (reference range, 140-440 × 103/μL), prothrombin time of 11.7 seconds (reference range, 9.9-11.4 seconds), activated partial thromboplastin time of 36.0 seconds (reference range, 25.7- 32.9 seconds), and serum zinc levels of 34.4 μg/dL (reference range, 72.4-124.4 μg/dL).

Results from initial punch biopsies from a purpuric macule on the right inframammary fold and a blister at the perineum were inconclusive.

B, Clinical findings of macroglossia and glossitis with purpura of the lips.

C, Punch biopsy specimen of a flaccid bulla showing the floor of a subepidermal blister lined by fibrin and a chronic inflammatory infiltrate.

D, Scattered short eosinophilic amorphous bands in the dermis.

She had IgG λ-type multiple myeloma complicated by anemia and lytic lesions in the calvarium, which was managed conservatively with transfusions.

However, she declined any further investigations for her peripheral neuropathy.

(To convert zinc to micromoles per liter, multiply by 0.153.)

A repeated biopsy from a hemorrhagic blister at the left groin was performed (Figure, C and D).A, Purpura and erosions at the buttocks.


He disclosed full compliance with his HIV highly active antiretroviral therapy (HAART), which included ritonavir, darunavir, etravirine, and raltegravir.

He also reported taking sumatriptan as needed for headaches.

The patient reported a 1-month history of “puffy and bumpy” lips.

He also described his lower lip as sometimes becoming “dry and scaly” during this time but denied any bleeding from the area.

Findings of a complete review of systems were unremarkable, other than occasional headaches.

On physical examination, there were several erythematous papules at the vermillion border of the lower lip within a background of edema (Figure, A and B).

In addition, the patient had slight fissuring of the tongue, but the remainder of the oral mucosa was normal and intact.

Numerous laboratory tests were performed, including a complete blood cell count, complete metabolic panel, CD4 count, HIV viral load, and assays for C-reactive protein, erythrocyte sedimentation rate, angiotensin-converting enzyme, and rapid plasma reagin; all results were normal except for a slightly elevated angiotensin converting enzyme level (84 µg/L; normal, 9-67 µg/L).

His CD4 count was within normal limits (520 cells/µL) and HIV viral load was undetectable.

A biopsy was performed on the right lower lip (Figure, C and D).Clinical images (A and B) show persistent, nontender swelling of the lips in a patient with human immunodeficiency virus, showing erythematous papules at the vermillion border and edema of the lower lip.


C, Sebaceous tumor with a modestly increased ratio of basaloid cells to sebocytes.The patient’s medical history included diabetes mellitus type 2, hypercholesterolemia, hypertension, and depression.

Review of her family medical history revealed that her paternal grandfather died from melanoma and that her father died from colon cancer.

She stated that most of the men in her family had died from some form of cancer by the fourth decade of life.On physical examination, a tender, centrally depressed, firm, pink 1.1-cm nodule was present on her upper cutaneous lip (Figure, A).

She was otherwise asymptomatic.A, Centrally depressed, firm, pink 1.1-cm nodule on the upper cutaneous lip and skin-colored papule on the left medial cheek (above marker dots).

Three other skin-colored to pink papules were present on her face and neck.

Shave biopsies of all 4 skin lesions were performed (Figure, B and C).

B, Cup-shaped tumor demonstrated keratinocyte atypia with a central core of keratinaceous debris.


He was recently hospitalized for confusion, short-term memory loss, vomiting, and diarrhea.

He also experienced hair loss (Figure 1), a facial rash, hoarseness, and painful peripheral neuropathy in his feet.

He reported difficulty opening his eyelids during hospitalization but denied any history of diplopia.

His blood pressure on admission was 150/102 mm Hg, his pulse was 118 beats/min, and ophthalmic examination findings demonstrated decreased visual acuity and dyschromatopsia.

Results of a complete blood cell count, comprehensive metabolic panel, and erythrocyte sedimentation rate were within reference limits, and computed tomography of the head without contrast showed no abnormalities.

A lumbar puncture showed normal opening pressure with a mildly elevated protein level in the cerebrospinal fluid.Alopecia was noted in our patient in addition to temporal thinning of the lateral half of the eyebrows.On our examination, best-corrected visual acuity was 20/70 OU.

Extraocular motility was full in both eyes, and confrontational visual field test findings were full in all quadrants.

The patient missed 4 color plates on Ishihara pseudoisochromatic testing.

The slitlamp examination revealed an unremarkable anterior segment, and results of dilated ophthalmoscopy showed temporal optic nerve pallor in both eyes.

The macula, vessels, and retinal periphery were unremarkable on examination.


He denied any history of diabetes or past ocular problems and reported having mild hypertension for which he was taking lisinopril.

He had been experiencing nonprogressive diminished vision in his left eye for 6 weeks.

Review of systems was positive for fatigue of his tongue while eating but he denied any jaw claudication, fevers, malaise, joint pain, or weight loss.

His best-corrected visual acuity was 20/25 OD and 20/30 OS.

Pupillary and anterior segment examination in both eyes were unremarkable with the exception of bilateral nuclear sclerotic cataracts.

Dilated fundus examination of the right eye showed a nerve fiber layer infarct (NFLI) inferior to the optic nerve (Figure 1A).

In the left eye, there were several scattered NFLIs in the peripapillary region (Figure 1B).

Fluorescein angiography (FA) showed relatively normal flow without evidence of occlusion or vasculitis.

An extensive inflammatory and infectious laboratory workup revealed a hemoglobin level of 12.6 g/dL and elevated erythrocyte sedimentation rate and C-reactive protein level of 54 mm/h and 6.16 mg/L, respectively (to convert hemoglobin to grams per liter, multiply by 10, and C-reactive protein to nanomoles per liter, multiply by 9.524).

Antinuclear antibody testing was positive (1:80 with homogenous pattern).

Further workup including human immunodeficiency virus testing was nonrevealing.Fundus photographs of the right and left eye demonstrating nerve fiber layer infarcts in the peripapillary region.


She had a history of alcohol, tobacco, cocaine, and marijuana use but denied current illicit drug use.

She had not taken any medications prior to the appearance of the lesions.

Three weeks previously, she noticed painful erosions throughout her mouth.

A week later, painful blisters appeared on her upper extremities, trunk, and thighs.

She also reported 2 pruritic and painful lesions on her scalp that had appeared 6 months prior, shortly after a chemical hair treatment.

The patient reported a 2.25-kg weight loss, subjective fevers, and chills but no urinary symptoms.On admission, the patient was tachycardic (113/min), but she was afebrile and other vital signs were normal.

Physical examination revealed crusted plaques on her scalp bilaterally (Figure).

Erosive stomatitis involving the lower lip, buccal mucosa, hard palate, soft palate, and tongue was noted (Figure).

Multiple well-circumscribed, round-to-oval bullae, erosions, and hyperpigmented patches were noted on her upper extremities, trunk, and thighs (Figure).

Laboratory evaluation revealed a serum creatinine level of 7.1 mg/dL (627.6 μmol/L), up from a baseline (10 days prior) level of 0.9 mg/dL (79.6 μmol/L).

Urinalysis revealed a specific gravity of 1.015 and was positive for hyaline casts and protein but negative for white blood cells, red blood cells, and bacteria.

A complete blood cell count was unremarkable.

Results of human immunodeficiency virus screen and urine drug screen were normal.Left, Crusted plaques on scalp of patient.


On day 8 after birth, a 0.5-cm, circular, crusted papule with a surrounding rim of erythema on the left hip was noted (Figure, A).

The patient’s premature birth was complicated by acute respiratory distress that necessitated intubation and necrotizing enterocolitis that required parenteral nutrition.

At birth, the patient was found to be mildly anemic (hemoglobin level, 11.0 g/dL [to convert to grams per liter, multiply by 10]) and thrombocytopenic (platelet count, 120 × 103/µL [to convert to 109/L, multiply by 1]) with concomitant intraventricular hemorrhage.

A cerebrospinal fluid culture result was positive for Staphylococcus epidermidis, but the results of additional blood cultures were negative for organisms.

A punch biopsy of the lesion was performed (Figure, B and C).A, Crusted circular papule with a surrounding rim of erythema and induration on the left hip.

B, Biopsy specimen revealing epidermal necrosis with fungal elements within the superficial dermis (hematoxylin-eosin, original magnification ×20).

C, Biopsy specimen highlighting branching and septate hyphae within the superficial dermis (specimen was stained with Gomori methenamine silver, original magnification ×40).

Although afebrile, he was treated empirically for sepsis with vancomycin hydrochloride and cefepime hydrochloride.


He reported a history of moderate alcohol consumption, drinking 1 beer per day during the week and approximately 5 to 8 beers over the weekend, but denied any use of nutritional supplements or illicit drugs.

There was no recent travel outside the state.

Human immunodeficiency virus test results on admission were negative.

The patient noted swelling on the right side of the neck and a 5-kg weight loss over the past 2 months.

Physical examination revealed scleral icterus, jaundice, and a fixed right supraclavicular lymph node conglomerate measuring 6 × 3 cm.

There was no cervical, left supraclavicular, axillary, or inguinal lymphadenopathy.

Computed tomography of the neck, chest, abdomen, and pelvis demonstrated a large right supraclavicular lymph node, extensive mediastinal lymphadenopathy, a large extracardiac mass abutting the left atrium, hepatomegaly, and multiple splenic lesions.

Laboratory evaluation demonstrated a total serum bilirubin level of 10.5 mg/dL with a direct component of 8.4 mg/dL (to convert to micromoles per liter, multiply by 17.104).

Mild leukopenia and slight thrombocytopenia in the absence of associated anemia was noted on initial complete blood cell count.


Her medical history was significant for chronic gastritis, which was being treated with esomeprazole 20 mg; a laparoscopic cholecystectomy 18 years prior; and excision of a 26-mm Merkel cell carcinoma of the left knee with negative results of the sentinel lymph node biopsy (stage II) 19 months prior.

Results of the patient’s follow-up examinations were negative until a high-resolution computed tomographic scan showed a 45 × 40-mm intraluminal protruding mass with slightly enlarged lymph nodes along the lesser curvature of the gastric fundus (Figure, A).

Results of fluorine 18–labeled fluorodeoxyglucose and gallium citrate Ga 68–labeled 1,4,7,10-tetraazacyclododecane-N,N',N'',N'''-tetraacetic (DOTA)-D-Phe1-Try3-octreotide (DOTATOC) positron emission tomography confirmed the presence of a metabolically active mass in the gastric fundus (maximum standardized uptake value, 6) with intense 68Ga–DOTATOC uptake (maximum standardized uptake value, 24) as well as mild 68Ga–DOTATOC uptake in 2 lymph nodes of the lesser curvature.A, Multislice computed tomographic scan showing the 45 × 40-mm mass in the gastric fundus.

B, Endoscopic image showing the endophytic lesion in the posterior wall of the gastric fundus at the esophagogastric junction.Preoperative workup was completed via esophagogastroduodenoscopy, which showed the presence of the polypoid lesion in the posterior wall of the gastric fundus at the level of the esophagogastric junction (Figure, B).

Multiple biopsies were performed at the time of the endoscopy.


His medical history was uneventful, and there was no weight loss.

However, the patient’s father had died of a pancreatic carcinoma the previous year at the age of 65 years.

A similar episode had occurred 1 month before admission that improved spontaneously.A physical examination did not reveal any clinical abnormities, but the patient reported dysuria and abnormally frequent urination.

A computed tomographic scan of the abdomen revealed nephrolithiasis with a 4-mm kidney stone on the right side and a slightly congested right kidney.

During computed tomography, we incidentally found a 10 × 10 × 8-cm mass in the tail of the pancreas (Figure 1), as well as thrombosis of the splenic vein.

The patient’s laboratory values, including cancer antigen 19-9 and carcinoembryonic antigen levels, were normal.Computed tomographic (CT) scans of the abdomen reveal the mass in the pancreas (arrowheads).


The patient had a history of an ovarian cyst treated conservatively, and cosmetic breast augmentation.

She had a 10 pack-year smoking history and denied alcohol or illicit drug use.

Examination revealed distant heart sounds but otherwise had unremarkable results.

An echocardiogram demonstrated a mass in the left ventricular myocardium.

Cardiac magnetic resonance imaging was obtained to further assess the mass lesion.

This revealed multiple intramyocardial masses involving the left ventricle, the largest of which measured 2.7 × 2.2 cm; aortopulmonary window lymphadenopathy; and moderate pericardial effusion (Figure).

Computed tomographic imaging of the chest, abdomen, and pelvis with contrast failed to reveal discrete masses or lymphadenopathy elsewhere.

A transcutaneous biopsy of the left ventricular mass was nondiagnostic.


In September 2013, she began receiving trastuzumab treatment and received adjuvant radiotherapy (5000 Gy in 25 fractions) 1 month later.

In June 2014, she developed a generalized nonpruritic, nontender rash, without fevers or other constitutional symptoms.

Physical examination showed multiple red-brown plaques and papules of various sizes on the chest, abdomen, back, and limbs (Figure 1).

Laboratory evaluation revealed pancytopenia (white blood cells, 1460/μL; hemoglobin, 8.3 g/dL; and platelets, 99 000/μL [leukocyte differential: 0% blasts, 0% promyeloctes, 0% myelocytes, 0% metamyelocytes, 0% banded neutrophils, 30.1% segmented neutrophils, 4.1% eosinophils, 0.7% basophils, 0.7% monocytes, 64.4% lymphocytes]).


She had no fever or any other systemic symptoms.

She was otherwise in excellent health, with no history of allergies, no recent travel, and no animal exposure or trauma to her arm.Swelling and keloid formation within red ink area of tattoo.On examination, the patient was afebrile and appeared healthy.

Topical hydrocortisone cream (1%) applied for 1 week had provided no benefit.

Marked swelling and keloid formation within the red ink area of the tattoo were noted.

There was no drainage, local warmth or tenderness, or pustule formation.

Notably, there was no swelling or discoloration over the black ink area of the tattoo.


He previously made an informed decision to undergo prostate-specific antigen (PSA) screening for prostate cancer.

His digital rectal examination (DRE) revealed an enlarged prostate without nodules.

His PSA history is displayed in the Table.The patient’s slow rise in prostate-specific antigen (PSA) level and enlarged prostate are consistent with benign prostatic hyperplasia, and his probability of prostate cancer is less than 10%.The patient’s rise in PSA level means his probability of prostate cancer is more than 50%.The patient’s probability of prostate cancer is approximately 6% for a high-grade cancer and 18% for a low-grade cancer.Variability in the patient’s PSA level makes it likely the tests were done in different laboratories.


He had no other symptoms.The patient's medical history included hypertension (controlled with lisinopril and hydrochlorothiazide), a low-density lipoprotein level of 155 mg/dL, and a high-density lipoprotein level of 44 mg/dL.

He did not smoke or have family history of premature coronary artery disease (CAD).

He reported substernal chest pain, lasting less than 5 minutes, which sometimes occurred if he ran more than 2 miles.

The patient’s physical examination results were unremarkable, blood pressure was 134/80 mm Hg, body mass index was 26 (calculated as weight in kilograms divided by height in meters squared), and resting electrocardiogram (ECG) results were normal.The patient had no chest pain during ETT.

Results are reported in the Table.Further testing is unnecessary because the patient is asymptomatic and has high exercise capacity.Further testing is needed because of the ST depressions during recovery.Further testing is unnecessary because ST depressions are not significant unless 2 mm or greater.Further testing is needed because inferolateral ST depressions indicate obstructive coronary artery disease in the right coronary artery, the left circumflex artery, or both arteries.


She stated that it began before her diagnosis of acute myelogenous leukemia and the initiation of treatment with hydroxyurea 4 years later.

Her additional daily medication regimen included donepezil hydrochloride, melatonin, and aspirin, 81 mg.Findings from the patient’s physical examination revealed background erythema with numerous rough horny spicules at the follicular ostia on her face, ears, and neck; the upper part of her chest; and her bilateral forearms.

She denied having pruritus or pain, but her skin had a rough sandpapery sensation.

She reported that the involvement extended to her neck, the upper part of her chest, and her bilateral forearms.

Findings from the rest of her examination revealed a pigmented macule on her right cheek.

Two punch biopsy specimens were obtained from her right cheek and right postauricular area and submitted for histopathologic examination (Figure).Histopathologic images (hematoxylin-eosin) of the punch biopsy specimen from the right side of the lateral neck.

She had previously received treatment with long courses of triamcinolone acetonide cream, 0.1%, bacitracin ointment, and a combination antibiotic ointment of neomycin sulfate, polymyxin B, and bacitracin, with no improvement of her skin’s condition.

She associated the onset of the textural changes with her diagnosis of polycythemia vera.


The patient had no history of medical problems.

He was born in Spain and had received his childhood immunizations.

He remembered insect bites on his feet, but the lesions later became ulcerated and painful.

The patient denied experiencing fever, arthralgia, or a sore throat.Findings from the physical examination revealed 6 painful ulcerated, exudative nodules with a grayish membrane over the ulcers on the dorsal aspect of his feet (Figure 1).

No signs of lymphangitis or lymphadenopathy were detected.

A 4-mm punch biopsy specimen from one lesion was obtained and stained with hematoxylin-eosin and Gram stain for histopathologic analysis.

Another skin specimen was cultured for microbiologic analysis.


According to her mother, new lesions had appeared during the past weeks on the shoulders.

Physical examination revealed coarse facial features, hepatomegaly (7 cm below the costal arch), distinctive lumbar kyphosis, and muscular hypotonia compared with her twin brother.

Dermoscopy showed faint clouds of nonhomogeneously distributed light brown pigment.A, Polycyclic, brown, partly livid shimmering macules covered large areas of the back, neck, buttocks, and lower extremities.

B, Fusiform and dendritic cells were found scattered in the dermis (hematoxylin-eosin, original magnification ×100).

C, Immunohistological staining of the same specimen (original magnification ×200).

S-100 protein positivity identified these cells as melanocytes.

D, A triangle-shaped first lumbar vertebral body is shown.


The woman’s medical history was significant for type 2 diabetes mellitus (DM), hypertension, recurrent urinary tract infections, onychomycosis, end-stage renal failure, and a history of living, unrelated donor renal transplant 12 years earlier, kidney transplant rejection, and prior episodes of syncope.

Medications included tacrolimus, mycophenolate mofetil hydrochloride, prednisone (1 mg/d), losartan potassium, and insulin.

Family history was notable for her father having died of lung cancer and her mother had heart disease and DM.

Social history did not reveal any unusual exposures.

Neurologic findings revealed reasonably preserved mental status, with bedside examination revealing normal attention, language, and orientation but mild memory deficits for short-term recall (2 of 3 words recalled at a 5-minute delay) and long-term fund of knowledge.

Cranial nerve, motor, sensory, and reflex examination results were significant only for gait ataxia, with an inability to perform tandem gait.

Urinalysis revealed a urinary tract infection, but computed tomography (CT) of the head showed extensive mass lesions with bilateral edema.

Magnetic resonance imaging (MRI) of the brain delineated expansile mass lesions of the splenium of the corpus callosum, with T2–fluid-attenuated inversion recovery hyperintensity in the bilateral parietal lobes, left thalamus, and midbrain (Figure, A); administration of contrast revealed multiple ring-enhancing lesions (Figure, B).

Physical examination results showed a transplant surgical scar and onychomycosis.

Blood test results were consistent with DM.

Findings from cerebrospinal fluid (CSF) examination included a white blood cell count of 9/µL, with differential examination showing 84% lymphocytes, 13% monocytes, and 3% neutrophils; red blood cell count of 1080/µL; protein level, 180 mg/dL; and glucose level, 87 mg/dL.

Flow cytometry revealed B and T lymphocytes but no monoclonal populations of cells.

Polymerase chain reaction amplification tests on CSF revealed no evidence of cytomegalovirus or herpes simplex virus 1 or 2 genetic material.

Serum and CSF serologic test results were negative for antibodies to toxoplasma; testing using polymerase chain reaction on blood for Epstein-Barr virus (EBV) revealed minimal (very low positive) viral DNA at 52 IU/mL.

A CT scan of the chest, abdomen, and pelvis showed a small, subpleural nodule; fatty liver; diverticulosis; failed native kidneys; and normal transplanted kidney.

Dexamethasone sodium phosphate and levetiracetam were administered.

The patient underwent a diagnostic procedure.Brain magnetic resonance imaging showing unsuspected mass lesions.

A, A T2 fluid-attenuated inversion recovery (FLAIR) sequence illustrating prominent T2 hyperintensity in the right more than the left parietal white matter suggestive of edema, an expansive mass lesion on the right more than the left splenium of the corpus callosum, and an infiltrative mass lesion in the left thalamus extending into the mesencephalon.

Whole-body positron emission tomography revealed hypermetabolic regions in the brain.


He was born at full term weighing 3.63 kg after a normal pregnancy, labor, and delivery.

He grew appropriately until 3 months of age, after which his weight dropped from the 50th percentile to the fifth percentile in 2 months despite maintenance of a fairly adequate caloric intake.

The patient had multiple episodes of emesis.

His head was of normal size, although it appeared large relative to his small body size.

Results of his gastrointestinal evaluation were normal.

At 6 months of age, he developed a constant rapid nystagmus of the right eye.On presentation, he was a happy, engaged, alert child with an emaciated appearance (Figure, A).

During the examination, the patient was socially interactive and visually attentive.

He had normal, optokinetic responses and brisk pupillary responses with no relative afferent pupillary defect.

He had a rapid pendular horizontal nystagmus, with no associated strabismus, head nodding, or torticollis (Video).

The patient looked readily toward objects held in the peripheral visual field of either eye.

The retinal examination showed normal-sized optic discs without swelling or pallor.

The patient had no history or findings suggestive of neurofibromatosis type 1.A, On presentation, the patient appeared emaciated but alert.


However, the therapy was complicated by avascular hip necrosis that required total hip arthroplasty, and his visual symptoms recurred with corticosteroid tapering.At presentation, his visual acuity was 20/150 OD and 20/15 OS.

The anterior segment was normal in both eyes.

Dilated ophthalmoscopic examination of the right eye revealed a diffuse subretinal yellow mass and an exudative retinal detachment temporal to the fovea (Figure 1).

Ophthalmoscopic examination of the left eye was normal.

B-scan of the right eye showed a dome-shaped choroidal lesion with an apical height of 3.4 mm and medium to high internal reflectivity.

Fluorescein angiography demonstrated heterogeneous leakage, and optical coherence tomography of the macula showed subretinal fluid with irregular retinal and choroidal thickening.

Results from extensive workup for infectious and autoimmune etiologies (including serum angiotensin-converting enzyme, lysozyme, lumbar puncture, magnetic resonance imaging of the brain and orbits, and computed tomography of the chest) were negative, except for positive purified protein derivative skin testing and positive interferon-γ release assay (QuantiFERON-TB Gold; Cellestis, Inc).Large choroidal tuberculoma at presentation.

In a fundus view of the right eye, a moderate amount of subretinal fluid is seen adjacent to the lesion, involving the fovea center.

B-scan (not shown) measured an apical height of 3.4 mm.

Oral prednisone provided visual improvement.


She reported recently injuring her hand on a metal fence at home and biting her nails frequently.

She lives on a farm in Ohio and has extensive direct contact with sheep and cows; family pets include a cat, a dog, and a hamster.

She reported mild tender lymphadenopathy of the right axilla but denied fever.Examination revealed an erythematous, 1 × 1.5-cm, well-defined eroded pustule with central crusting and an erythematous border (Figure).

There were several slightly enlarged, mildly tender lymph nodes noted in the right axilla.Eroded and crusted pustule with surrounding inflammation on the thumb.Complete blood cell count, erythrocyte sedimentation rate, and basic metabolic panel results were unremarkable.

Findings on radiography revealed focal soft-tissue swelling with no evidence of foreign body, subcutaneous gas, or osseous involvement.

There was no known recent travel or contact with anyone with a similar lesion.


He denied any heartburn, hemoptysis, pain, neck masses, or smoking history.

Prior treatment with 2 rounds of oral antibiotics and 1 round of oral steroids from his primary care physician did not improve his symptoms.

He described a progressively worsening voice with use to the point where he was nearly aphonic by the end of his workday.

Objectively, the patient’s voice was rough, diplophonic, and very strained.

Videostroboscopic examination in the clinic revealed a broad-based submucosal mass in the anterior two-thirds of the right true vocal fold (Figure, A) that disrupted vibration of both vocal folds owing to its size and anterior location (Figure, B and Video).

Findings from the remainder of his head and neck examination were unremarkable.

The patient was taken to the operating room for microdirect laryngoscopy under general anesthesia (Figure, C).

A microflap incision along the lateral aspect of the right true vocal fold mass was performed, and a firm, submucosal, tan-colored, seemingly encapsulated, multilobulated mass was removed en bloc with narrow margins and sent for permanent section analysis (Figure, D).

The mass was deep to the epithelium of the true vocal fold and superficial to the vocal ligament.A and B, Clinical views of endoscopic appearance of the anterior right true vocal fold mass.

C and D, Intraoperative endoscopic views.

D, A microflap incision was performed along the lateral aspect of the lesion and a multilobulated, firm submucosal mass deep to the epithelium but superficial to the vocal ligament was resected.


She denied other sinonasal symptoms, history of epistaxis, nasal trauma, or surgery.

Clinical evaluation revealed a soft-tissue mass filling the left nasal cavity and based on the mucosal surface of the anterolateral nasal vestibule.

Noncontrast paranasal sinus computed tomography showed a 1.2 × 0.8-cm ovoid soft-tissue mass opacifying the posterior aspect of the left nasal vestibule (Figure, A, arrowhead).

B-D, Histopathologic images from the nasal cavity mass, original magnifications ×100.

Endoscopic excision under local anesthesia was performed to remove a broad-based soft-tissue mass from the left nasal vestibule mucosa with a cuff of grossly healthy submucosa.

A tissue specimen was biopsied (Figure, B-D).

The patient had an uneventful postoperative course, and her epistaxis symptoms were resolved at the 5-month follow-up.A, Noncontrast paranasal sinus computed tomographic image.


Rapid correction to 136 mEq/L occurred, resulting in lethargy, aphasia, and ataxia.

Over the subsequent 2 weeks, the hyponatremia resolved and the patient was left with slight dysarthria and difficulties with fine-motor movements.

Laboratory evaluation revealed a sodium level of 109 mEq/L.

Magnetic resonance imaging (MRI) demonstrated an abnormal signal within the basal ganglia and insular cortex.

A 2.5 × 1.5 × 1.8-cm mass was found in the superior right maxillary sinus with extension into the infundibulum (Figure, A).

Computed tomographic (CT) scans of the sinuses without intravenous contrast demonstrated that the mass had calcifications.

The submucosa contained a small, round, blue-cell tumor growing in circumscribed lobules and nests separated by vascularized fibrous stroma.

The neoplastic cells had uniform, small, round nuclei with scant cytoplasm.

Cells were arranged in a pseudorosette pattern (Figure, B).

The nuclei demonstrated dispersed, salt and pepper nuclear chromatin and inconspicuous nucleoli.

The cells were surrounded by a neurofibrillary matrix.

There were prominent microcalcifications.

The tumor cells were diffusely positive for immunohistochemical marker synaptophysin (Figure, C).

Results from cytokeratin staining were negative (Figure, D).A, T1-weighted postgadolinium magnetic resonance image, coronal view.

Owing to persistent hyponatremia (sodium level, 125-130 mEq/L) and an identifiable lesion, the patient was taken to the operating room for biopsy.

He underwent a maxillary antrostomy with near-complete removal of the mass.

He was diagnosed as having idiopathic syndrome of inappropriate antidiuretic hormone secretion (SIADH).

B, Hematoxylin-eosin, original magnification ×100.

C, Tissue positivity for synaptophysin, original magnification ×200.

D, Tissue negativity for cytokeratin, original magnification ×200.


She reported a distant history of breast cancer and a recent history of an oral cavity lesion, which was not biopsied or followed up.

She did not have any known tuberculosis exposure, recent foreign travel, exposure to unpasteurized food, history of immunodeficiency, or alcohol or tobacco use.

She did not have fever, chills, cough, dysphagia, or odynophagia.

Physical examination revealed a healthy-appearing woman with normal vital signs.

She was found to have bilateral cervical lymphadenopathy, which included fixed and bulky nodes in level IB and IIA and nontender level IV and V nodes.

An oral cavity examination revealed no evidence of masses or lesions, floor of mouth and base of tongue were soft, and the palatine tonsils had no lesions or ulcers.

Flexible laryngoscopy revealed no evidence of pharyngeal or laryngeal lesions.

Contrast-enhanced computed tomographic (CT) scans of the neck (Figure) revealed bilateral lymphadenopathy with central necrosis.Computed tomographic scan with contrast.

A, At the level of mandible.
B, At the level of thyroid cartilage.
C, Through the sphenoid.
D, Through the temporomandibular joint.


Her medical history included hypertension, diabetes mellitus, and right-sided chronic otitis media of 4 years’ duration successfully treated surgically 1 year earlier (tympanoplasty type 1).

On oral endoscopic examination, mild bilateral hyperemia of the tonsillar area and posterior pharyngeal wall were noted.

A submucosal pulsatile mass was clearly visible in the right retropharyngeal area (Figure, A and B; Video).

No other clinically significant abnormalities were noted.

She was reevaluated after 15 days.A and B, Endoscopic examination of the oropharynx revealing a submucosal pulsatile mass in the right retropharyngeal area.

Abnormal medial course of the right internal carotid artery (arrow).

Aberrant internal carotid artery in the retropharyngeal space.

Part of the clinical findings were suggestive of laryngopharyngeal reflux disease, and oral esomeprazole, 40 mg/d, was prescribed.

Head and neck magnetic resonance angiography was recommended (Figure, C and D).


When presenting for his fourth and final dose of ipilimumab, he reported central headaches, severe fatigue, poor appetite, intermittent nausea, and a mild rash.

On examination, vital signs were within normal limits.

Physical examination had largely unremarkable results except for a slightly red, raised rash over his chest and proximal extremities.Laboratory testing showed the following: thyrotropin, 0.02 mIU/L (reference range, 0.3-5.0 mIU/L), and free thyroxine, less than 0.25 ng/dL (reference range, 0.5-1.2 ng/dL; to convert to picomoles per liter, multiply by 12.871).

Cosyntropin stimulation test showed a cortisol peak level of 0.9 µg/dL (reference range, >20 µg/dL; to convert to nanomoles per liter, multiply by 27.588).

He had low corticotropin (<5 pg/mL; reference range, 7-51 pg/mL; to convert to picomoles per liter, multiply by 0.22) and testosterone levels (<0.1 ng/mL; reference range, 2-11 ng/mL; to convert to nanomoles per liter, multiply by 0.0347).

Magnetic resonance imaging (MRI) of the brain is shown in the Figure.Magnetic resonance imaging of the brain with contrast.

He then underwent inguinal lymph node dissection and was found to have 9 lymph nodes involved with melanoma (stage IIIC melanoma).He was then treated with ipilimumab (3 mg/kg), a monoclonal antibody to cytotoxic T lymphocyte antigen-4 (CTLA-4), every 3 weeks, as part of an investigational adjuvant therapy clinical trial.

Several months earlier, he presented to the emergency department with shortness of breath.

Imaging revealed pulmonary emboli and incidental groin lymphadenopathy.


The patient noted no other symptoms.His medical history included atopic dermatitis and pulmonary tuberculosis.

There was no family history of gastrointestinal pathology.

He had not undergone any previous abdominal surgery, except inguinal hernia repair.

No history of sexually transmitted diseases was found.

The anal lesion appeared 1 year earlier and grew slowly to the current size.

The patient reported bleeding from the rectum after defecation and denied weight loss or fever.

It was ulcerated, covered by purulent exudate, and very painful.

Physical examination revealed a 12 × 10-cm hard mass on the left side of the anus (Figure 1A).

The scrotum was mildly tender to palpation.

Digital rectal examination and rectoscopy were not performed because of the pain and fecal incontinence.

Routine blood, liver, and renal function test results were normal, as were results for carcinoembryonic antigen and cancer antigen 19-9.

Chest radiography showed no abnormalities.

Computed tomographic scan of the pelvis showed a hypodense 12 × 7 × 3-cm mass extending to the anus, anal canal, and lower perirectal space (Figure 1B).

Abdominal computed tomography showed no pathology.Clinical photograph of the giant perianal mass in the left perianal region (A) and abdominal computed tomographic scan showing the mass in the anus (B).


She had not received any medication, including contraceptive pills or hormones, for more than 10 years.Nine years before this examination, the patient underwent elective splenectomy and hepatic biopsy at another institution.

However, she did not know the reason for removal of the spleen, and results of the histopathologic examination were not available.

She had undergone a cesarean section at age 25 years.

The patient had no history of trauma or other previous medical events.An abdominal computed tomographic scan revealed a well-defined, solid, heterogeneous mass, completely intrahepatic, with no enhancement and no liquid component, causing slight displacement of the right hepatic vein (Figure 1).Cross-sectional computed tomographic image of the abdomen shows a large, intrahepatic, 20-cm solid mass.

The patient was asymptomatic, and there were no significant findings on abdominal physical examination— the liver was not palpable.

The ultrasonographic scan showed a hepatic mass in the right lobe composing approximately 50% of the liver parenchyma.

Results of whole blood analyses, including α-fetoprotein, were within the reference ranges.


Her medical history included hypertension, diabetes, pulmonary sarcoidosis, and acid reflux, for which she takes amlodipine, carvedilol, repaglinide, hydroxychloroquine, and pantoprazole.

Her history also included chronic renal insufficiency and chronic hepatitis C, for which she takes no medications.

She reported no fevers, new skin exposures, oral ulcers, arthritis, alopecia, or photosensitivity and no worsening pulmonary symptoms of cough or shortness of breath.

The rash did not improve after 2 weeks of applying topical triamcinolone ointment (0.1%).Physical examination revealed annular coalescing scaly patches with erythematous borders on her forehead, neck, back, and upper and lower extremities (Figure, panels A and B).

Laboratory workup revealed an antinuclear antibodies titer of 1:80 with a speckled pattern, elevated Sjögren syndrome–related antigen A (SS-A) level (>8 AI), and no elevation of Sjögren syndrome–related antigen B (SS-B), ribonucleoprotein, double-stranded DNA, Smith, or anti-histone antibodies.

Complete blood cell count, erythrocyte sedimentation rate, and C-reactive protein level were within normal limits.

Creatinine level was elevated but stable at 1.8 mg/dL (159.1 μmol/L).

Skin biopsy revealed an inflammatory pattern of vacuolar interface dermatitis (Figure, panel C).A, Widespread annular and polycyclic scaly patches on the trunk and extremities.


He was taking sertraline for treatment of anxiety disorder, and had a 15-year-old son.

He reported no headache, erectile dysfunction, breast tenderness or mass, arthralgias, edema, or increase in glove, ring, or shoe size.

His examination was significant for the presence of bitemporal visual field defects on confrontation testing.

Laboratory tests were performed (Table), which revealed low serum testosterone and thyrotropin and elevated serum prolactin levels.

A neuro-ophthalmic examination revealed the presence of symmetric superior temporal visual field defects on perimetry.

He had no acromegalic features, gynecomastia, galactorrhea, or abnormal virilization.

Magnetic resonance imaging (MRI) was obtained to examine his brain.The patient has hyperprolactinemia due to a nonfunctioning pituitary adenoma.The patient has hyperprolactinemia due to thyroid disease.The patient has hyperprolactinemia due to a prolactinoma.


Her medications included metformin, lansoprazole, venlafaxine, diltiazem, atorvastatin, oxycodone/acetaminophen, ramopril, reglan, zolpidem, and clopidogrel.

She denied any history of trauma and had not applied anything topically in this area of skin.

She denied fevers, systemic symptoms, joint pain, and skin thickening.

She was treated with clobetasol cream (0.05%), and the plaque resolved in 4 weeks with postinflammatory hypopigmentation.Ten months later, the patient developed a tender, pink, indurated 7-cm plaque with telangiectasias and central ulceration in the same location, with no other cutaneous findings (Figure, B).

Physical examination revealed an 8-cm solitary, erythematous plaque with vesiculation and central erosion on the right lateral area of her abdomen (Figure, A).

The remainder of the physical examination was unremarkable.

A punch biopsy showed a vacuolar interface dermatitis pattern, but a definitive clinical diagnosis was not established.

No precipitating factors could be identified.


She had previously undergone coronary artery bypass grafting with simultaneous aortic valve replacement and ileal conduit urinary diversion as a result of to recurrent upper urinary tract infections.

On day 7 of her hospital stay, she developed severe, unremitting left ankle pain with purpuric lesions on the skin.

Laboratory findings were significant for neutrophil-predominant leukocytosis (leukocyte count, 19 400/μL [to convert to ×109/L, multiply by 0.001]).Physical examination revealed multiple stellate, purpuric plaques with central flaccid bullae on the medial and lateral aspects of the left ankle (Figure, A).

The remainder of her skin examination findings were unremarkable.

Punch biopsy specimens were obtained along the border of normal and lesional skin (Figure, B and C), and she underwent transesophageal echocardiography.A, Stellate purpura with overlying flaccid bulla on the medial aspect of the ankle.

B, Partially necrotic epidermis with intraepidermal bulla formation with marked perivascular infiltrates in the deep dermis and subcutaneous tissue (hematoxylin-eosin, original magnification ×25).

C, A small blood vessel occluded with fibrinoid material with a perivascular lymphoneutrophilic infiltrate (hematoxylin-eosin, original magnification ×400).


His medical history was significant for type 2 diabetes mellitus and hypertension, which were managed with metformin, glimepiride, and atenolol.Physical examination revealed hyperpigmented annular plaques with violaceous borders on his scalp and the superior part of his forehead (Figure, A).

The eruption began during the summer 3 months before presentation.

There were violaceous papules on the dorsal aspect of the hands (Figure, B), extensor surface of the arms, and the nape of the neck.Physical examination findings.

A, Hyperpigmented annular plaques with violaceous borders on the scalp.

B, Violaceous papules on the dorsal aspect of the hands.

C, Histopathologic analysis of violaceous eruption on the hand.

Lymphocytic infiltrate at the dermoepidermal junction (hematoxylin-eosin, original magnification ×10).A punch biopsy specimen was obtained and sent for histopathologic evaluation (Figure, C).


The lesions subsequently involved her chest, abdomen, and back and flared with sun exposure.

Biopsy samples were obtained for histopathologic evaluation.A, This case shows well-demarcated plaques with an overlying scale crust occurring in a photodistributed pattern on the central face.

C, Hematoxylin-eosin, original magnification ×10.Laboratory findings were significant for positive antinuclear antibody titers at 1:640, lymphopenia, and normocytic anemia.

Test results were negative or within normal limits for levels of antiribonucleoprotein, antihistone, antiphospholipid, anti-Smith, anti-Ro/Sjögren syndrome antigen A, and anti-La/Sjögren syndrome antigen B antibodies, C3, C4, CH50, rapid plasma reagin, and creatinine; erythrocyte sedimentation rate; and a comprehensive metabolic profile.

Urinalysis results were within normal limits.

A diagnosis of lupus erythematosus (LE) was favored, but the lesions failed to improve on a regimen that included hydroxychloroquine sulfate, fluocinonide ointment, 0.05%, and tacrolimus ointment, 0.1%.

B, Hematoxylin-eosin, original magnification ×4.

A biopsy specimen was obtained (Figure, B and C).


The patient had received a diagnosis of human immunodeficiency virus (HIV) infection 4 months before, with a nadir in his CD4 count of 11/μL.

He started highly active antiretroviral therapy, with improvement in his CD4 count to 101/μL most recently.

In addition to highly active antiretroviral therapy, he received combined sulfamethoxazole and trimethoprim and azithromycin prophylaxis.

During the past few months, he had reported increasing fatigue and intermittent fevers thought to be owing to immune reactivation syndrome.

His visual acuity was 20/150 OD and 20/100 OS, and intraocular pressures were 6 and 10 mm Hg, respectively.

On slitlamp examination, both eyes were injected with diffuse mutton-fat keratic precipitates and had more than 50 cells per 1×1-mm slitlamp high-power beam in the anterior chamber.

Results of a dilated ophthalmoscopic examination revealed bilateral vitritis, hyperemic optic nerves, and extensive whitening likely involving all layers of the retina (Figure 1).

After 48 hours of treatment, his condition did not improve.Marked vitritis, hyperemia of the optic nerve, and coalescent areas of retinal whitening involving the posterior pole are seen in the left eye.

He was hospitalized and started therapy consisting of intravenous (IV) acyclovir sodium, 10 mg/kg every 8 hours, and prednisone, 30 mg/d.

Samples for a laboratory workup for infectious causes were obtained.


He had no ocular history, was not taking any medications, and had no known drug allergies.

He smoked 2 to 4 packs of cigarettes per day, consumed 1 to 3 alcoholic drinks per day, and denied illicit drug use.

He had experienced eye redness for 1 week, which resolved with use of artificial tears; a mild posterior headache; and paresthesias of the left thumb and index and middle fingers.His medical history was significant for epilepsy as a child, although he had been seizure free for more than 10 years without medication.

He denied recent travel, vaccinations, systemic illnesses, or influenza-like symptoms.His best-corrected visual acuity was 20/20 OD and 20/100 OS.

Amsler grid testing revealed a central scotoma in the left eye.

No afferent papillary defect was apparent.

Results of the external and anterior segment examinations were unremarkable, and no vitreous inflammation was noted.

Results of the neurologic examination revealed decreased sensation to light touch, vibration, and temperature in his left upper and lower extremities.A, Subretinal and retinal pigment epithelial lesions (arrowheads) are visible in the left eye.

Figure 1 shows findings of the posterior segment examination.

The arrowheads outline the border of the area that was hypofluorescent in the early frames (not shown).


The patient lives in the southeastern United States and had no reported history of unusual exposures or insect or tick bites.A, A blanching, erythematous, macular rash present on the patient’s cheeks.

Physical examination findings were significant for ill appearance, bilateral nonexudative conjunctivitis, shotty bilateral anterior cervical lymphadenopathy, diffuse abdominal tenderness (greatest in the right upper quadrant), and associated rebound and guarding.

There was also a blanching, erythematous, macular rash on his cheeks (Figure, A) and an intermittent, erythematous, reticular rash on his chest, abdomen, arms, and legs (Figure, B) that spared his palms and soles and flared with fever.

Laboratory studies were significant for an elevated aspartate transaminase level of 264 U/L (reference range, 12-47 U/L; to convert to microkatals per liter, multiply by 0.0167) and an alanine transaminase level of 251 U/L (reference range, 17-63 U/L; to convert to microkatals per liter, multiply by 0.0167).

A complete blood cell count revealed leukopenia with a white blood cell count of 28 300/µL (to convert to ×109/L, multiply by 0.001) (neutrophils, 64%; lymphocytes, 18%; monocytes, 4%; eosinophils, 2%; basophils, 1%; and bands, 11%), a low-normal hemoglobin level of 11.4 g/dL (to convert to grams per liter, multiply by 10), and thrombocytopenia with a platelet count of 610 × 103/µL (to convert to ×109/L, multiply by 1).

Computed tomography of the abdomen revealed a dilated appendix (7 mm) with mucosal hyperemia and an internal appendicolith; acute appendicitis could not be excluded radiographically, so the patient was admitted for further workup because of a concern for acute abdomen.

The remainder of his examination findings were unremarkable.

B, An example of an intermittent, erythematous, reticular rash present on the patient’s left arm.


She had no significant medical history, had quit smoking cigarettes 4 year prior to presentation, but had a 20 pack-year smoking history.

She had no pain or neurosensory disturbances related to the lesion; however, she did have difficulty tolerating a regular diet owing to the bulk of the mass.

Findings from the physical examination were notable for a 4.9-cm exophytic, nodular, slightly mobile mass of the left lower posterior alveolar ridge, involving the buccal and lingual gingiva.

Previous biopsy demonstrated squamous mucosa with ulceration and chronic inflammation.

Contrasted computed tomography revealed an exophytic complex mass with areas of calcification and ossification inferiorly and a necrotic, cystic irregularly enhancing portion superiorly (Figure, A-C).

The mass was excised, and teeth 20 to 26 were removed.

The alveolar ridge was recontoured, and the incision was closed primarily.A-C, Computed tomographic (CT) scans.

An additional biopsy was performed (Figure, D).

D, Histopathologic image of biopsy specimen.


She had no significant use of tobacco or alcohol in the past.

She had not experienced any dysphagia, dysphonia, dyspnea, fevers, or weight loss.

Findings from an otoscopic examination was unremarkable.

Nasopharyngoscopy was performed and failed to reveal any masses, ulcerations, or mucosal lesions.

A magnetic resonance image (MRI) revealed an enhancing 1 × 6-mm lesion in the left side of the posterolateral tongue base (Figure, A).

A biopsy of the mass revealed an intermediate-grade infiltrating neoplasm forming solid sheets and glandular structures (Figure, B).

The tumor cells stained positive for CK7 and p63, and negative for CK20, p16, and S-100 by immunohistochemical analysis.

Stain for mucicarmine was positive in glandular areas (Figure, C).

After establishing the diagnosis, the patient was taken to the operating room for a left base of tongue resection via suprahyoid approach along with a left-sided neck dissection of levels I to IV.

The tumor was removed with negative margins, and no positive cervical lymph nodes were found on final pathologic analysis.A, Magnetic resonance (MRI) image of a lesion in the left side of the posterolateral tongue base.

B, Intermediate-grade infiltrating neoplasm forming solid sheets and glandular structures.

Hematoxylin-eosin, original magnification ×20.

C, Mucicarmine stain in the glandular area, original magnification ×40.


During the course of the second chemotherapy treatment, she developed left-sided mandibular pain.

At initial evaluation by the otolaryngology service on hospital day 32, she had decreased sensation at the left mandibular branch of the trigeminal nerve and ecchymoses along the mandibular buccal-gingival borders bilaterally with induration of the left floor of mouth and buccal mucosa (Figure, A).

A computed tomographic scan revealed cellulitic changes along the buccal cortex of the mandible and a small 2 × 12-mm abscess formation.

Magnetic resonance imaging revealed a 7 × 10 × 35-mm abscess involving both gingival and lingual aspects of the left anterior mandible (arrowheads) (Figure, B).

Biopsy specimens of the right mandibular gingiva are shown in the Figure, C and D.A, Patient photograph.

C and D, Histopathologic images from biopsy specimens.

She was febrile at admission and treated empirically with antifungal, antibiotic, and antiviral medications in the setting of cultures that were negative for organisms.

The initial chemotherapy regimen failed, requiring a more aggressive regimen, which left her pancytopenic.

She continued to receive broad spectrum antimicrobial and antifungal coverage.

By hospital day 38, the patient had developed evidence of ischemia and necrosis along the gingival and lingual aspects of the left mandibular alveolar ridge, extending past midline to involve mucosa on the right side.


There was no history of dysphagia, hoarseness of voice, dyspnea, or constitutional symptoms, such as fever, weight loss, or night sweats.

Clinical examination revealed a 7 × 6-cm, well-defined, firm, nontender swelling extending from the angle of the mandible to the clavicle.

Oropharyngeal examination revealed a mucosal bulge on the lateral pharyngeal wall with normal overlying mucosa.

A computed tomographic (CT) scan of the neck was performed, which revealed a solid 7 × 8 × 10-cm right carotid space mass, with a few cystic areas and coarse specks of calcification within (Figure, A, yellow arrowhead).

It showed heterogeneous postcontrast enhancement, predominantly around the calcific foci.

It extended from the C2 to D1 vertebral level and displaced the right common carotid artery and internal jugular vein anterolaterally (Figure, A, red arrowhead).

Fat planes around the mass were well maintained (Figure, B, arrowheads), and there was no bone destruction.

A biopsy was performed from the mass (Figure, C and D).A, Axial postcontrast computed tomographic (CT) image of the neck.

B, Coronal postcontrast CT image of the neck.

C, Hematoxylin-eosin, original magnification ×200.

D, Hematoxylin-eosin, original magnification ×400.


The patient had a history of myelodysplastic syndrome (refractory anemia with excess blasts–2), prostate cancer treated with prostatectomy and radiation therapy 5 years prior, and colonic adenocarcinoma treated with right hemicolectomy 6 years prior.

Four months before presentation, his myelodysplastic syndrome transformed into acute myeloid leukemia (AML).

However, remission was successfully induced with mitoxantrone hydrochloride and etoposide therapy, as confirmed by bone marrow biopsy, and he was prescribed continuing melphalan therapy on an outpatient basis.Three days prior to presentation, the patient on awakening noticed an acute onset of blurred vision in his left eye without any pain, photophobia, diplopia, vision loss, or floaters.

Visual acuity was 20/20 in the right eye and 20/30 in the left.

External examination had unremarkable results.

Pupillary and motility assessments had normal results.

Intraocular pressure was elevated bilaterally, measuring 29 mm Hg in the right eye and 41 mm Hg in the left.Slitlamp examination of the right eye revealed a 0.5-mm hypopyon with small hemorrhages on the iris surface (Figure 1A).

In the left eye, examination demonstrated a 1.5-mm hypopyon mixed with hemorrhage, 1+ cells in the anterior chamber, and small hemorrhages on the iris surface (Figure 1B).

Bilaterally, gonioscopy revealed open angles with few hemorrhages in the angle but no neovascularization.

Dilated fundoscopic examination had unremarkable results bilaterally, with no retinal hemorrhages or optic disc swelling.Color slitlamp photographs illustrating bilateral hypopyon (black arrowheads) with iris surface hemorrhages (white arrowheads).

He was randomized to experimental drug CPX-351 for induction, but treatment was discontinued as a result of renal failure.

He had no history of ocular surgery or trauma.


Routine laboratory test results showed total bilirubin of 4.74 mg/dL (to convert to millimoles per liter, multiply by 17.104) and amylase of 1.041 U/L (to convert to microkatals per liter, multiply by 0.0167).

An abdominal ultrasonography scan demonstrated gallstones and a mildly dilated common bile duct (CBD).

Magnetic resonance imaging of the abdomen confirmed these results and revealed cholelithiasis.

Multiple gallstones were found within a dilated region of cystic duct.

The patient consequently underwent urgent laparoscopic cholecystectomy with intraoperative cholangiography (Figure, A).

Intraoperative cholangiography revealed an unusual anatomical variant and subsequent transcystic choledochoscopy was performed, which demonstrated a double lumen at the distal CBD (Figure, B).


He did not report any previous abdominal surgery.

The patient stated that he had not had any procedures with intravascular instrumentation in the past year, dental cleanings, intravenous drug use, cutaneous abscesses, or recent trauma.

The pain was sharp and constant with intermittent radiation to the back and associated anorexia with a 10-kg weight loss.

Physical examination revealed he was afebrile and in normal sinus rhythm; there was minimal epigastric abdominal tenderness without signs of peritonitis and no palpable masses.

Femoral pulses were palpable and symmetric.

Laboratory examination revealed mild anemia (hematocrit, 35% [to convert to a proportion of 1.0, multiply by 0.01]), no leukocytosis, and an elevated erythrocyte sedimentation rate (71 mm/h).

Blood and urine cultures were negative for organisms.

A computed tomographic (CT) angiogram showed asymmetric attenuation surrounding the infrarenal aorta (Figure 1).

On comparison, a CT scan that was performed 6 months before presentation had identified no aneurysmal disease.Computed tomographic scan with arterial phase intravenous contrast with asymmetric attenuation surrounding the infrarenal aorta.


She reported having a rectangular area of discolored skin for the past 10 years that developed as a result of a complication during an interventional radiology procedure for treatment of a splenic aneurysm.

She denied international travel, drug use, incarceration, and high-risk sexual behavior.The patient had a history of uterine cancer at age 25, for which she underwent hysterectomy and chemotherapy.

She also had a history of breast cancer in her 40s, for which she underwent lumpectomy and tamoxifen therapy.

She had undergone surgical excision of a gastric polyp in her early 50s.

She had no history of radiation therapy.On physical examination she was well-appearing and afebrile, with normal vital signs.

Two months prior to presentation this lesion became painful and enlarged, without improvement with triamcinolone cream or oral antibiotics.

She also reported recent fevers, night sweats, nausea, and fatigue.

There was a 12 × 7–cm indurated pink and deep purple plaque on the right side of the abdomen, with 2 focal areas of ulceration (Figure).

Extending outward from this plaque were finger-like projections of purple subcutaneous papules.

Inferior to the plaque there was an approximately 3-cm, tender, orange-to-yellow patch.


The headaches were severe enough to interfere with daily activities, occurred several times weekly, and were associated with nausea, vomiting, photophobia, and sensitivity to noise.

Funduscopic and neurologic examination results were normal.

A diagnosis of migraine headaches was made, but therapeutic trials with nonsteroidal anti-inflammatory drugs and sumatriptan were unsuccessful.


The patient explained that he usually plays soccer and sweats abundantly.

Physical examination revealed creamy yellow concretions along several hair shafts, in both armpits, with strong axillary odor (Figure, A).

These concretions did not disappear when cleansed with alcohol.

Hair samples of the affected areas were sent for microscopy examination (Figure, B-D) and microbiologic culture.

Confirmation of the suspected diagnosis was made with the results of complementary tests.A, Clinical photograph of axillary hairs shows creamy yellow concretions along several axillary hairs.

B, Direct microscopic examination of the hair shaft (original magnification ×40).

C, Periodic acid–Schiff stain (original magnification ×400).

D, Grocott silver stain (original magnification ×400).

Treatment with antiseptic soap and a miconazole nitrate cream was initiated.

He did not apply deodorant or any other products in the underarm, and he ensured proper hygiene of the area.

After 2 weeks of treatment, the lesions had resolved and the patient had normal axillary hairs.


He had initially developed lesions on his legs, which then spread to his neck, chest, and buttocks.

This eruption was asymptomatic, and the patient reported no history of vesiculation.

His mother noted minimal evolution of the lesions, except for recent flattening of those on the legs.

Physical examination showed numerous discrete (1 to 3 mm) smooth brown papules concentrated on the neck, chest, anterior and lateral thighs, and buttocks (Figure 1).

Several lesions had a positive Darier sign (Figure 1A).A, Multiple small brown papules of the chest.

Localized erythema developed around several lesions after firm stroking.

B, Scattered small brown papules of the lateral thigh.There was no family history of similar lesions.

A punch biopsy of a papule on the left thigh was performed, and the specimen was submitted for pathological review.


Her history was remarkable for rheumatoid arthritis treated with oral gold salts 15 years ago, but the total dosage of gold salts could not be determined.

These pigmented lesions corresponded exactly to areas that had previously received laser treatment.

A skin biopsy specimen of the lesion on the right side of the woman’s face was obtained, and histopathologic evaluation was conducted.A, Diffuse blue to slate-gray patches developed on the face, corresponding exactly to areas that had previously received laser treatment.

Rechallenge with the original Q-switched Nd:YAG laser was administered on the right forearm, and a similar slate-gray macule developed immediately (Figure 1B).

B, A rechallenge test administered on the right forearm with the original Q-switched Nd:YAG laser yielded a similar slate-gray macule (arrowhead).


One year later, the patient complained of a 1-month history of gradually worsening vision in the right eye.

On examination, her best-corrected visual acuity was 20/20 OD and 20/20 OS.

An external examination revealed ptosis of the right upper eyelid covering 40% of the surface of the eye.

In each eye, the pupil, intraocular pressure, motility, and confrontational visual field were normal.

An anterior segment examination revealed mild nuclear sclerotic cataracts in both eyes.

A dilated fundus examination of the right eye was notable for revealing infarcts in several nerve fiber layers along the arcades and nasal to the optic disc and a few microaneurysms nasal to the optic disc.

Fluorescein angiography of the right eye (Figure, A) revealed multiple areas of staining nasal to the nerve and inferotemporal to the nerve and to the areas of pinpoint leakage within the macula.

No abnormalities were noted during the fundus examination of her left eye.

Her visual acuity was 20/400 OD and 20/20 OS.

A fundus examination of the right eye revealed thickening in the macular region.

Optical coherence tomography of the right eye (Figure, B) revealed a central macular thickness of 454 μm and the presence of subretinal fluid in the subfoveal region.A, Fluorescein angiography of the right eye illustrating areas of staining nasal to the nerve and inferotemporal to the nerve and to the areas of pinpoint leakage within the macula.

She was observed and followed up every 4 months.


He had seasonal allergies but was otherwise healthy.

He had not been wearing his contact lenses since the episodes started.

A, The photograph shows eyelid edema and erythema, conjunctival injection, and a raised inflamed papule on the upper cheek.

Conjunctival cultures for bacteria or viruses (including adenovirus and herpes simplex virus) were negative.The patient’s visual acuity with eyeglasses was 20/20 OU.

Findings from examination of the right eye were significant for lower eyelid follicles and mild conjunctival injection.

A nontender preauricular lymph node was noted as well as a raised erythematous papule on the patient’s upper cheek (Figure 1A).

Findings from examination of the skin revealed multiple raised papules on the right elbow and knee that were diagnosed as warts by the patient’s dermatologist (Figure 1B).

The patient’s symptoms persisted despite previous treatment regimens with topical corticosteroids for atopic conjunctivitis and topical antibiotics for staphylococcal blepharitis.

These papules had been present for about 6 months and, despite the use of topical salicylic acid and cryotherapy, they continued to spread.External photograph of the patient's right eye at presentation.


Medications included metoprolol and aspirin.

On examination, he was alert and oriented and vital signs were normal; body mass index was 24.

He reported unintentional weight loss without fevers or decreased appetite.

Neurologic examination revealed right eye heterotropia and nasal upshoot indicative of a fourth cranial nerve palsy (Figure 1A), left ptosis, flattening of the right nasolabial fold (Figure 1B), and bilateral restricted upgaze and ataxia (Video).

Results of a basic metabolic panel and complete blood cell count were normal.

Screening for human immunodeficiency virus, Lyme disease, and drug use was negative.

Contrast-enhanced magnetic resonance imaging (MRI) of the brain was unremarkable.

Cerebrospinal fluid (CSF) sampling revealed elevated protein (75 mg/dL [reference range, 10-42]), lymphocyte predominant pleocytosis (21-66 cells/uL [reference range, 0-11]), and oligoclonal bands (OCBs).

Pleural thickening was seen on routine chest radiography; chest computed tomography (CT) revealed mediastinal lymphadenopathy, subcentimeter pulmonary nodules, and calcified pleural plaques.A, Right fourth cranial nerve palsy.

On adduction, the right eye turns upward.

This finding (nasal upshoot) suggests the presence of a fourth nerve palsy.


When the patient was aged 4 weeks, the lesion became ulcerated and she was admitted to our hospital.

The patient had no systemic symptoms and was discharged and scheduled for an outpatient dermatology appointment.Physical examination showed a well-nourished, well-developed infant whose gluteal region had well-demarcated ulcers with scalloped borders on either side of the midline, superior to the anal verge.

The base of the ulcers was covered with fibrinous material and the residue of topical medications.

Bright red matted telangiectasias extended from the anus to the ulcers (Figure).Two well-demarcated ulcers covered with white fibrinous material.

She was initially treated at an outside hospital with intravenous clindamycin hydrochloride for presumed perianal cellulitis and was discharged with a regimen of oral clindamycin hydrochloride.

She was given intravenous antibiotics and mupirocin, 2%, ointment, triamcinolone, 0.1%, ointment, clotrimazole, 1%, cream, nystatin cream, and zinc oxide paste.

Results of cultures for bacteria and herpes simplex virus were negative.


Her medical history was significant for localized invasive ductal carcinoma of the right breast treated with wide local excision 13 years previously.

At presentation she was considered disease-free.

Six months later the patient developed discomfort around her right ear, prompting a referral to the local otolaryngology service.

Findings from the clinical examination, including otoscopy, were unremarkable.

A magnetic resonance imaging (MRI) scan revealed an 8-mm lesion within the right parotid gland with a spiculated border and ill-defined surrounding enhancement extending close to the stylomastoid foramen (Figure, A).

This was of low T2 signal with no perineural spread evident.

A fine-needle aspirate and core biopsy were obtained under ultrasonographic guidance.

The cytologic findings showed loosely cohesive groups of atypical epithelial cells.

Histologic examination of the core biopsy revealed an infiltrative lesion composed of cords and nests of medium-sized cells surrounded by a densely hyalinized stroma (Figure, B).

The cells contained hyperchromatic vesicular nuclei with moderate amounts of eosinophilic cytoplasm (Figure, C).

Immunohistochemical analysis showed the cells were diffusely positive for cytokeratin 7 (CK7), estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (Figure, D).A, Axial fast spoiled gradient echo gadolinium-enhanced magnetic resonance imaging (MRI) scan with fat suppression demonstrating lesion of the right parotid gland (arrowhead).

This resolved with oral steroids and antiviral drugs consistent with a presumed diagnosis of idiopathic facial nerve (Bell) palsy.


Initially the lesion appeared to be acutely inflamed with erythema, overlying crusting, and tenderness to palpation.

The child was otherwise healthy, and the parents stated that he had no systemic symptoms such as fever or weight loss.

On physical examination, a 1.5-cm superficial, ovoid firm lesion was noted in the left postauricular area (Figure, A).

While the lesion was attached to the skin, it was mobile over the mastoid bone.

There were no middle ear abnormalities on physical examination.

Ultrasonography of the lesion revealed a nonvascular, well-circumscribed 1.7 × 1.4 × 0.6-cm lesion in the soft tissue posterior to the left ear.

It demonstrated a heterogenous echotexture but was predominantly hypoechoic without internal vascularity or distinct calcifications.

Pathologic examination revealed a neoplasm extending from the reticular dermis into the subcutaneous adipose tissue (Figure, B).

There were lobules of lipidized histiocytic cells with eosinophils in a background of collagen (Figure, C).

The lesion stained negatively for S-100 and CD1a (Figure, D).A, Gross photograph of left postauricular mass.

B, High-powered (original magnification ×100) view depicting some pale areas representing lipidized cells.

C, High-powered (original magnification ×400) view demonstrating pale, foamy cells (xanthoma cells).

The child was treated with a course of antibiotics.

The lesion had distinct borders and separated easily from the surrounding soft-tissue attachments.

It was completely excised, including the overlying skin.

Four weeks after the initial evaluation, the acute inflammation had resolved, but the lesion had increased in size.

Excisional biopsy under general anesthesia was performed owing to rapid enlargement and unclear etiology of the lesion.

B-D, Histopathologic images (hematoxylin-eosin).


His medical history was significant for hypertension and coronary artery bypass surgery.

He reported numbness of the lower lip and difficulty on swallowing.

On intraoral examination, the mass was hard in consistency with relatively normal overlying mucosa.

Computed tomographic (CT) images with bone window showed a grossly expansile, multilocular, low-attenuation lesion of the anterior segment of the mandible (Figure, A and B).

The images demonstrated severe erosion of the facial and lingual cortices with a remarkable scalloping pattern, and multiple wispy, ill-defined intralesional septa.

Soft-tissue CT images indicated a cystic and solid nature of the mass (Figure, C and D).


She stated that she had no other symptoms, and her family medical history was not remarkable.

On examination, the rigid indirect laryngoscopy revealed yellowish floppy granular proliferation affecting the bilateral arytenoids and posterior aspects of the aryepiglottic folds, with symmetrical vocal cord motion (Figure, A).

The main lesions were clearly demarcated from the surrounding normal mucosa.

The specimens mounted on the hematoxylin-eosin slides showed eosinophilic amorphous material underlying the epithelium (Figure, B).

Staining for thioflavin T revealed yellow-green fluorescence (Figure, C).

The fibrillar component emitted a characteristic apple-green birefringence under polarized light after binding to Congo red dye.

No clinical evidence of systemic involvement and/or plasma cell dyscrasia was found.A, Endoscopic examination demonstrated symmetric yellowish lesions affecting the arytenoids and posterior aspects of the aryepiglottic folds, with a patent airway and mobile vocal folds.

B, Eosinophilic amorphous material underlying the epithelium (hematoxylin-eosin, original magnification ×200).

C, Thioflavin T exhibited a typical yellow-green fluorescence after binding to amyloid fibrils (original magnification ×200).

The patient then underwent microlaryngeal surgery with biopsy under general anesthesia.

The nidus was fragile and bled copiously when traumatized.


On examination, she had a 6-cm nontender mass in the submentum.

Her floor of mouth (FOM) was soft, and there was no cervical lymphadenopathy.

Ultrasonography (US) (Figure, A) revealed a well-circumscribed, avascular, homogeneous, isoechoic lesion, measuring 6.2 × 6.0 × 6.0 cm along the FOM and left submandibular regions.

Magnetic resonance imaging (MRI) of the neck revealed the lesion within the FOM, above the mylohyoid muscle.

The lesion involved the root of the tongue in the midline and extended to the left, causing significant thinning of the left mylohyoid muscle without extension through it.

The lesion demonstrated a fluid signal with T2 hyperintensity (Figure B), T1 hypointensity (Figure, C), and peripheral rim enhancement.

Mild restricted diffusion was also noted.

The mass was encapsulated and positioned above the mylohyoid muscle and extended into the FOM between bilateral genioglossus muscles.

The mass was removed entirely via transcervical excision.A, Sagittal midline ultrasonography shows a floor of mouth lesion with uniform low-level echoes.

B, Axial T2-weighted magnetic resonance image (MRI) revealing a hyperintense lesion involving the floor of mouth.

C, Coronal postcontrast MRI revealing a T1 hypointense unilocular lesion involving the floor of the mouth and root of the tongue.

Attempted open biopsy at the time of thyroidectomy revealed only adipose tissue.

The patient underwent transcervical excision of the mass (Figure, D).

D, Intraoperative photograph during mass excision.


He noted a childhood history of plantar warts and believed these lesions to be identical in appearance.

He had received his third cycle of R-CHOP (rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine sulfate, prednisone) 2 weeks prior to presentation as well as an injection of granulocyte-colony stimulating factor.

He also complained of a pruritic rash on his left thigh that had started several days before the appearance of his plantar foot lesions.

It was exquisitely tender to palpation, and the patient was visibly uncomfortable when walking.

The patient was afebrile, and his vital signs were within normal limits.

Physical examination revealed grouped, brown, flat-topped papules on his distal plantar left foot (Figure).

He also demonstrated erythematous papules and plaques on his posterolateral thigh.

Laboratory studies revealed pancytopenia, with a white blood cell count of 2800/μL, hemoglobin level of 11.6 g/dL, and a platelet count of 81 × 103/μL.

His lactate dehydrogenase level was elevated at 914 U/L, and results of his comprehensive metabolic panel were unremarkable.

He was anticipating his fourth cycle of treatment the day of his presentation.

He did not recall any injury or unusual exposure.

(To convert white blood cell count to ×109/L, multiply by 0.001; to convert hemoglobin to grams per liter, multiply by 10; to convert lactate dehydrogenase to microkatals per liter, multiply by 0.0167.


She had been prescribed total parenteral nutrition prior to referral.

On presentation, her physical examination was remarkable for mild epigastric tenderness.

The results of laboratory testing, including a complete blood cell count, chemistry values, liver function tests, and amylase and lipase levels, were unremarkable.

Computed tomography demonstrated focal gastric thickening.

Esophagogastroduodenoscopy with endoscopic ultrasonography was performed that confirmed a submucosal gastric mass (Figure, A).

A fine-needle aspiration biopsy revealed benign and reactive glandular cells and debris.

Magnetic resonance cholangiopancreatography demonstrated a 2.4-cm hypervascular and exophytic mass in the gastric antrum and locoregional lymphadenopathy (Figure, B).A, Endoscopic ultrasonography of the gastric antrum mass reveals an area of gastric thickening (arrowheads) corresponding to computed tomographic findings.

A fine-needle aspiration biopsy was nondiagnostic, showing gastric antral-type mucosa without pathologic changes (inset).

B, The coronal image in T2 phase reveals a 1.8 × 2.4 × 1.5-cm hypotense lesion (arrowhead) in the gastric antrum.

The lesion was also enhanced on T1 arterial phase sequencing.

During endoscopy, this area was visualized grossly as a bulge in the atrium along the incisura.


The patient described a history of sleep apnea, a remote transient ischemic attack with left-sided weakness, and a prior thyroidectomy.

She had increasing fatigue during the last 6 months, as well as worsening anxiety.

On physical examination, the neck was supple, with no palpable masses or lymphadenopathy, and had a well-healed transverse neck incision.

Magnetic resonance imaging revealed a 1.1-cm, round, partially enhancing, cystic mass near the tail of the parotid gland that appeared hypointense on T2-weighted imaging (Figure 1).

An enlarged and distended venous structure that measured up to 7 mm was also visualized in the area.

Laboratory work revealed no abnormalities.Magnetic resonance images of the parotid gland.

T1-weighted image (A) and T2-weighted image (B) revealing a round, partially enhancing, cystic mass near the tail of the parotid gland (white and red arrowheads).


She was not taking any medications because 2 weeks after starting celecoxib, her joint pain resolved and she discontinued use without recurrence of pain.

The patient had no family history of autoimmune diseases.

She reported no joint swelling or morning stiffness.

The patient reported no history of fever, weight loss, photosensitivity, malar rashes, skin thickening, oral or nasal ulcers, weakness, Raynaud phenomenon, sicca symptoms, chest pain, shortness of breath, or abdominal pain.

She previously saw her primary care physician who prescribed celecoxib (for joint pain) and ordered antinuclear antibody (ANA) testing, which was positive at a value of 1:80 (Table).

On examination, her vital signs, including blood pressure, were normal; and results of skin, thyroid, musculoskeletal, mucus membranes, cardiovascular, pulmonary, and neurologic examinations were all normal.

She was then referred to the rheumatology clinic.


She had a history of type 2 diabetes mellitus, hypertension, hyperlipidemia, and allergic rhinitis.

Her medications included metformin, lisinopril, and verapamil.

Her cardiac and pulmonary examinations were normal.

The spleen was palpable 5 cm below the left costal margin.

Laboratory evaluation revealed a white blood cell (WBC) count of 91 ×103/μL, with 54% neutrophils, 1% blasts, 2% basophils, 8% metamyelocytes, 23% myelocytes, and 1% promyelocytes (increased immature granulocytes).

Hemoglobin level was 11.7 g/dL and platelet count was 290 000 (Figure 1).


His medications included amiodarone, furosemide, nifedipine, insulin glargine, and allopurinol.

The lesions were pruritic at times and the patient reported no improvement with chlorhexidine wash or hydrocortisone, 1%, cream.

He denied preceding trauma, recent travel, or new medications.A, Red, scaly papules on the patient's forearm.

He was otherwise asymptomatic, and review of his systems revealed no abnormalities.

B, Punch biopsy specimen from the center of a papule on the forearm shows pseudoepitheliomatous hyperplasia, spongiosis with vesiculation, intraepidermal neutrophilic microabscesses, focal subepidermal bulla formation, and dermal infiltrate of neutrophils, lymphocytes, and histiocytes (hematoxylin-eosin, original magnification ×4).Physical examination revealed numerous red to violaceous scaly papules symmetrically distributed on both forearms.

Laboratory tests revealed a serum creatinine level of 3.79 mg/dL (normal range, 0.70-1.40 mg/dL) and serum iodine level of 42 305 ng/mL (normal range, 40-92 ng/mL).

A punch biopsy was obtained from the center of a papule on the right forearm (Figure, B).


On further questioning, the patient noted that between her hospitalizations she had gone home and cleaned her fish tank, played with her pet cat, and gardened in her indoor cactus garden.

She said she had not recently traveled, and was not taking any immunosuppressive medications.

A few days after that discharge, the patient noticed a painful ulceration on the right distal forearm, at the site where a peripheral intravenous catheter had been inserted during her initial hospitalization.

On physical examination, the patient had an ulcerated plaque on the right forearm with 2 tender, 1- to 2-cm red nodules in the right antecubital fossa (Figure, A).

A skin biopsy and culture were performed from the forearm lesion (Figure, B and C).A, An ulcerated plaque on the right forearm.

Note 2 tender, 1- to 2-cm red nodules in the right antecubital fossa.

Hematoxylin-eosin, original magnification ×20.

The patient had been discharged approximately 2 weeks prior, after an admission for congestive heart failure.


The patient reported using an aluminum-containing antiperspirant spray for years before the onset of the eruption but had since discontinued use of deodorants or antiperspirants without improvement in her lesions.

Her medical history was significant only for epilepsy, and her daily medications included lamotrigine and cholecalciferol.Physical examination revealed multiple red-brown to purplish follicular papules and nodules in bilateral axillae with focal areas of scarring (Figure 1).

The areas involved were not itchy or tender but bothered her cosmetically.

No facial lesions were noted.Clinical examination findings.

Multiple red-brown papules within the axilla bilaterally.She did not improve with multiple medications, including topical antifungals, topical corticosteroids, oral ketoconazole, topical dapsone, doxycycline (40 mg/d), minocycline (100 mg twice daily), a combination of amoxicillin and clavulanate, and intralesional triamcinolone acetonide.

A 4-mm punch biopsy was performed on the right axilla for evaluation.


He had been born at full term and was otherwise healthy.

His medication regimen included a pediatric multivitamin.

It also appeared to encroach on the visual axis in the downgaze position.

The parents reported that the patient had started to rub his eyelid intermittently, causing irritation and a minimal amount of associated bleeding.Lesion on the right lower eyelid of an 11-month-old patient.

On examination, the patient’s pupils were equal in diameter and reactive to light, his ocular motility was full, and the lesion did not obstruct his vision.

Findings from external examination were significant for a single 3 × 2 × 2–mm, red-brown, raised, solid, fixed papule at the center of the lower eyelid margin.

There was no madarosis and no evidence of epiphora or conjunctivitis.

On examination 1 month later, the papule had grown slightly, with a 1 × 1–mm area of ulceration.

The lesion was initially diagnosed as a hemangioma and the decision was made to monitor it.

There was no history of trauma to the area.