A 61-year-old male patient who was operated due to laryngeal carcinoma six months ago. First, MDCT and then, whole body PET-CT scan (643 MBq F-18-FDG i.v.) was performed for the patient due to the lesion monitored on the right apical in PA radiography of the patient, who was followed up stably. The patient’s routine blood test results were within the normal ranges. A lesion of 15x10 mm with radially spiculated extensions, in irregular appearance and containing a few microcalcifications was monitored in the apical region of the right lung in thoracic CT (, ). No lymphadenopathy was detected in the mediastinum. It was observed during the PET-CT that the lesion had a moderate F-18FDG uptake (2.40 SUVmax) (). Apart from that, no significant pathologic finding was detected in the chest. In addition, no focus was detected during the PET-CT scan outside the thorax. The patient was first considered to have metastasis in the light of the existing findings. A wedge resection was performed for the patient’s lesion (). Microscopic examination of the surgical material showed a group of fungal hyphae, and the patient was diagnosed aspergilloma. The patient was not given any antifungal treatment because the entire region was cleaned within the surgical borders and there was not any other focus.


A 36-year-old lady presented with complaints of redness, foreign body sensation, and watering for 2 days in the left eye. She gave a history of dust entering the eye while boarding a roadside cab. She had unaided visual acuity of 6/6 in both eyes. The right eye was asymptomatic. Left eye examination revealed hyperemic bulbar and palpebral conjunctiva and motile minute white bodies on the conjunctival surface. There was no corneal involvement. Anterior chamber, lens, and posterior chamber examinations were normal. On direct ophthalmoscopy, bilateral fundus oculi was found healthy. Examination of left eye under slit lamp revealed several highly motile worm-like organisms of about 1-2 mm long moving on the external surface of the conjunctiva. These organisms moved away from the slit lamp beam to the fornix. They were immobilized using 0.5% propacain drops and were removed using McPherson Forcep under slit lamp examination. And, few were placed into a freshly opened vial containing tear drop solution for further investigation. The eye was irrigated with saline solution. The specimen was sent to microbiology laboratory for identification.
Light microscopy of wet mount prepared from the specimen showed spindle-shaped body with a pair of sharp, dark brown oral hooks, connected to a large internal cephalopharyngeal skeleton. The body was divided into segments, and each segment had tufts of numerous brown appendages at the margins. These findings were suggestive of first instar larvae of O. ovis []. The rest of the ocular examination was normal, so diagnosis of unilateral external ophthalmomyiasis was made.
The patient was advised for instillation of anti-inflammatory and antibiotic eye drops. The patient gradually improved and was completely asymptomatic on her next visit after 7 days.


A 53-year-old African-American man with a history of peptic ulcer disease, anxiety, renal insufficiency (baseline creatinine level, 1.7 mg/dL) was admitted for gross hematuria and left flank pain. He works as a mechanic, is married, and was a former smoker. His family history is significant for prostate cancer and high blood pressure. He was recently diagnosed with CML during an admission for weight loss, easy bruising, and fatigue. A bone marrow biopsy showed hyperplastic granulocytes with a maturation pattern consistent with CML. Further genetic analysis showed cells with a translocation between chromosomes 9 and 22, the genetic hallmark of CML. The cells were also positive for the genetic product of the translocation, a defective or deregulated tyrosine kinase, also known as the BCR-ABL protein, which is essential to the pathogenesis of the disorder. During that admission, he developed hematuria and bloody stools. A computed tomography scan of his abdomen and pelvis showed mild left hydronephrosis without obvious mass or stone, and his hematuria resolved. His gastrointestinal bleeding work-up included an esophagogastroduodenoscopy and colonoscopy. Several polypectomies resulted in prolonged bleeding, which ultimately resolved.
Before definitive treatment for his CML could be started, he again developed hematuria with mild left flank pain. Upper tract imaging was negative for an overt renal mass, and a cystoscopy found gross blood from the left ureteral orifice (). Ureteroscopy was performed, but no obvious cause of bleeding was found. Cytology showed left renal pelvis urine abundant in acute and chronic inflammatory cells with no evidence of malignancy.
Because of persistent bleeding without a treatable source, the patient was sent to interventional radiology for an angiography examination. A pseudoaneurysm was noted in the left renal artery at a small branch in the lower pole, and it was subsequently embolized (). The patient's bleeding stopped and his hematocrit remained stable until 2 days later when he became hypotensive because of sudden blood volume loss. He required vasopressors and intensive care admission. A repeat arteriogram revealed a site of bleeding into the retroperitoneum remote from the initial embolization (A). The patient continued to have hemodynamic instability and continued blood loss (B). Ultimately, he was taken for an emergent left nephrectomy ().
Final pathology of the removed kidney, several days later, showed CML infiltration with diffuse extramedullary hematopoiesis.
Postoperatively, the patient required prolonged respiratory support and hemodialysis. Hydroxyurea and colchicine were initiated to control the patient's leukocytosis and tumor lysis syndrome. He experienced 2 episodes of cardiac arrest and required prolonged vasopressor support. He was started on imatinib, a tyrosine kinase inhibitor, which has been shown to be an effective targeted therapy for CML. Fortunately, his condition improved and he was discharged on hospital day 71 on hemodialysis.


A 21-year-old male was diagnosed to have double outlet left ventricle with normally related great arteries, subaortic ventricular septal defect (VSD), and severe pulmonary stenosis for which he underwent VSD closure and placement of RV to PA conduit (16 mm Dacron) at the age of 6 months. He was subsequently lost to follow-up and was asymptomatic until 1-year ago when he started to have mild dyspnea on exertion. On evaluation, he had stable vitals and ejection systolic murmur of grade 2/6 with late peaking at the upper left sternal border.
Echocardiography showed dilated right atrium (8.5 cm × 7 cm) and right ventricle (8 cm × 7 cm). He also had severe RV dysfunction along with tricuspid valve inflow restrictive pattern. Pulsed Doppler of the tricuspid valve during diastole showed higher velocities during the early filling phase (e>a) [] and on tissue Doppler velocities assessment e’> a’ [] inferior vena cava (IVC) size was 2.59 cm on inspiration and IVC variation with respiration was 30%. There was severe stenosis of RV to PA conduit with peak gradient of 80 mmHg. The antegrade diastolic flow was detected [] which started after a gap, which correlated with isovolumic relaxation time phase. There was moderate tricuspid regurgitation with a maximum pressure gradient 72 mmHg. The anatomical features were defined by computerized tomography scan [Figure and ].
He underwent RVOT reconstruction with bovine pericardium and pulmonary valve replacement with a 21 mm bioprosthetic perimount valve (Edwards Life Sciences, Irvine, California, USA) after excision of the previously placed conduit. Postoperative course was uneventful and he was successfully extubated on the 2nd postoperative day.
Postoperative echocardiography showed well opened RVOT, peak gradient of 20 mmHg, laminar flow in branch pulmonary arteries, mild PR, RV systolic dysfunction in the form of RV fractional area change of 28%, and tricuspid annular plane systolic excursion (TAPSE) of 1.16 cm. RV diastolic dysfunction was present (Tricuspid valve inflow e > a and TDI a > e) suggestive of pseudonormalization. There was no diastolic antegrade flow seen across RVOT [] as was seen preoperatively, left ventricular ejection fraction was normal.


The patient was a 3-year-old previously healthy male who developed cough, congestion, and recurrent fevers with a maximum temperature spike of 102°F in the first week of January 2015. He was seen by his primary care physician 3 days prior to admission and was prescribed oral amoxicillin for possible streptococcal throat infection. During the next 2 days, the patient developed decreased oral intake with nonbloody, nonbilious vomiting and lethargy. He was brought to our hospital emergency department where he was found to be hypotensive (blood pressure: systolic/diastolic, 50-70/30-50s mm Hg), tachycardic (to the 130-150 beats/min), and obtunded with waxing and waning mental status. Bedside heart ultrasound demonstrated a large pericardial effusion with concerns of tamponade, and he underwent emergent pericardiocentesis, with 80 cc of yellow serous fluid drained. He was also intubated for increased work of breathing and altered mental status. He was then transferred to the intensive care unit and was started on epinephrine and norepinephrine drips to maintain normal blood pressure. His immunizations were current for age, except for the influenza vaccine, which he usually received annually; he had missed the current season because of change of medical insurance. His father had an upper-respiratory infection the week before the patient got sick.
Infectious diseases service was consulted for assistance with diagnosis and management of the patient. On our examination of the patient in the intensive care unit, his temperature was 102.3°F and heart rate 168 beats/min. He was on conventional ventilator support (settings: rate = 20; PEEP: 5; PIP: 22; FiO2: 40%; oxygen saturation: 97%), with blood pressures of 40-120/34-67 mm Hg. His weight was 15.7 kg (91st percentile). He was intubated and sedated. He had generalized edema, pupils round and reactive bilaterally, and no conjunctival injection or oral lesions. He had the full range of motion at the neck with no masses. Lungs were clear to auscultation bilaterally. His cardiovascular examination was remarkable for distant heart sounds with pericardial rub, increased capillary refill of 5 s with cold peripheral extremities, regular rate and rhythm, and no murmurs; the pericardial drain was in place with serous discharge. His abdomen was distended and firm.
His initial laboratory values were as follows: complete blood cell count of white blood cells (WBCs) of 13 × 10³/µL, with a differential of neutrophil 48%, bands 7%, lymphocytes 31%, and eosinophil 2.5%; platelet count of 148 × 10³/µL; and hemoglobin of 13 g/dL. His sedimentation rate was 9 mm/h and C-reactive protein <0.5 mg/dL. His blood urea nitrogen, serum creatinine, aspartate aminotransferase, alanine aminotransferase, and urine analysis were normal. B-type natripeptide was 102.9 pg/mL (normal <100 pg/mL).
Chest X-ray showed generous heart with perihilar atelectasis (). Ultrasound of the abdomen showed no intussusception, normal appendix, and small pockets of free fluid in the right upper and lower quadrants, with upper quadrant-free fluid appearing complex, with gallbladder wall thickening. EKG showed normal sinus rhythm, low voltage QRS, and nonspecific T wave abnormality. Echocardiography of the heart showed moderate to large circumferential pericardial effusion, with greatest dimension along the diaphragmatic surface (~1.8 cm), right atrial wall collapse during end diastole, qualitatively normal right-ventricular size and systolic function, and qualitatively mild to moderate concentric left-ventricular hypertrophy.
His winter respiratory panel from nasal wash specimen was positive for influenza A, reverse transcription polymerase chain reaction (RT-PCR) positive (H3N2). The blood cultures were collected before starting antibiotics were negative. The pericardial fluid Gram stain showed many WBCs and moderate red blood cells but no organism; aerobic, anaerobic, and viral culture were negative. Molecular testing for bacterial, fungal, and viral pathogens on pericardial fluid were sent to University of Washington 2 days after initiation of oseltamivir and antibiotics and were negative for influenza A/B, respiratory syncytial virus, entero/parechovirus, cytomegalovirus, parvovirus B19, adenovirus, and universal bacterial and fungal PCR. An aliquot of pericardial fluid and blood were also sent to the John Welsh Molecular Diagnostic Laboratory at Baylor College of Medicine for influenza PCR, which was negative. His purified protein derivative (PPD) test was negative.
Broad-spectrum IV antibiotics, vancomycin and cefotaxime, IV steroids, and oseltamivir via nasogastric tube were administered. Because of the patient’s persistent critical status and concern for poor absorption of oral oseltamivir, IV peramivir was administered at a dose of 10 mg/kg/dose every 24 hours for 5 days. Within 24 hours of IV peramivir administration, the patient recovered dramatically; he was extubated, and both epinephrine and norepinephrine drips were discontinued. Two days later, the pericardial drain was removed.
During recovery, the patient was noted to have truncal ataxia, possibly related to an influenza A induced encephalopathy, and he improved gradually over the following week. Follow-up echocardiography was normal. He was discharged home after 10 days of hospitalization. shows his clinical response and recovery. He and his family members received tetravalent influenza vaccine before discharge. He had a follow-up with the physical rehabilitation clinic a month later where he was found to be at his baseline function.


A 12-year-old male child was brought to the Ophthalmology Emergency Clinic with a history of decrease in vision of his right eye (oculus dextrus [OD]) of 1-week duration. There was no history of redness or pain OD. Trauma, ocular surgery or any major systemic disease in past was ruled out. On examination, the best corrected visual acuity OD was −6/9 with (0.25/−0.50 cyl × 90 [no improvement with pin hole]). In the left eye (oculus sinister [OS]) it was 6/5 with 0.50/−0.25 cyl 90. In both eyes (oculus uterque [OU]) anterior segment, direct and consensual pupillary reaction, intraocular pressure (12 mmHg), and extraocular muscle movements were normal. Color vision (Ishihara PseudoIsochromatic Chart) was normal OU.
Amsler chart testing OD showed metamorphopsia but was normal OS. Visual field charting (Humphreys Visual Field Analyzer C-120) was normal OU. Fundus evaluation showed the disparity in the cup-disc ratio (OD 0.1 and OS 0.3). Optic disc OD was hyperemic with blurred margins. There were horizontal striae in the posterior pole between the optic disc and the fovea and the parafoveal and perifoveal region deeper to the retinal blood vessels. The retinal blood vessels and the fovea appeared normal OS [ and ], optical coherence tomography (OCT) of macula OD showed folding of the inner retinal layers in the posterior pole, with a central thickness of 254 μ and a parafoveal thickness between 400 and 420 μ. Macular region OS was normal []. B-scan ultrasonography (USG) OD showed diffuse thickening of the choroid and sclera and was normal OS []. Fundus fluorescein angiography (FFA) showed early leakage of the dye from the disc OD and normal dye transit OS []. Magnetic resonance imaging (MRI) of the brain was normal, but right orbit showed diffuse isointense swelling that became hyperintense with contrast on T1-weighted and hypointense on T2-weighted images. The left eye was normal [-].
Complete blood count, differential count, erythrocyte sedimentation rate, C-reactive protein, sickledex, anti-nuclear antibodies, anti-cardiolipid antibodies, rheumatoid antibodies, antiphospholipid antibodies, serology for TORCH, VDRL, were normal. Chest X-ray was normal. Mantoux test was negative. Angiotensin conversion enzyme assay was normal.
A presumptive diagnosis of idiopathic posterior scleritis was made and the patient was treated with pulse methylprednisolone 1 g/day for 3 days followed by oral prednisolone 1 mg/kg body weight. This was tapered gradually over next 8 weeks.
Visual acuity improved to 6/6 (0.25/−0.50 cyl × 90) with a resolution of disc edema and flattening of the retinal striae within 4–6 weeks of initiation of above treatment [ and ].


A 61-year-old male patient with concurrent prostatic adenocarcinoma and an enhancing right-sided renal mass was referred to our robotic oncology center for evaluation and treatment. He had no comorbidity or previous surgery. Patient's sexual health inventory for men questionnaire score was 14, body mass index was 25.4 kg/m2, and digital rectal examination was normal. Serum creatinine and prostate-specific antigen were 1.0 mg/dL and 6.7 ng/mL, respectively. The prostatic biopsy revealed adenocarcinoma Gleason score (GS) 6 (3+3), in one core with core percentage volume of 50%. On pelvic magnetic resonance imaging, the prostate volume was 29 mL, and there was no typical cancerous lesion in the prostate and no evidence of extracapsular extension, seminal vesicle invasion or pelvic lymph nodes enlargement. A contrast-enhanced computed tomography scan of the abdomen and pelvis showed 1.6-cm enhancing endophytic mass in the posteromedial portion of right kidney suggestive of RCC. Bone scan showed no metastasis. The patient underwent RS-RARP and selectiveclamp RAPN in the same setting. Based on Partin's table our patient has 80% probability of organ confined disease and 0% computed risk for lymph node metastasis []. Pelvic lymph node dissection may be omitted for patients when predicted probability of lymph node metastasis based on clinical information is less than 3% [].


A 15-year-old female patient had reported to the Department of Orthodontics with the chief complaint of a malpositioned upper left tooth. A clinical examination of the patient was done. It was observed that the patient had a symmetrical mesoprosopic face. The patient had a convex profile and a prominent nose. The smile arc of the patient was nonconsonant [].
On intraoral examination, it was observed that the maxillary midline was shifted toward the left and the mandibular midline was shifted toward the right; canine relation was Class I on the right side and a buccally blocked canine was present on the left side. Anteriorly, the overbite was in an edge to edge relation. The patient had a Class I molar relation on the right side and Class II molar relation on the left side. The patient had bilateral posterior crossbite with respect to the first molars [].
The maxillary arch was U-shaped and symmetric, and the mandibular arch was wide, symmetric, and U-shaped.
The cephalometric findings revealed a normodivergent growth pattern with a Class I skeletal base [].
An orthopantomogram was also recorded which showed erupting third molars in all four quadrants [].
On considering the diagnostic criteria, a decision was made for unilateral first premolar extractions alignment of the dentition into the arches and correction of bilateral posterior crossbite.
Preadjusted edgewise MBT.022 slot brackets were bonded in both arches, and initial alignment was done using 016 NiTi wire without involving the blocked out canine into the continuous wire. A NiTi expander was inserted for correction of posterior crossbite. An archwire sequence of 018 NiTi, 016 × 022 NiTi, and 017 × 025 NiTi was followed. Extraction of maxillary right first premolar was performed. An open coil spring was placed with respect to the blocked out canine for space creation and midline correction in the maxillary arch []. After sufficient space had been created, the left maxillary canine was bonded and aligned within the arch using active lacebacks. Mandibular right first premolar was extracted to maintain the canine relation and the overbite. Mandibular left canine was retracted into the extraction space using closed coil spring. Space created was used for midline correction and the correction of crowding of the mandibular incisors.
A 019 × 025 SS wire was placed in both arches for 6 weeks along with asymmetric elastics for achieving a canine guided occlusion [].
Bracket repositioning was done and 014 NiTi wires were used for final finishing and detailing.
An ideal Class I occlusion was achieved in the patient with a positive overjet and overbite. The smile appearance improved and the esthetic profile of the patient was maintained [Figures and and ]. Post treatment Orthopantomogram showed ideal mesiodistal angulations of the dentition [].


A 46-year-old nondiabetic male presented with pedal edema of 1-month duration. He was hypertensive taking amlodipine 5 mg/day for last 1-year. He denied the history of smoking or alcoholism. Past history was insignificant except for an appendicectomy, 20 years back. On examination, he was normotensive, obese Class II (body mass index [BMI]-42). Fundus was normal. Systemic examination was unremarkable.
The evaluation revealed proteinuria (3.032 g/day), bland urinary sediment, and a serum creatinine of 1.3 mg/dl. Serum albumin was 3.8 g/dl. Lipid profile was abnormal with high total cholesterol (213 mg/dl) and low-density lipoprotein (153 mg/dl) values. Thyroid profile was normal. Immunological markers were negative, and complements were normal. In view of significant proteinuria, a renal biopsy was performed with a provisional diagnosis of membranous nephropathy.
Renal biopsy included 13 glomeruli, all enlarged in size and showed variably sized nodules, which were cellular and were Periodic-acid-Schiff (PAS) and silver positive. Vessels and tubulointerstitium were unremarkable except for focal lymphocytic infiltrates. Immunofluorescence was negative for IgM, IgA, IgG, C3C, C1q, k, and λ. With the above findings being consistent with diabetic nephropathy, he was reevaluated, and diabetes mellitus was ruled out. HbA1C was 5.2%, and glucose tolerance test was within normal limits. Workup for other causes including amyloidosis, LCDD, and immune deposition diseases was negative. Electron microscopy (EM) which revealed diffuse flattening of foot processes with marked widening and ill-defined lobularity of the mesangium without any electron dense deposits. The negative features on EM and immunofluorescence rule out other differentials of nodular glomerulosclerosis including monoclonal immunoglobulin deposition disease, fibrillary and immunotactoid glomerulonephritis, fibronectin glomerulopathy, and collagenofibrotic glomerulopathy [Figures –].
With the above findings, the diagnosis of idiopathic nodular glomerulosclerosis was made, and the patient was discharged on telmisartan. Further follow-up of the patient at 3 monthly intervals revealed a progressive decline in proteinuria to <1 g/day.


A 45-year-old female presented with myalgias, decreased appetite, and mild pedal edema of 15 days’ duration. She was moderately built and underweight. BMI was 16.5. Systemic examination was unremarkable. Investigations revealed serum creatinine 8.9 mg/dl and 24 h urinary protein excretion 710 mg/day. Serum albumin was 3.4 g/dl. Urine microscopy revealed bland urinary sediment without any microscopic hematuria. Ultrasound showed normal-sized kidneys with increased echotexture and maintained corticomedullary differentiation. She was given 3 sessions of hemodialysis, and a renal biopsy was performed. Renal biopsy showed 12 glomeruli, all glomeruli were enlarged with nodules and were PAS and silver positive. Vessels and tubulointerstitium were unremarkable. Immunofluorescence was negative for IgM, IgA, IgG, C3C, C1q, k, and λ. EM did not show any electron dense deposits and was suggestive of nodular glomerulosclerosis. Her HbA1C was 5%. Fundus examination was normal. Blood sugars were normal. Autoimmune workup was negative. Workup for other causes of nodular glomerulosclerosis such as amyloidosis, LCDD, and immune deposition diseases was negative. Lipid profile was normal except for a mildly decreased high-density lipoprotein level (38 mg/dl). She remained dialysis dependent.


The 5-month-old previously normal, well-growing [weight = 5.3 kg, length = 60 cm, weight/height = -1 SD to -2 SD as per the World Health Organization (WHO) growth chart, head circumference = 40.5 cm] immunized female child presented with fever since 6 days followed by fast breathing for 2 days. Roentgenogram of the patient's chest [] showed left-sided large pneumothorax with shift of the mediastinum on the right and was referred to our center for further management.
On admission, she was euthermic, irritable [heart rate = 168/min, respiratory rate = 68 bpm, blood pressure = 98/60 mmHg, peripheral capillary oxygen saturation (SpO2)=88% on room air] with reduced chest expansion on the left side. Her breath sounds were decreased on the left side with a hyperresonant note. She was started on high-flow oxygen and was shifted to the pediatric intensive care unit (PICU). On admission to PICU, the left-sided intercostal drainage tube was placed [], which drained gush of air followed by thick, white-colored pleural fluid that was exudative. The complete blood picture of the patient showed hemoglobin level = 10 gm%, total leukocyte count (TLC) =37,400/mm3 (P 80% and L 15%), and C-reactive protein (CRP) level was positive (18.3 mg/dL), human immunodeficiency virus enzyme-linked immunosorbent assay (HIV ELISA) was negative. Ceftriaxone injection, Ampiclox, and Clindamycin were started, along with other supportive measures.
Gradually, her respiratory distress was alleviated over a period of next 24 h but roentgenogram [] of the chest showed incomplete expansion of the left side with multiple cavitations even after 5 days, hence computed tomography (CT) scan of the chest [] was done that showed collapse consolidation of the left lung with multiple cavitations and some cavity in the lower lobe communicating with pleural cavity and suspected to be CCAM. Left thoracotomy with decortication with lower lobe lobectomy was done in view of suspected CCAM. Gross surgical sample [] revealed a wedge of lung measuring 10 cm × 8 cm × 5 cm. Pleural surface was congested and cut surface was firm with no or little normal looking lung parenchyma. Microscopic examination [] of the patient showed signs of pleuritis with underlying suppurative inflammation of the lung indicative of abscess. Adjacent lung tissue showed vague lobulated architecture with interlobular fibrosis, definite increase in the number of bronchiolar structures, and small alveolar spaces lined by plump cuboidal epithelium. Overall symptoms in correlation with clinical and radiological findings were consistent with type III CCAM.
Later, she became hemodynamically stable with improved air entry to the left side of the chest. Roentgenogram of the chest [] showed resolution of the pneumothorax following which the implantable cardioverter defibrillator (ICD) tube was removed. Later blood and pleural fluid cultures were sterile; hence, the patient was started on oral antibiotics and was discharged after pneumococcal and flu vaccination. On follow-up after 4 weeks, her growth and respiratory functions were found to be normal.


Informed consent was obtained from the patient for being included in this case report and for publication of the accompanying images.
A 44-year-old male patient presented to our outpatient clinic for multiple infiltrated plaques on his scalp for 4 years. A dermatological examination showed multiple plaque lesions of annular erythema with central atrophy and raised borders (Fig. ). An inflammatory and granulomatous reaction in the dermis of the skin, originating beneath the surface epithelium (Fig. a), and granulomas consisting of epithelioid histiocytes and multinucleated giant cells (Fig. b) were detected during the histopathological assessment of the diagnostic biopsy specimen. A systemic screening was performed when available evidence supported a diagnosis of cutaneous sarcoidosis. The chest X-ray showed bilateral hilar enlargement, and the computed thoracic tomography revealed many lymph nodes in the perivascular region, paratracheal region, subcarinal region, and in both hilar regions, where the short axis of the largest lymph node in the right hilus reached up to 1.4 cm in diameter. The patient was diagnosed with cutaneous sarcoidosis based on the typical lung involvement, elevated angiotensin-converting enzyme levels, and histopathologic findings.
After designing a treatment plan during a control visit, the patient reported that they had found and used a solid soap which contained G. lucidum and goat’s milk from a herbal shop (GanoSoap®, Gano Exel Industries Sdn. Bhd., Malaysia). The patient indicated that they kept the soap foam on the lesion for 1 h, and then rinsed it and repeated the procedure for a total of 3 days. A dermatological examination showed that almost all of the lesions had disappeared (Fig. ). After 6 months, the lesions recurred and the patient applied the same soap again. The lesions disappeared within a week and the scalp lesions are in remission.


The first case was an 11-week-old male, a product of full term normal vaginal delivery with a birth weight of 3.6 kg. The parents are first-degree relatives. The pregnancy was complicated by gestational diabetes mellitus. He presented at the age of 2 months with a history of right lower limb edema and chronic diarrhea since birth. The right lower limb edema started soon after birth, associated with redness and warmth. Later on, the edema became generalized and noticeable on the face and both lower limbs (). The diarrhea was up to 6 times per day, loose, non-greasy with no mucus or blood. There was mild abdominal distention. His feeding and activities were normal. Right lower limb cellulitis was suspected and treated with antibiotics. There was no history of recurrent infections, chronic, or genetic diseases in the family. Physical examination revealed right lower limb pitting edema but no redness or warmth. The abdomen and both testicles were mildly distended. His laboratory tests revealed low total serum protein, low serum albumin, low serum calcium, and high alkaline phosphatase. ().
Initial serum immunoglobulin E (IgE) <7.00 IU/ml (normal range: 11-162 IU/ml) and immunoglobulin G (IgG) 0.48 (normal range: 2-6.8 g/l) were low, while immunoglobulin A (IgA) and immunoglobulin M (IgM) levels were normal. Repeated total IgE was high but IgG remained low. Toxoplasma, others, Rubella, cytomegalovirus, and herpes simplex (TORCH) screen, and hepatitis profile were negative. The 24-hour urine for protein was negative. Serum cholesterol was low while serum triglycerides were normal. Allergy tests were negative. Stool microscopy was positive for fat globules but stool alpha 1 anti-trypsin was not performed. Thyroid stimulating hormone level (TSH) was high indicating subclinical hypothyroidism, which normalized on subsequent testing. Ultrasound abdomen was unremarkable. Upper gastrointestinal endoscopy showed normal esophagus mild diffuse gastritis, while first and second part of the duodenum showed prominent submucosal folds with whitish appearing villi throughout. Duodenal biopsies showed hugely dilated lymphatics in the lamina propria indicating intestinal lymphangiectasia. The patient was given albumin infusion with furosemide and started initially on amino-acids based formula (Elecare) followed by MCT based formula (Monogen), fat-soluble vitamins, multivitamins, oral iron, and calcium supplementations. The edema significantly improved and continued after 9 months of follow-up.


A 12-year-old male who was initially diagnosed as a case of mesenteric lipoma after a history of puffy eyes, scrotal swelling, and recurrent diarrhea of 2 months duration. The diarrhea was 3-4 times per day, loose with no mucous, blood, or steatorrhea. He had occasional mild abdominal pains not associated with vomiting, weight loss, or changes in appetite. He had a history of recurrent attacks of wheezing and shortness of breath, but no history of atopic conditions. He had no history of recent upper respiratory tract infections or urinary complaints. He was a product of a full term normal vaginal delivery with an Apgar score of 9 and 9 at one and 5 minutes. His birth weight was 2.9 kilograms. He had a right foot hypertrophy since birth. He was fully vaccinated. The parents are non-consanguineous, and they have 8 other siblings who are not suffering from any chronic or genetic diseases. At the age of 10 years, an abdominal mass was felt accidently, but he was reassured as his abdominal ultrasound (US) was unremarkable. On physical examination, he had course facial features but no dysmorphism. There was a bilateral pitting pedal edema more prominent on the right lower limb. His weight was 27 Kg and his height was 127 centimeters both on the 25th percentile. Abdominal examination revealed mobile, palpable masses in the left hypochondrial and lumbar region, a scrotal edema, and extensive multiple cutaneous warts on his genitalia. All other systems were normal including fundus examination. The laboratory work up () revealed low serum total protein (44 g/L), low albumin (28 g/L), low globulin (17 g/L), and low serum cholesterol. His full blood count showed lymphopenia. Serum thyroid stimulating hormone level was high indicating subclinical hypothyroidism. Serum 25 hydroxycholecalciferol (30 nmol/l, normal >50) and serum calcium were low. Erythrocytes sedimentation rate, C-reactive protein, coagulation profile, liver enzymes, and renal function test were all within normal range. Human immunodeficiency virus (HIV) serology was negative. Urine and stool routine microscopy were normal. His abdominal US was reported as normal, although a retrospective review showed ‘a halo sign’ indicating thickened intestinal wall ().
Abdominal CT scan showed a diffuse mass predominantly of fat density infiltrating the mesentery. Ultrasound guided fine needle biopsy of abdominal masses was negative for malignancy, and it revealed mature fibro-adipose tissue and benign peritoneal mesothelial cells. Barium meal and follow through showed thickened bowel wall with nodularity. Low red blood cells indices, low serum iron (5 umol/l, normal range 6-27), and low serum ferritin (36 µg/l, normal range 52-421) were consistent with iron deficiency anemia. While the patient was on his regular diet, stool alpha 1 anti-trypsin was elevated (normal value: 0-0.62 mg/g) indicating PLE. Upper gastrointestinal endoscopy showed creamy white dots covering the second part of duodenal mucosa. Colonoscopy showed nodular rectum, sigmoid, and ascending colon. Microscopic examination revealed hugely dilated lymphatics in the duodenal mucosa and submucosal ().
Lower esophagus biopsies showed chronic, non-specific esophagitis with no eosinophils. Gastric and rectal mucosa were normal. Helicobacter pylori test was negative. The patient was diagnosed with PIL. He was kept on low-fat, high protein diet along with MCT oil, fat-soluble vitamins, iron, and calcium supplements. In addition, he received nebulized salbutamol and pulmicort for his chest symptoms. On follow-up, the patient showed improvement. Three years later, the patient presented again with diarrhea, occasional colicky abdominal pain, chronic productive cough, and stammering speech. On examination, he had bilateral lower limb edema more on the right side and bilateral crepitations in his chest. A high-resolution chest CT scan showed thickening of central lung interstitium and interlobar septa, few small nodules with peri-lymphatic distribution, and central peribronchial cuffing. There were no hilar or mediastinal lymphadenopathy, and no pleural or pericardial effusion. These changes are consistent with pulmonary lymphangiectasia (). The patient was managed with albumin infusion and diuretics. On follow-up, the patient improved but he was not adherent to the restricted diet.
Ethical approval for this study was obtained from the Pediatric Department, Salmaniya Medical Complex, Bahrain.


A 35-year-old woman presented with two month history of a swelling in her left eye which increased rapidly in size to involve the left temporal region. Within this period she developed rapidly progressive proptosis and blurring of vision leading to complete blindness. Also the patient had no pain at the time of presentation and no history of swelling at any other site of body was present.
Upon physical examination, there was a lobular firm, nontender mass of size 15 × 7 cm, extending from left orbit to the left temporal region. In addition to axial proptosis, the left eye showed restricted movement in all directions. Her palpebras exhibited prominent chemosis []. She was unable to perceive light in her left eye. Her cornea was intact. The round pupil was 6mm across and sluggishly reactive to light. The disc of the left optic nerve was edematous. On extensive examination there were no subcutaneous swellings, café au lait spots or Lisch nodules. Computed tomography (CT) scan showed large lobulated extra-axial mass arising from left sphenoid wing and temporal lobe apex; extending into lateral extra-coanal space of left orbit and temporal fossa destroying temporal lobe []. Magnetic resonance imaging (MRI) of the orbits and brain with and without contrast enhancement showed left sphenoidal based extra-axial marginated in-homoginously enhancing mass at the lateral side of the left optic nerve buckling the ipsilateralantero temporal lobe []. Other systemic observations of the patient were normal. No evidence of any distant metastasis was found on clinical or radiologic evaluation.
On this occasion, the tumor was exposed through a left lateral orbitozygomatic approach. The tumor was highly vascularised, densely adhered to the zygomatic bone and had eroded the lateral orbital wall and temporal bone of left side. Optic sheath and the duramater of temporal lobe were intact. Near total dissection of the tumor was done with microsurgical technique. The histopathological diagnosis was MPNST [] which was subsequently confirmed on the basis of immunopositivity for S-100. Immunohistochemically, tumoral cells were positive for S-100 []. Smooth muscle actin, desmin, Leu 7 and myelin basic protein (MBP) were all negative. Postoperatively, the patient recovered rapidly. Post-operative CT scan showed minimal residual mass in the orbit []. At discharge, she had improved cosmoses with stable neurological status []. Vision in her left eye improved to finger counting at one meter and extra-ocular movements were normal. She was further referred to the cancer institute where she received external beam radiotherapy. On one year follow-up, the patient is doing well with no local recurrence or any distant metastasis.


A 35-year-old man was admitted to our hospital because of weight loss, nausea, vomiting and diffuse abdominal discomfort with one-week duration. He had no known previous diseases and did not take any medication. He had lost approximately 10% of weight during the last year prior to admission. His abdomen was enlarged and tender with spontaneous epigastric and right hypochondrium pain without rebound tenderness. The relevant laboratory findings were: hemoglobin 13.2 g/dL; leukocytes 5,450/mm3; platelets 138,000/mm3; lactate dehydrogenase 2,448 U/L, aspartate aminotransferase 183 U/L, alanine aminotransferase 80.9 U/L, total bilirubin 0.4 mg/fL, albumin 3.1 g/dL, amylase 2 U/L, γ-glutamyl transferase 160 U/L and C-reactive protein 6.4 mg/dL. Coagulation and kidney function tests were normal. HIV serology was positive and the CD4 T cell count was 99 cells/μL. Abdominal computed tomography (CT) scan showed hepatosplenomegaly and diffuse peritoneal thickening with small cystic areas (). Small bowel wall thickening was also seen. Upper digestive tract endoscopy was performed: the esophagus showed non-detachable white plates (); the stomach did not show abnormal findings (, ); the inspection of the duodenal bulb revealed marked edema and hyperemia with some violaceous areas (, ); finally, the second and third portions of duodenum showed no abnormal findings (). Several biopsy samples were taken. Histopathological examination of the esophagus biopsies showed multiple spores and hyphae of Candida albicans. The duodenal bulb biopsies showed a diffuse infiltrate of monotonous medium-sized lymphoid cells, with round nuclei, multiple small, basophilic nucleoli and basophilic cytoplasm (). The atypical cells were reactive to CD20, CD10, c-myc and bcl-6 and not reactive to bcl-2 and CD3. The Ki67 antibody was consistent with a very high proliferation index (close to 100%) (). Epstein-Barr virus was detected by in situ hybridization. This histopathological findings were consistent with the diagnosis of BL of the duodenal bulb. The patient was also submitted to ultrasound-guided peritoneal biopsy and the peritoneal samples were also compatible with the diagnosis of BL. Cranial CT scan and lumbar puncture excluded central nervous system involvement. Chest CT scan showed no relevant aspects. Bone marrow biopsy revealed 80% of atypical cells with Burkitt phenotype and the translocation (8,14). On the basis of those findings, the patient was diagnosed with BL stage IV, using the modified Ann Arbor staging system. He was started on highly active antiretroviral therapy and received systemic chemotherapy with CHOMP (cyclophosphamide, doxorubicin, vincristine, methotrexate and prednisolone). One week later, he developed a tumor lysis syndrome but he recovered and is asymptomatic two months after the diagnosis.


A 44-year-old white man was admitted to our hospital because of acute pulmonary edema. His past medical history was significant for chronic tobacco use and recurrent episodes of arthralgias over the course of 2 years, which were treated symptomatically by the patient by self-medication with analgesics, without any specific medical management.
The patient had been well until 2 months earlier, when he began to have worsening of his physical state, anorexia, weakness, weight loss, and diffuse myalgias. Three days before admission, he complained of acute left flank pain unassociated with trauma. It was sudden in onset, intense, and associated with nausea. In addition, the patient reported a significant decrease of urine volume (<0.5 L urine in 24 hours) and dyspnea. Physical examination showed high blood pressure (170/100 mmHg), his temperature was 38.7°C, and his respiratory rate was 34 breaths per minute. His weight was 71 kg (he weighed 81 kg 2 months earlier). Chest auscultation revealed bilateral rales. Cardiac examination findings were unremarkable. The abdomen was tender, mainly over the left upper quadrant, and had no palpable hepatosplenomegaly. He had 1+ lower-extremity edema. Exam of the lower limb found petechial purpura on his left leg, with livedo reticularis. Otherwise, the examination was normal.
Laboratory findings revealed a rapidly progressive renal failure with a serum creatinine level of 1.71 mg/dL (normal value, 0.6–1.2 mg/dL), which increased to 4.02 mg/dL over the next 2 days; a blood urea nitrogen level of 57 mg/dL (normal value, 7–20 mg/dL), which also increased to 123 mg/dL; a hypervolemic hyponatremia of 124 mEq/L (normal value, 135–145 mEq/L); and normal serum electrolytes otherwise. Twenty-four hour urinary protein levels were 0.6 g/24 hours (normal value, <0.03 g/24 hours), and urinary sediment was positive for microscopic hematuria. Hemoglobin was 9.7 g/dL (normal value, 13–16 g/dL), white blood cell count was 18,300/mm3 (normal value, 4,000–1,000/mm3), and platelets were 626,000/mm3 (normal value, 150,000–300,000/mm3). Erythrocyte sedimentation rate was 80 mm/hour (normal value, <15 mm/hour), with a C-reactive protein level of 11.3 mg/L (normal value, 6–12 mg/L). Aminotransferase and creatinine kinase levels were normal. Lactate dehydrogenase levels were elevated (1,243 U/L; normal value, <250 U/L). CH50 was not checked, but complement component C3 was normal, at 80 mg/dL (normal, 80–170 mg/dL), and C4 was strongly reduced, at 6 mg/dL (normal, 16–40 mg/dL). Rheumatoid factor and antinuclear antibodies were present. There was no monoclonal paraprotein detected both on serum and urine protein immuno-electrophoresis. In addition, five blood samples for cultures (both aerobic and anaerobic) were sent to the laboratory in view of the patient’s fever, leukocytosis, and high erythrocyte sedimentation rate, all of which were negative.
Chest radiography showed cardiomegaly with bilateral pulmonary infiltrates, suggesting acute pulmonary edema. Renal ultrasound showed normal-sized kidneys without evidence of hydronephrosis, but it allowed us to identify a subcapsular renal hematoma that measured 63×52 mm in the upper pole of the left kidney, which was confirmed by abdominal computed tomography (CT) scan (). Multislice computed angiotomography scanning identified the hematoma and ruled out microaneurysms of the main renal arteries, other vascular abnormalities, and renal tumors (). Hemodialysis therapy was started because of oliguria, continuous decrease of renal function, and persisting pulmonary edema despite high doses of furosemide (500 mg/day), and then the patient was operated on with conservative surgery for renal hematoma. A drain was placed and then withdrawn after 3 days.
Renal biopsy was performed, during surgery, the third day after admission and was submitted for light microscopic and immunofluorescence examination (). The specimen consisted of renal medulla and cortex with 14 glomeruli. One glomerulus was globally sclerosed. Some glomeruli were ischemic. The preserved glomeruli were enlarged and showed diffuse mesangial expansion. There was significant hypercellularity of glomeruli with numerous infiltrating neutrophils, minimal endocapillary proliferation, and one cellular crescent. There were thickening and reduplication of the glomerular basal membrane, suggesting membranoproliferative glomerulonephritis. In two glomeruli, we noted intracapillary amorphous deposits compatible with microthrombi. Small vessels showed extensive necrotizing angiitis. Some vessels had also leukocytoclastic angiitis. There was considerable tubular necrosis and interstitial edema with minimal leukocyte infiltrates. Unfortunately, the immunofluorescence sample did not contain glomeruli.
The patient underwent an extensive workup to determine the cause of his renal vasculitis. The laboratory tests were sent immediately after we received the kidney biopsy results, 72 hours after the biopsy had been performed. Serological studies for antineutrophil cytoplasmic antibodies, antiglomerular basement membrane antibodies, anti-double-stranded DNA antibodies, and anti-Smith antibodies were negative, excluding respectively pauci-immune vasculitis, Goodpasture’s syndrome, and lupus vasculitis. There was neither apparent sepsis nor visceral abscess on computed tomography scan. Transthoracic echocardiography showed no vegetations, thus excluding infectious endocarditis. Skin-biopsy specimen of a purpuric lesion showed leukocytoclastic vasculitis without immunoglobulin A deposition, and therefore did not support the diagnosis of Henoch-Schönlein purpura. Tests for cryoglobulinemia were positive, including the presence of cryocrit (12%) with type II mixed cryoglobulin (immunoglobulin G/immunoglobulin M kappa). We made additional investigations to determine the cause of mixed cryoglobulinemia, and assessment for hepatitis C virus (HCV) RNA and hepatitis B virus DNA by polymerase chain reaction was negative. Tests for Sjögren’s syndrome were positive with the presence of anti-Ro (SS-A), anti-La (SS-B), lymphocytic infiltrate in minor salivary gland biopsy (grade 3 according to Chisholm and Mason grading system), and positive Schirmer’s test. Screening for lymphoma remained negative despite initial elevated lactate dehydrogenase levels. There were neither peripheric or visceral adenopathies nor lymphomatic infiltration on osteomedullary biopsy. All these data confirmed that the patient had SRK caused by type II mixed cryoglobulinemia-associated Sjögren’s syndrome.
The patient received 3 days of pulses of methylprednisolone (1 g/day), followed by oral prednisone (1 mg/kg/day) with a decreasing regimen and 6 monthly pulses of intravenous cyclophosphamide (1 g) as induction of remission. The patient remained febrile during hospitalization, with temperatures ranging between 38.5°C and 38.8°C, until he received the third pulse of methyl prednisolone, which was administered 12 days after admission. Azathioprine (100 mg/day) was started as maintenance treatment. The patient had spectacular improvement of his physical state. Arthralgias and the other symptoms disappeared, proteinuria fell to only trace amounts, and renal function returned to its baseline value (0.9 mg/dL) over the next 2 weeks, and C4 levels were again normal. Resorption of the renal hematoma was complete over the next 5 weeks. Cryoglobulins remained undetectable. Renal function and lactate dehydrogenase were still normal. Ethical approval was not needed in the present case report, because it didn’t include research or experiments. There was no risk of causing harm or violating the patient’s right, since it was presented in a way that respected the patient’s privacy and confidentiality. The patient gave oral consent when informed that the data will be published.


A 25-year-old male presented to us with pain in the right flank for 1 day. He had history of ureterorenoscopic removal of a right ureteric stone 1 year earlier. His vital signs, general physical examination and abdominal examination revealed no abnormality. Urinalysis was normal, and abdominal ultrasound raised a suspicion of small calculi in the right kidney. Non-contrast computed tomography (NCCT) abdomen revealed a few subcentimetric calculi in both kidneys without hydronephrosis or hydroureter. However, it also revealed a large appendicolith of 2.5 × 2.1 cm2 size. [Figure and ] (mineral core), composed mainly of calcium and struvite on spectral analysis [Figure and ]. His routine investigations were essentially normal. He underwent laparoscopic appendectomy using a 10-mm supra-umbilical camera port and two 5 mm ports at the supra-pubic region and the left iliac fossa, respectively. A pre-ileal appendix was found hidden in flimsy adhesions posterior to the terminal ileum. An incidental Meckel's diverticulum was also found [], which was not pathological and was left alone. The mesoappendix was cut using Harmonic scalpel (Johnson and Johnson make) and the appendix was cut at the base between ligatures []. It was removed using a glove bag after enlarging the supra-umbilical incision because of the large stone size — 2.5 cm × 3.0 cm [Figure and ]. The patient had an uneventful recovery.


A27-year-old primigravida was referred to us at 23 weeks of gestation, with a history of leaking per vaginum for two weeks. There was no history of fever or bleeding per vaginum in the first trimester.
Ultrasound done at our center showed a single live fetus, with parameters corresponding to 21 weeks. Imaging was difficult because of severe oligoamnios. Single vertical pocket measured 7 mm. The fetus was detected to have a lower limb anomaly. The left lower leg was short [] with the tibia and fibula measuring16mm compared to 31 mm on the right side. The left foot was not seen. The findings were suggestive of amputation of the left leg. Movement of the left lower limb confirmed amputation and absence of the foot []. On the right side, a constriction was seen in the calf []. The working diagnosis was amniotic band syndrome.
Labor was induced in view of maternal sepsis and she delivered a dead female fetus weighing 460g. The left lower limb showed amputation at the mid calf. There was an area of constriction on the right lower limb and below the constriction, the limb was edematous. The upper limbs were normal. The postnatal picture confirmed our diagnosis of amniotic band syndrome []. The fetal karyotype was normal.


A 25-year-old primigravida came for a first trimester ultrasound at 12 weeks of gestation. The first trimester was uneventful. USG done showed a fetus with parameters corresponding to 12-13 weeks of gestation. A membrane was seen attached to the lower limb, restricting the movement of the limb [, ]. An ultrasound done at 19 weeks showed limb anomaly. The right foot was acutely dorsiflexed with oligodactyly- only one toe could be seen and the left foot had inversion []. There was syndactyly in the left hand and oligodactyly in the right. A band was seen connecting the hands []. The features were suggestive of ABS. The couple when counseled regarding the findings opted for termination in view of the morbidity. The pregnancy was terminated and the findings were confirmed. The fetal karyotype was normal.


A 28-year-old primigravida with a fourth degree consanguineous marriage, came to us for an anomaly scan at 19 weeks. The fetus was detected to have multiple anomalies - bilateral cleft lip and palate [], distorted calvarium [], severe frontal bossing with discontinuity of the frontal bone [], and a band was seen near the fetal head moving along with the fetus [].
The couple, when counseled, opted for termination of the pregnancy. The fetus was found to have bilateral cleft lip palate, the right eyelids were missing. In the scalp there was a localized area of aplasia cutis and a membrane was attached to that area []. The fetal karyotype was normal.


An 88-year-old male urologist with a history of atrial fibrillation, iron deficiency anemia and unprovoked pulmonary thromboembolism, presented to our hospital in January 2014 after a fall leading to rhabdomyolysis and quadriceps tendon rupture. Upon laboratory investigations, he was found to have normocytic normochromic anemia with a hemoglobin level of 9.8 g/dL, mean corpuscular volume of 94.3 fl and reticulocyte count of 2.3%. White blood cell count was 14.6×103 per µL (58% neutrophils, 12% lymphocytes, 30% monocytes, 0% basophils and 0% eosinophils) and platelet count was 191×103 per µL. Absolute monocyte count was elevated at 4.4×103 per µL (normal range 0.0-0.9×103 per µL). Iron deficiency anemia and megaloblastic anemia due to hypovitaminosis B12 or folate were excluded. Presence of anemia and persistent monocytosis suggested underlying bone marrow pathology such as myelodysplasia or chronic myelomonocytic leukemia, and warranted a bone marrow examination.
A bone marrow aspirate and biopsy showed mild trilineage hypercellularity with myeloid to erythroid cell ratio of 4.7:1; however monocytes were not noted to be elevated (). Immunohistochemical stains demonstrated CD138 positive, CD20 positive, monoclonal kappa plasma cells accounting for 10% cellularity (). Flow cytometry demonstrated plasma cells positive for kappa chain, CD38, CD138, CD20, partial CD45, dim CD27 and CD200, and negative for CD19, CD56, CD117, CD28 and CD81. Cytogenetic analysis by FISH (fluorescence in situ hybridization) demonstrated translocation t(11;14) () and deletion chromosome 17p13 (TP53) but did not detect rearrangements of chromosome 1p or 1q, gain of chromosome 5q, deletion of chromosome 13 (or 13q), t(14;16) or t(4;14). Unexpectedly, karyotype analysis detected Philadelphia chromosome [t(9;22)(q34;q11)] in 8 out of 20 metaphases analyzed (). Serum protein electrophoresis and immunofixation showed immunoglobulin D kappa monoclonality with M-spike of 1 g/dL. A skeletal survey was unremarkable for any characteristic myeloma bony lesions, as was magnetic resonance imaging of the spine. Serum calcium and renal function were normal. Serum free kappa chains were elevated with an increased kappa:lambda chain ratio (). Immunoglobulin levels were depressed except for markedly elevated immunoglobulin D level (). At the same time, quantification of chimeric BCR-ABL mRNA transcripts was done by reverse transcription polymerase chain reaction (RT-PCR). There were no plasma cells detected on peripheral smear examination. He was therefore diagnosed with IgD kappa smoldering multiple myeloma (Durie-Salmon stage I and International Staging System I) and chronic phase chronic myelogenous leukemia simultaneously. Therapy was not initiated and a watch and wait approach was implemented with serial clinical and laboratory assessments.
In May 2014, after two months of initial diagnosis, he developed profound fatigue, severe nocturnal sweating and low grade fevers. On laboratory evaluation, he had a sudden increase in white blood cell count to 40×103 per µL, increase in serum kappa chain level and decrease in immunoglobulin levels (). A peripheral blood smear examination showed presence of circulating plasma cells, plasmacytoid lymphocytes and abnormal lymphocytes which were previously not present (). He had rapidly progressed from an asymptomatic smoldering myeloma stage to PCL.
Therapy for MM and PCL was instituted as RVD (lenalidomide, bortezomib and dexamethasone) regimen that resulted in disappearance of plasma cells from peripheral circulation. Imatinib for treatment of CML was not started along with RVD to avoid potentially dangerous adverse effects from combined proteasome inhibitor and tyrosine kinase inhibitor therapy given patient’s advanced age and co-morbidities. However, he exhibited worsening leukocytosis and thrombocytosis with counts as high as 90×103 per µL and 2069×103 per µL, respectively. BCR-ABL mRNA transcripts were found elevated at 180.38%. He was subsequently started on imatinib (400 mg daily) for CML. Both RVD and imatinib were continued which he tolerated well with diarrhea as the only side effect which was well controlled with antidiarrheal medication.
Over the next few weeks, he demonstrated subjective improvement as well as improvement in free kappa chain, LDH, BCR-ABL mRNA transcripts and immunoglobulin D levels. A trend of myeloma parameters longitudinally over time is summarized in . A complete clinical remission, however, was not achieved. The immunoglobulin levels continued to decline. In September 2014, he was admitted to the hospital and succumbed to fulminant septic shock consequent to pneumonia.


A 27-year-old male patient with an unremarkable medical history was referred to the Department of Oral and Maxillofacial Radiology with a complaint of pain in the region of the lower right molar teeth.
An intraoral examination revealed irregular morphology of the mandibular permanent third molar. This morphology suggested the presence of the union of an extra cusp on the lingual aspect of a wisdom tooth. This union led to the development of a groove formation that caused periodontal problems. The gingiva around the right mandibular third molar appeared to be reddish in color, with loss of stippling and an inflamed appearance ().
A panoramic radiograph indicated the fusion of a supernumerary tooth with the permanent third molar and the presence of a dilated follicular space associated with this abnormal formation. This irregular enlargement exhibited a sharply delineated area of radiolucency around the fused supernumerary tooth (). However, the panoramic radiograph was not sufficient to visualize this dental formation and its surrounding tissues because it only provided information in the mesiodistal plane. With the consent of the patient, a CBCT image was taken to observe the abovementioned teeth, the periradicular lesion, and the relationship thereof with the peripheral structures.
The CBCT scans of the right side of the mandible in all orthogonal planes showed a fused supernumerary molar on the lingual aspect of the third molar (). Around the periradicular region of these malformed teeth, a cystic lesion was identified in the axial, coronal, and sagittal planes (). Additionally, an axial section revealed perforations of this cystic lesion on the buccal and lingual borders of the compact bone (). Furthermore, the presence of a retromolar canal was incidentally identified on a sagittal CBCT image ().
A treatment plan was developed, including the extraction of the fused teeth and the cystic lesion. The fused teeth were extracted with an inferior alveolar nerve block (); subsequently, the cystic lesion was curetted and sent to the Department of Pathology for a definitive diagnosis. Based on pathological and histological examinations, it was identified as a paradental cyst ().


A 29-year-old man presented with a nonhealing ulcer over the anterior aspect of the right leg of 4 months duration for which he was treated with various antibiotics and topical medications. He also complained of a fleshy lesion in the mouth for the last 2 years. He gave a history of bathing in a pond for the last 7 years.
There was an irregular ulcer measuring 6 cm × 3.5 cm over the anterior aspect of right leg showing peripheral healing and central red granulation tissue []. On close examination, small brownish spots were observed. Oral examination showed a pedunculated red mass studded with black spots hanging by the side of the uvula []. Histopathologic examination of both the lesions revealed features of rhinosporidiosis. Both the lesions were surgically excised, and the base of the ulcer was treated by radiofrequency ablation. The patient was further started on dapsone 100 mg OD. On follow-up, the ulceration healed but new oral lesions were noted after 3 months.


A healthy 23-year-old homosexual male presented to the emergency room with complaints of vertigo, right facial weakness, and diplopia. Neurological examination found limitation in right abduction, right gaze nystagmus with marked oscillopsia, and right peripheral facial nerve paralysis. Brain MRI showed a hyperintense focus in the right pons, weakly enhanced, adjacent to the area of the abducens and facial nuclei. Frontal periventricular hyperintense foci were also demonstrated without enhancement.
The patient was hospitalized with a suspected inflammatory process, chiefly multiple sclerosis (MS). The differential diagnosis also included a vascular or neoplastic process. A lumbar puncture examination revealed pleocytosis with multiple lymphocytes, which normalized on repeat exam. Cytology and oligoclonal bands were normal. Blood tests for antinuclear antibody (ANA), C3, C4, anti-neutrophil cytoplasmic antibody (ANCA), and rheumatoid factor were normal. HIV was negative. Blood tests aimed at ruling out a vascular etiology, including antiphospholipid antibody (APLA), cardiolipin IgM and IgG, beta 2 glycoprotein, D-dimers, circulating anticoagulants, and a transcranial Doppler examination were normal. As no definite diagnosis of MS was reached, the patient was diagnosed with a clinically isolated syndrome, and was treated with IV solumedrol 500 mg/day for 5 days, followed by oral prednisone 20 mg/day, with marked improvement in his signs and symptoms.
A month later, following discontinuation of prednisone, the patient returned with a headache and worsening of diplopia and facial weakness, which again improved after recommencing 60 mg/day prednisone. Repeat MRI showed the pontine focus to be more enhanced, rendering the diagnosis of MS less plausible. Angiotensin-converting enzyme was negative; anti-Ro and anti-La were negative for neuro-Sjögren, and aquaporin 4 was negative as well, refuting a diagnosis of neuromyelitis optica. The patient was discharged with slow tapering off of prednisone treatment and with no definite diagnosis.
Ten months later, the patient complained of visual deterioration OD and constriction of his right lower visual field. On examination, best-corrected visual acuity (BCVA) was 20/100 OD and 20/20 OS. Intraocular pressure was normal in both eyes. There was a right afferent pupillary defect, and Ishihara color vision score was 1/12 OD and 12/12 OS. Nystagmus was still seen, but cranial nerve functions were normal. There was mild anterior uveitis OD with +1 cells and no flare. Mild vitritis, with few cells, was seen OU. Fundus examination of the right eye revealed superior optic disc edema accompanied by hemorrhages and blood vessel sheathing. The macula was elevated, with intraretinal hemorrhages in the upper half of the macula, and star-shaped exudates in its lower half. A superior hemivein occlusion was noted, composed of dilatations and tortuosity of the superior retinal veins, a frosted branch angiitis pattern, and hemorrhages in the upper half of the retina. Retinal hemorrhages were also seen inferior to the optic disc (fig. ). Fundus examination of the left eye revealed star-shaped exudates in the upper half of the macula.
Fluorescein angiography of the right eye demonstrated a superior hemivein occlusion with occlusive vasculitis (fig. ). Optical coherence tomography (OCT) demonstrated vitreal cells and neuroretinitis findings in both eyes. Both eyes demonstrated different stages of neuroretinitis (fig. ). A 30-2 stimulus III visual field test showed an almost complete lower-half scotoma OD, fitting the superior distribution of retinal damage and a small superonasal central scotoma. OS visual field test demonstrated constriction of the superonasal quadrant and a small superotemporal central scotoma. The bilateral central pattern fitted a small central homonymous scotoma, possibly representing an insult to the tip of the occipital lobe.
Systemic physical examination revealed only a purple, flat, painful lump, approximately an inch across, on the right shin typical of erythema nodosum, and was otherwise normal. On further history-taking, the patient negated other uveitic signs and symptoms, including mouth or genital aphthae, gastrointestinal or respiratory symptoms, other rashes, travel to exotic areas, or exposure to animals.
Due to the finding of frosted branch angiitis in a young homosexual patient, a vitreal tap was performed to rule out CMV infection, and intravitreal ganciclovir 2 mg/0.1 ml was injected. A uveitic workup including a complete blood count and chemistry was normal; C-reactive protein (CRP) was high (88 mg/l, normal value 0–5 mg/l); ANA, C3, C4, C and P ANCA were normal; a coagulation panel, including PT and PTT, was normal, β2 glycoprotein was normal, and homocysteine was found to be elevated 4 times the normal level (59.8 µmol/l, normal level 5–15 µmol/l).
Blood serologies for infectious causes, including Venereal Disease Research Laboratory test, treponema pallidum hemagglutination, toxoplasma IgM and IgG and Bartonella IgM and IgG were negative. A repeat HIV test was negative, as well as vitreous PCR for CMV. Mantoux examination was anergic, and a chest radiograph and computed tomography were normal.
Treatment with folic acid and B vitamins was started due to homocysteinemia. The patient was treated with IV methylprednisolone 1 g/day for 3 days, followed by prednisone 60 mg/day, with gradual tapering. Three weeks later, BCVA was 20/28 OD, color vision significantly improved to 11/12, with significant clinical improvement (fig. ). OCT showed absorption of most of the subretinal fluid (fig. ). Eventually, on follow-up visits, the patient confessed to having had mouth aphthae 5 times a year for the past 3 years. HLA-B51 examination was taken and found positive, validating the diagnosis of BD. Prednisone was tapered down and azathioprine (Imuran, GlaxoSmithKline, Triangle Park, N.C., USA) 50 mg/day was started. Due to patient complaints of insufferable side effects, prednisone treatment was tapered off.
For the rest of the follow-up, the patient demonstrated repeat deteriorations whenever prednisone dosage was lowered, similar to the deterioration that occurred in the central nervous system disease after the discontinuation in prednisone. Two weeks following the cessation of prednisone and under a regimen of azathioprine 150 mg/day, the patient returned complaining of visual deterioration, this time OS. BCVA OS was 20/32. No anterior uveitis or vitritis were seen. Blurring of the nasal edge of the optic disc was noted and OCT demonstrated a small amount of subretinal fluid, representing recurrence of neuroretinitis. Prednisone 60 mg/day was recommenced, and azathioprine dosage was increased to 150 mg/day. A week later complete resolution of subretinal fluid was seen, and BCVA OS improved to 20/20.
A month later, while on prednisone 20 mg/day and azathioprine 150 mg/day, the patient presented to the emergency department with acute colitis involving his left colon and sigmoid colon. He refused to undergo colonoscopy and was treated with antibiotics and a prednisone dosage of 30 mg/day, with resolution of the bowel inflammation.
Five months later, under 12.5 mg/day prednisone and 150 mg/day azathioprine, the patient complained again of visual deterioration OS. BCVA OS was 20/100 and 20/22 OD. Few cells were seen in the vitreous OS, accompanied by optic disc margin blurring with a prepapillary exudate. The macula was elevated (fig. ). OCT demonstrated recurrence of neuroretinitis (fig. ). Prednisone dosage was increased to 60 mg/day, and azathioprine 150 mg/day was continued. A week later, substantial improvement was seen: BCVA improved to 20/25, and the macular edema and optic nerve lesion resolved (fig. ).
As the patient presented with several flare-ups under prednisone treatment of more than 10 mg/day and azathioprine 150 mg/day, treatment with azathioprine was replaced with infliximab (Remicade, Janssen Biotech, Malvern, Pa., USA). Under treatment with infliximab infusions and 20 mg/day prednisone, no flare-ups of uveitis or systemic manifestations of BD were noted.


A 52-year-old Saudi woman presented to our outpatient dermatology clinic complaining of multiple painful bumps on her trunk and upper extremities, which had been present for the last 25 years. Recently, the lesions had become more painful to touch and increased in both size and number. She also had a history of uterine leiomyomatosis for which she underwent hysterectomy 17 years ago. A family history revealed that her mother, 2 sisters and 2 maternal aunts also had a history of multiple uterine leiomyomatosis.
A physical examination revealed several smooth, nonmobile nodules that were reddish to brown in color, arranged in a cluster on her right arm (fig. ), left forearm and trunk. The nodules were both firm and tender to touch, ranging in diameter from 0.5 to 2 cm. The most prominent and painful nodules were removed and submitted for histological analysis, which showed a relatively well-circumscribed dermal proliferation of intersecting fascicles of spindle cells (fig. ). The cells exhibited cigar-shaped nuclei and growth in between collagen bundles. The findings were consistent with a diagnosis of benign dermal leiomyoma.
Based on the patient's unique clinical presentation in conjunction with her surgical and family histories, a diagnosis of Reed's syndrome was confirmed. The patient was referred for genetic counseling and for evaluation of renal malignancy. Renal ultrasound and magnetic resonance imaging (MRI) were negative for renal pathology. No symptoms indicative of renal cell cancer were found.
The patient returned to the clinic after 5 years, complaining of more painful lesions.
In this instance, the patient's dermal lesions on her right arm were treated with liquid nitrogen cryotherapy. The therapy consisted of two 30-second freeze thaw cycles with a 1 mm margin. After 2 weeks of cryotherapy, the patient reported a decrease in the pain and size of the lesions (fig. ). One year after cryotherapy treatment, the patient reported nonrecurrence of the lesions, with absence of pain at the site of the lesions.


A 79-year-old male patient was scheduled for holmium laser enucleation and morcellation of the prostate to treat BPH. He exhibited acute obstructive symptoms of the lower urinary tract and gross hematuria. His weight and height were 59.7 kg and 166.5 cm. He was previously healthy and had no other medical history. Preoperative laboratory findings and chest X-ray findings were within normal ranges. Preoperative electrocardiography showed a normal sinus rhythm, and echocardiography showed normal left ventricular function. The volume of the prostate gland, measured preoperatively using endorectal ultrasonography, was 98 ml, including 75 ml for the transitional zone of the prostate.
Upon arrival at the operating room, his systolic/diastolic blood pressure was 120/90 mmHg, heart rate was 70 bpm, and peripheral oxygen saturation was 99%. Routine monitoring was conducted such as electrocardiography, peripheral oxygen saturation, non-invasive blood pressure, end-tidal carbon dioxide, and body temperature. Anesthesia was induced with 250 mg of sodium thiopental, 50 mg of rocuronium, and sevoflurane, and was maintained with sevoflurane (2–3 vol%), N2O (1 L/min), and oxygen (1 L/min), with supplemental rocuronium. Continuous arterial blood pressure was monitored via the left radial artery using a 20 G catheter. Initial arterial blood gas analysis in 50% oxygen showed values of pH 7.42, arterial partial pressure of carbon dioxide (PaCO2) 44 mmHg, arterial partial pressure of oxygen (PaO2) 245 mmHg, bicarbonate (HCO3–) 28.5 mEq/L, base excess 3.4, Na+ 141 mEq/L, K+ 3.7 mEq/L, and hematocrit 40%.
Following repeated massive bladder irrigation with saline, ~150 ml of blood clots were evacuated using an Ellik evacuator and the bladder distension was relieved immediately. Next, holmium laser enucleation and morcellation of the prostate was initiated using an isotonic saline solution for bladder irrigation. At this moment, his vital signs showed a systolic/diastolic blood pressure of approximately 130/80 mmHg, heart rate of 85 bpm, and oxygen saturation at 100%. Peak airway pressure was 11 cmH2O. One hour after the beginning of the procedure, the peak airway pressure increased to 23 cmH2O. On auscultation, the lung sounds were clear. At the end of the surgery, it reached 28 cmH2O. However, oxygen saturation was maintained at 99%. No significant hemodynamic changes developed during the surgical procedure, and estimated blood loss was less than 100 ml. The total operation time was approximately 110 min. During the operation, a total of 45000 ml of saline was used for bladder irrigation. After completion of the procedure, 2 mg of neostigmine and 0.4 mg of glycopyrrolate for neuromuscular blockade reversal were administered intravenously. The patient was extubated after recovery from neuromuscular blockade, which was confirmed by hand grip and head lift.
Immediately after tracheal extubation, he experienced severe respiratory difficulty with low SpO2 (~90%) and complained of severe abdominal pain. Physical examination revealed a tense and distended abdomen. The patient's systolic/diastolic blood pressure was 110/85 mmHg with heart rate of 95 bpm. After applying a 100% O2 mask, arterial blood gas analysis indicated values of pH 7.15, PaCO2 56 mmHg, PaO2 72 mmHg, HCO3– 20 mEq/L, base excess -9.7, Na+ 144 mEq/L, K+ 3.8 mEq/L, and hematocrit 38%. He was re-intubated using 5 mg of midazolam and 30 mg of rocuronium, and his peak airway pressure was 25 cmH2O at this time. Chest X-ray showed acute pulmonary venous congestion and subsegmental atelectasis in both lower lobes. He received 20 mg of furosemide intravenously. The cystogram showed no leakage of contrast media (). An urgent computed tomography (CT) scan of the abdomen and pelvis was performed without tracheal extubation. The CT scan showed massive fluid collection in the abdominal pelvic cavity suggesting bladder wall injury but with no demonstrable discontinuity of the bladder wall (). To relieve intraperitoneal fluid collection, ultrasonography-guided aspiration was performed without complications () and approximately 270 ml of fluid was drained.
The patient was transferred to the intensive care unit (ICU) and was closely monitored. Ultrasonography-guided aspiration was repeated and 320 ml of fluid was drained. Physical examination revealed a soft abdomen. Six hours after arrival at the ICU, careful extubation was performed. His systolic/diastolic blood pressure remained stable, around at 110/60 mmHg, with heart rate of 70 bpm. Urinary output was maintained at 80–100 ml/h after ICU admission without renal impairment. The patient recovered uneventfully and was discharged on postoperative day 2.


A 43-year-old male patient underwent total colectomy for multiple carcinomas in ascending and transverse colon, followed by adjuvant chemotherapy. According to the pathologic report, the pathologic T stage was T2 and T1, for ascending and transverse colon cancer, respectively and N stage was N1c, and tumors showed mucin production (10 %). There was no evidence of other organ metastasis on the initial imaging work up. However, two years later, segmental intrahepatic bile duct dilatation in liver segment 2 (S2) was depicted on the postoperative follow up abdominal computed tomography (CT) scan and there was 4 cm low density mass lesion around the dilated bile duct at the S2 periphery (). For further workup, Gadoxetic acid-enhanced pancreas magnetic resonance imaging (MRI) was performed. We again noted dilated bile duct in S2 with peripheral mass formation (). Within the dilated bile duct, intraductal lesion which showed high signal intensity (SI) on T2-weighted images (T2WI) and low SI on T1-weighted images (T1WI) was identified. After contrast administration, both the intraductal lesion and the peripheral mass did not show avid arterial enhancement and persistent low SI on the delayed phase. The mass demonstrated high SI on diffusion-weighted images (DWI) and low apparent diffusion coefficient (ADC) value. The serum tumor marker, carbohydrate antigen (CA) 19-9 was elevated up to 310.61 U/mL, and carcino-embryonic antigen (CEA) was 15.06 ng/mL. Our first impression was invasive intraductal papillary neoplasm of the bile duct (IPNB), however intraductal metastasis from colon cancer was also considered. He underwent left lateral segmentectomy. However, the histologic diagnosis was metastatic adenocarcinoma from colon with exuberant mucin production and extensive necrosis (40%).


A 55-year-old male patient was referred to our hospital for evaluation of a hepatic tumor. The patient had alcoholic liver disease, and symptoms including jaundice and itching sense had been developed one week ago. Liver function tests showed normal range of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The serum tumor marker, α-fetoprotein (AFP) was also normal range. However, CA 19-9 was elevated up to 465.85 U/mL. There was an intraluminal growing polypoid enhancing mass at the primary confluence of bile duct, extending to the second order branch of right intrahepatic bile duct on CT scan (). On MRI, this lesion depicted as high SI on T2WI, and low SI on T1WI. After, contrast administration, it showed arterial enhancement. It showed washout on portal and delayed phase. And low SI on hepatobiliary phase, and definite diffusion restriction (-). This lesion caused biliary obstruction, resulted in peripheral intrahepatic bile duct dilatation. And the serum total bilirubin level was 17.2 mL/dL, and direct bilirubin was 12.9 mL/dL. Our impression was intraluminal growing hilar cholangiocarcinoma. The patient underwent right hemihepatectomy and caudate lobectomy. However, the histopathologic diagnosis was intraductal growing hepatocellular carcinoma (HCC), confined to the bile duct wall.


A 78-year-old asymptomatic woman was referred to our hospital for further examination of multiple cardiac tumors in the left atrium and left ventricle, which had been detected on echocardiography conducted before chemotherapy for the third recurrence of breast cancer.
The patient was initially diagnosed with right breast cancer in 2003. She had undergone total mastectomy and lymph node dissection before adjuvant chemotherapy. Histopathological analysis indicated scirrhous carcinoma. The first recurrence of the breast cancer was diagnosed in 2007 due to right axillary adenopathy. She had again undergone operation before receiving chemoradiation, and hormonal therapy was started. The second recurrence was detected in 2013, when computed tomography (CT) was performed during a routine outpatient visit. The CT scan revealed right-sided pleural effusion and a mass shadow in the sternum. After switching to another hormonal medication, the pleural effusion disappeared. The third recurrence was confirmed by skin biopsy of a rash on the postoperative scar. Therefore, the regimen was changed to treat the third recurrence of breast cancer. Adriamycin was selected for the patient, and echocardiography was performed for cardiac screening. There were no signs or symptoms such as fever, shortness of breath, platypnea, and systemic embolization until cardiac tumors were accidentally detected on echocardiography. She had never undergone echocardiography previously. She had no family history of cardiac myxoma. Physical examination and laboratory tests showed no spotty skin pigmentation or endocrine hyperfunction. Transthoracic and transesophageal echocardiograms showed 4 tumors in the left atrium and left ventricle ( and ). Coronary angiography showed feeding arteries from the left circumflex coronary artery to the tumors and no obstructive coronary lesion. Although we were not confident about the diagnosis, we decided on surgical resection because the mobile tumors located in the left semilunar cusp of the aortic valve and anterior mitral leaflet carried the risk of causing embolism or obstruction. On pathological examination, all 4 tumors were identified as myxomas (), since they showed myxoma cells with a stellate appearance proliferate in a myxoid background in nests and linear syncytia (). The patient's postoperative course was uneventful with no recurrences as determine by echocardiographic examination during the 12-month postoperative follow-up.


A 71-year-old female was admitted with progressive dyspnea on exertion for 3 days. A transthoracic echocardiogram (TTE) and transesophageal echocardiogram revealed a huge (8.1 × 1.44 cm), highly mobile, echolucent, snake-shaped left atrial (LA) mass with moderate to severe eccentric mitral regurgitation (MR) ().
She underwent surgical removal of LA mass which was 7.0 × 3.3 cm of cardiac myxoma with degenerative change and mitral valve repair using a 26 mm Cosgrove-Edwards ring (Edwards Lifesciences LLC, NY, USA) annuloplasty band with new chorda formation for the A 1, 2 leaflets.
At 18 days after surgery, a complete blood count revealed white blood cell of 9130 103/uL, hemoglobin of 9.7 g/dL, and platelet of 188 103/µL, and reticount was 2.96%. A blood smear exam showed mild normocytic normochromic anemia with anisocytosis and polychromasia. A blood biochemical analysis revealed serum lactate dehydrogenase (LDH) of more than 1800 IU/L, total bilirubin of 1.46 mg/dL (indirect bilirubin, 0.7 mg/dL), aspartate transaminase of more than 2800 IU/L, alanine transaminase of 1471 IU/L, blood urea nitrogen of 34.5 mg/dL, and creatinine of 1.36 mg/dL. There were no specific findings on ultrasonography of kidney and several laboratory tests for autoimmune disease which were conducted to exclude other causes of acute kidney injury. A direct Coombs test was negative and serum haptoglobulin level was 2 mg/dL.
She had complained about dark urine and decreased urine output of 1 L/day on the 34 days after surgery. The vital sign were 130/70 mm Hg of blood pressure, 74/minute of heart rate, 36.3℃ of body temperature, and 20/minute of respiratory rate. Her urine exam was positive for microscopic red blood cell [3–5/high power field (HPF)]. Hemoglobin was 6.8 g/dL, platelet count was 88 103/µL, and creatinine was 1.99 mg/dL. There was no evidence of infection; the patient didn't complain fever and chilling, her C-reactive protein was 0. Also there was no evidence of DIC and she underwent esophagogastroduodenoscopy and colonoscopy to rule out gastrointestinal bleeding, but there was no evidence of bleeding. A blood smear exam () showed red blood cell fragmentation with a few schistocytes (6/HPF) and polychromasia. There were no specific changes of LDH and haptoglobin levels between the 34 days and 18 days after surgery. A follow-up TTE showed no significant interval change.
Associated with outstandingly elevated LDH level and the presence of circulating schistocytes, we considered MAHA which is a non-immune hemolytic anemia resulting from intravascular red blood cell fragmentation. Because the causes of intravascular hemolysis couldn't be distinguished only by laboratory finding and there was no interval change on follow-up TTE, we preferentially assumed red cell fragmentation syndrome which includes TTP-HUS.
With the overall impression of TTP-HUS, we couldn't wait for the result of ADAMTS13 level which has diagnostic value in acute TTP and it takes time about 1 month only available in one center of Korea, we start plasma exchange immediately and maintained this for 3 weeks. However, her anemia with schistocytosis, hyper-indirect bilirubinemia, and high LDH level were not controlled. During the plasma exchange, the creatinine showed a decreasing number of aspects but never decreased to the normal value and the peak level of creatinine was 1.99 mg/dL. The patient didn't undergo dialysis.
At 47 days after surgery, the TTE showed moderate eccentric MR with multiple jet striking the annuloplasty ring ().
The persistent anemia with schistocytosis and the secondary signs of hemolysis prompted a redo of, the MVR with a tissue valve (27 mm; St. Jude Medical, MN, USA) at 57 days after the initial surgery. The operative finding was an irregular and unclean coaptation surface margin of the mitral valve and but the mitral valve annulus was not dilated.
The anemia with schistocytosis and the secondary signs of hemolysis were immediately resolved after the repeat MVR. The creatinine levels were normalized 4 days after MVR. The patient is doing well, with no abnormal findings and has been followed up in outpatient clinic for 5 months.


A 62-year-old female presented with chief complaints of swelling in the left popliteal region since 6 months which progressed rapidly since 1 month after a local quack performed incision and drainage of the swelling. No other constitutional symptoms. On examination, a lobulated swelling of size 6 cm × 5 cm on the posterolateral aspect of the knee joint irregular in shape with smooth surface, well-defined margins, firm in consistency, skin not pinchable, and nonmovable. Tenderness present on deep palpation with the local rise of temperature. Lymphadenitis probably of tuberculous origin was suspected. X-ray revealed no bony involvement. X-ray chest was normal. Magnetic resonance imaging revealed large lobulated 5.5 cm × 3.7 cm × 6.6 cm soft tissue mass along posterolateral aspect of the left knee not infiltrating the bone []. Bone scan revealed increased blood pooling and delayed abnormal tracer uptake from same region representing neoplastic lesion. Incisional biopsy was performed. Intraoperatively, the swelling was in the intermuscular plane and found to be lobulated with focal areas of necrosis. Microscopy revealed fragmented cellular tumor with the lobular arrangement and focal chondromyxoid background. There were round to polygonal cells vacuolated cytoplasm convoluted nucleus with prominent chicken network type of calcification around the individual cells with focal areas of nuclear pleomorphism and mitotic figures. The lesion also contained multiple osteoclastic types of giant cells giving the impression of diagnosis to be chondroblastoma []. To rule out metastasis, computed tomography (CT) chest was done which revealed multiple random soft tissue nodules in both lungs signifying pulmonary metastasis. The oncologist confirmed the patient to be in the fourth stage hence was suggested for palliative radiotherapy. Chest X-ray taken after 1 month showed multiple opacities in the lung field which were not seen in the initial X-ray signifying the rapid and enormous progression of metastasis.


A dermatology consult was sought for a 65-year-old female who developed severe matting of scalp hair for 1 week. She was admitted under medical services for the management of azathioprine (50 mg once daily for a month) induced pancytopenia, which was prescribed for pulmonary sarcoidosis. She gave a history of loss of hair from frontal area of scalp, that came out in bunches, followed by spontaneous tangling of hair over the top of her head to form a stiff protuberant mass []. She denied shampooing the hair immediately prior to this. She had no features of scabies or lice and shampooed her hair once a week with a non medicated shampoo. There was no history of use of any chemical treatment for her hair such as streaking or straightening of hair. There was no associated pruritus or pain. She had no psychiatric comorbidity and was not emotionally and physically neglected. Examination of scalp revealed diffuse non scarring loss of hair over the frontal area and a mass of solid irregular matted hair located over the vertex, approximately 10 cm in height []. There was no foul odor, nits, or crust formation. Investigations revealed total leucocyte count of 0.9 × 109/L (reference range 4.0–11.0 × 109/L), hemoglobin of 7.4 g% (reference range 12–15.5 g%), and platelet count of 0.49 × 109/L (reference range 1.5–4.5 × 109/L). Examination revealed noncicatricial hair loss over the frontal region and elongated stiff protuberant mass of matted hair on the vertex which could not be detangled. Hair pull test was positive with anagen hairs. Microscopic examination revealed ragged irregular breaks in the cuticle. Pancytopenia was managed conservatively, and scalp hair were removed.


A 30-year-old female was referred for the sudden loss of hair and severe tangling of hair that could not be combed for 3 days. Her medical history was significant for the development of hydatidiform mole followed by methotrexate induced pancytopenia, severe stomatitis, and erythema multiforme over hands, feet, and upper trunk []. She was on methotrexate 25 mg once a day for 5 days, two cycles given over a period of 1 month. During her hospital stay, she found difficulty in combing her hair that became extensively tangled. Over next few days, she tried to comb her hair without success and found that her hair had been irreversibly matted and also the loss of hair over frontal area of scalp []. There was no history of skin or hair disease in past, and she regularly shampooed her hair once or twice a week. She was emotionally stable. Pertinent investigations revealed total leucocyte count of 1 × 109/L (reference range 4.0–11.0 × 109/L), hemoglobin of 8 g% (reference range 12–15.5 g%), platelet count of 0.55 × 109/L (reference range 1.5–4.5 × 109/L) and peripheral blood film predominantly normocytic normochromic. On examination, she had extensive noncicatricial alopecia involving the middle two-third of the scalp. An elongated, stiff mass of tangled hair extending downward was present. Hair pull test was positive. There were no signs of parasitic infestations or poor hygiene. Under light microscopy, the matted hair showed hair shaft fractures. She was managed conservatively for pancytopenia and scalp hair were shaved off as a part of treatment for plica.


A 64-year-old male patient underwent TPA for a 155mL prostate. There were no intraoperative complications. On the 5th postoperative day, after removal of the foley catheter, the patient presented recurrent episodes of gross hematuria with a bladder full of clots and anemia that required blood transfusion. Cystoscopy for clot evacuation showed a haematoma caused by arterial bleeding from the left side of the prostatic fossa. The patient underwent computed tomography (CT), which revealed a 2.2 × 1.5 cm hypervascular lesion matching the density of the adjacent iliac vessels on the left side of the residual prostate gland []. The patient was referred to our interventional radiology unit for selective arteriography. A 4 French (Fr) angiographic catheter was inserted via the left femoral artery and left internal iliac arteriography showed a pseudoaneurysm approximately 2 cm in size with venous filling during the early arterial phase, located at the distal portion of the left internal pudendal artery suggesting an AVF []. The left internal pudendal artery was catheterized super selectively with a 2.7 Fr microcatheter and embolization was carried out using two micro coils 3 mm × 40 mm []. After the procedure, the patient had no hematuria and was discharged after 3 days. At 6 months follow-up he had no hematuria, infection or ischemic complications.


A 19-year-old male suffering from facial disfigurement with the loss of his left eye was referred to the Department of Prosthodontics for maxillofacial prostheses. History revealed exenteration of orbit on the left side when the patient was 2-year-old due to the eradication of retinoblastoma causing gross facial hemiatrophy on the left side of the face over the period of time. Examination of the patient showed a large orbital defect on the left side [] with no definite bony or soft tissue undercuts to aid in retention of the prosthesis. The treatment aimed at the reconstruction of ocular surface as well as the soft tissue around it using medically graded silicone retained with silicone adhesives and tapes.
After evaluation and inspection of the anophthalmic socket and defect region [], the diameter of iris and pupil on the intact side was measured using a pair of Boley gauge caliper.
The eyebrow and eyelashes were lightly lubricated. Two direct impressions were made; one was the whole face, and other was just the defect area (for fabrication of the base for prosthesis support) using an irreversible hydrocolloid (Tropicalgin, Zhermack) supported by dental plaster (Kamaraju Co.). Subsequently, a cast was obtained using dental stone type III (goldstone) [].
Since the anophthalmic socket had a redundant eyelid tissue, which was functional during the movement of contralateral eye, it was intended to be blocked out [] before fabricating a heat polymerized acrylic resin (DPI, heat cure) base plate over it, which supported the overlying prosthesis. This base aided in orienting the prosthetic eye in the same plane as that of contralateral eye and to build-up the soft tissue over the atrophic side of the face surrounding the orbit.
A sheet modeling wax (Hindustan modeling wax no. 2) was adapted to fabricate a heat-cured base of acrylic resin after making a wax pattern over the cast obtained during impression made from the defect side. The assembly was acrylized. The resin base was retrieved, finished, and polished. The fit of the base was checked on the cast [] and later transferred to the patients face to check its stability by asking the patient to do functional movements such as smiling, opening and closing the eye, and raising the eye brow.
Measurements were made from the patient's facial midline to the center of the pupil, and from the inner canthus of the eye to the nasal bridge. Both the measurements were made when the patient was asked to look and fix the contralateral eye at distant gaze. These measurements were transferred to the cast to aid in the position of the ocular portion of the orbital prosthesis. A suitable stock ocular prosthesis closely matching the color, size, shape of the iris, and sclera of the other eye was selected as defect was relatively large. The eye was then secured in position on a bed of modeling wax based on measurements obtained, and the anteroposterior position was adjusted and verified on the patient when observed from the side profile and from the top of the head. Once the position was confirmed, the eyelids and the remaining portion was sculpted in wax and tried in the patient's orbital defect [Figure and ].
The wax sculpted prosthesis with the cast was flasked and dewaxed []. Room temperature vulcanizing medical-graded silicone material (M511 Cosmesil) was mixed, a mix of white, brown, and light red pigment stains were blended into the base color of silicon for intrinsic staining based on shade match with the patient's skin color. Silicone was packed and cured at room temperature for 24 h according to manufacturer's instructions. The following polymerization, the prosthesis was deflasked, retrieved, and finished.
A slit was made on the silicone extending from the medial canthus of the eyelid to the lateral canthus of upper and lower eyelid, and artificial eye lash (MAC Cosmetics) was inserted between it and adhered for natural appearance [].
After trial insertion, the acrylic part of the prosthesis was adhered to the socket with the help of a two-way silicon adhesive tape. The silicone part extending from the free ends of the resin plate was coated with a layer of silicone adhesive (Technovent) to camouflage with the soft tissue around the atrophic side of the face. The prosthesis looked more naturally pleasing as patient used spectacle on his day to day basis as well as the atrophic side of the face looked comparatively better after the periorbital rehabilitation [].
Home care instructions like gentle removal of prosthesis at night with the aid of silicone adhesive remover were given. The patient was instructed to avoid extreme heat and the use of soiled hands while handling prosthesis, as that can cause degradation and discoloration of prosthesis. Frequent follow-up was carried out. The patient should be asked to return back a day after the treatment for any tissue reaction. Periodic recall intervals of 1-week and 1-month, respectively.