A 48-year-old Egyptian obese woman, not known to have any medical illness before, was referred by ENT specialist as possible central dizziness with history of severe dizziness, nausea, and vomiting associated with blurring of vision and headache 1 day before. On examination, she was looking ill, with a temperature of 38.4°C, respiratory rate of 21/min, heart rate of 124/min, and blood pressure of 167/93 mmHg. Her chest, cardiovascular, abdomen, and neurological examination were unremarkable, except of mild early bilateral papilledema, neck rigidity, and ataxic gait. A CT scan of brain done with/without contrast in emergency department showed possible left sigmoid sinus partial occlusion. She was admitted and started on heparin infusion and ceftriaxone with good hydration plus amitriptyline, betahistine, cinnarizine, and heparin 5000 IU 6 hourly sc injections. Next day, MRI/MRV of brain was done and reported to be normal, but the platelet count dropped to 109/mm3, and GPT raised to 87 compared to normal result on baseline admission result; this supports stopping heparin therapy. On the third day afternoon, she was suffering from severe diffuse burning quality headache mainly on right tempro-occipital with severe central scalp scratching and pressing like pain last several hours and aborted only on pethidine intravenous injection. On the 4th day, lumbar puncture was done and the CSF was normal. The blood tests for CV, EBV, HIV, and H1N1 were also negative but serum dengue IgM was positive. A CSF sample for dengue IgM sent to private lab reported as positive. Throughout the 23 days admission period, the patient was almost afebrile but showed significant fatigue with bizarre headache appearing as persistent diffuse pressure like headache with attacks of severe bilateral temproparietal burning and central scratching pain associated with nausea, vomiting, dizziness, phonophobia, photophobia, anxiety, and near death phobia and bradycardia (4060) that required many cardiology and psychiatry on call review. On the 22nd day, the patient was discharged after showing reduction of headache attacks severity and frequency with normal blood count and liver enzymes. Then patient was on weekly out-patient neurology clinic follow up for several months using amitriptyline, respridone, and tramadol on need. Then gradually and slowly, headache attacks diminished in frequency and severity, resolving completely about 3 months after onset.


A 46-year-old male patient was brought to Emergency Department of Tertiary Care Centre at Bhavnagar, with, generalized stiffness, fever, generalized tremulousness mutism, perspiration, inability to swallow, intermittent tongue protrusion, sialorrhea, restlessness and insomnia for the last 3 days. Patient was seen by emergency team and was hospitalized in critical care unit. He was diagnosed with schizoaffective disorder of 11 year duration. He was under regular treatment of quetiapine 200 mg/day, divalproex sodium 500 mg/day and lorazepam 4 mg in two divided doses/day since 2006, confirmed by relatives and clinical case records. There was no past history suggestive of similar symptoms, medical disorder or substance use. The paternal uncle was having symptoms of self-talking, abusive, poor self-hygiene, roaming on roads who died at the age of 50 years.
On examination, patient was confused, not oriented to time and place. His temperature was 102°F, blood pressure 150/90 mm of Hg, heart rate 104/min, respiratory rate 20/min. He had generalized tremors, cog wheel rigidity in all extremities and orofacial dystonias. The pupils were normal size and reactive to light. Planters were flexor both sides. He was agitated and was pulling intravenous (IV) lines.
Clinically, NMS was suspected. Other differential diagnoses such us meningitis, encephalitis, substance/overdose or withdrawal, metabolic disturbances, seizure, heat stroke were ruled out. Serotonin syndrome was ruled out because of presence of severe rigidity, absence of hyperreflexia, clonus, diarrhea, in coordination and no use of serotonergic reuptake inhibitors. Lethal catatonia was ruled out because patient did not have initial psychotic symptoms. Blood and urine and cerebrospinal fluid (CSF) samples were sent for examination and culture. A head computed tomography scan, chest X-ray and urine analysis and CSF analysis were unremarkable. The physical and laboratory parameters are shown in .
Patient was admitted in intensive care unit and nasogastric tube and urine catheter was inserted. Quetiapine and divalproex were discontinued. Patient was given 6000 ml/day including dextrose and saline for hydration. Cold water sponging was done regularly to control hyperthermia. Bromocriptine 10 mg in four divided doses through nasogastric tube and intramuscular lorazepam 8 mg/day in two divided doses was started. There was hypernatremia (151 mEq/L) on day 1, which was corrected with successful fluid resuscitation. Vitals, electrocardiogram and urine output were monitored daily. As shown in clinical condition improved on day 3 and patient was able to take oral fluids. The patient was clinically stable and was ambulatory on day 5. There was reemergence of psychotic symptoms such as delusion of jealousy, auditory hallucinations, increased talkativeness and psychomotor activity on the 10th day. Clozapine 25 mg in divided was started with divalproex 500 mg/day. Dose was increased and patient was discharged on the 22nd day with 150 mg/day of clozapine and divalproex 1000 mg/day. Patient significantly improved on discharge and was advised for regular follow-up. Patient well- maintained with the same treatment on follow-up.


A 63-year-old white man with a history of hypercarbic-hypoxemic respiratory failure due to moderate COPD and with mild SAHS, presented with worsening fatigue, dyspnea, and development of peripheral edema. His initial polysomnography 10 years earlier revealed obstructive sleep apnea (OSA) with an AHI of 13.4/hour with oxygen desaturations to 62% on room air, entirely due to obstructive hypopneas. He was completely compliant with CPAP therapy at 11 cm of water pressure in addition to oxygen at 4 liters per minute (LPM), which had been demonstrated to adequately correct his sleep disordered breathing in the sleep laboratory. He was found to have emphysema with an forced expiratory volume in the first second (FEV1) of 67% of predicted. He quit smoking and was compliant with his bronchodilators and medical therapy for diastolic dysfunction.
Despite medical compliance, 8 years later he complained of worsening fatigue. Daytime oxygen requirements while walking rose to 6 LPM and nocturnal oxygen saturations fell to 70% on 5 LPM of oxygen with CPAP. He had to stop working because it was impractical for him to have such high oxygen flows at work. Repeat polysomnography was performed for retitration of CPAP therapy. This demonstrated correction with CPAP at 15 cm of water pressure and 4 LPM of O2, yielding an AHI of 0 with saturations >90%.
Echocardiography and cardiac catheterization showed diastolic dysfunction and no obstructive coronary artery disease or valvular disease. Diuretic therapy was intensified without improving oxygenation or symptoms. Computerized tomography of the chest with contrast showed baseline emphysema and no pulmonary emboli. Repeat pulmonary function was unchanged with FEV1 at 67% of predicted and stable lung volumes. Awake resting arterial blood gas on oxygen at 5 LPM was at baseline (pH: 7.45, PaCO2: 54 torr, PaO: 61 torr). A repeat nocturnal oximetry demonstrated desaturations to 75% on CPAP at 15 cm of water pressure with oxygen at 5 LPM. Interestingly, he never had erythrocytosis with a hemoglobin level of 13.6 g/dl.
He refused suggested tracheostomy in order to initiate nocturnal mechanical ventilation with a positive pressure ventilator, but agreed to have to TTOT in order to improve nocturnal oxygenation. A SCOOP® TTOT catheter was placed using a modified Seldinger technique. Subsequently, CPAP at 15 cm of water pressure was continued with TTOT at 4 LPM. Nocturnal oximetry on these settings showed no desaturations below 87% and <5 min with saturations below 90% []. A repeat blood gas after TTOT was not performed, as this would have required an indwelling arterial catheter to be representative of his true response to therapy while sleeping. Such maneuver was deemed too invasive for clinical therapy, considering his oximetry and overall clinical improvement. A daytime arterial blood gas, in a stable clinical state did demonstrate a decrease in PaCO2 to 48 while awake with TTOT. He had no complications of TTOT except for occasional mucous ball formation early in therapy and occasional tube dislodgment, which over time resolved with further patient education and the addition of guafenesin oral therapy. There were no problems related to air leaks or other pathology around the TTOT catheter site during CPAP therapy, and he markedly improved with decreased fatigue, dyspnea, and edema. He increased his activity level and lost 16 kg with diet and improved exercise tolerance. To determine if CPAP was still required, he was restudied without CPAP and with TTOT at 2 LPM. The overall AHI was 3.5/h, but with a supine AHI of 36/h. Saturations dropped to 87% with 17.2 min <89%. CPAP was reinstituted.
Over the ensuing year he improved further clinically. He intentionally cancelled his disability payments and returned to work as a car salesman with TTOT at 2 LPM with SaO2>90% with ambulation.


A 17-year-old male patient, student and nonsmoker, consulted a local physician at Murshidabad, West Bengal with high grade intermittent fever with chills but no rigors, cough with scanty mucoid expectoration, dull aching chest pain, and generalized weakness for 5 days. The patient's chest X-ray postero-anterior (PA) view at that time showed middle lobe consolidation []. The patient was treated as CAP with oral amoxicillin + clavulanic acid (625 mg) 8 hourly and levofloxacin (500 mg) daily was added afterwards. As the patient's condition deteriorated with documented weight loss of 5 Kg in 2 weeks, his father brought him to our hospital. On examination, the patient was very toxic with blood pressure 90/60 mmHg, pulse rate 130/min regular, respiratory rate 32/min with moderate pallor. Examination of the respiratory system revealed crepitations in the right mammary area. Examinations of other systems were normal. We treated the case as non-resolving pneumonia and did antibiotics adjustment with the intravenous cefoperazone-sulbactam (1.5 g) 8 hourly and oral clarithromycin (500 mg) twice daily along with the other supporting treatment. The investigations revealed hemoglobin 6.4 g%, total white cell count 15200/mm3 with 94% neutrophils; fasting blood sugar 86 mg/dl, urea 45 mg/dl, creatinine 0.8 mg/dl, total bilirubin 0.96 mg/dl, alanine transaminase 78 U/L, aspartate transaminase 82 U/L and alkaline phosphatase 238 U/L. Routine urine examination was normal and culture revealed no growth after 72 h of incubation. Blood culture (two samples) was negative for bacteria. His sputum smear was negative for acid-fast bacilli for 3 consecutive days. Enzyme-linked immunosorbent assay (ELISA) for HIV 1 and 2 was non-reactive. Mantoux test with 5 T.U. was negative. HBsAg and anti-HCV were negative. USG whole abdomen showed hepatosplenomegaly. The patient's condition deteriorated further with appearance of right-sided pleural effusion [] and hepatosplenomegaly. Examination of pleural fluid showed cell count of 560/mm3 with 70% lymphocytes, protein 3.4 gm/dl, sugar 46 mg/dl, lactate dehydrogenase 600 U/L and adenosine deaminase 36 U/L. The patient's contrast enhanced computed tomography (CECT) of thorax showed organization of right middle lobe consolidation with enlargement of right paratracheal and subcarinal lymph nodes with central necrosis []. Fibre-optic bronchoscopy revealed pus coming from the right main bronchus and a gelatinous mass in the posterior wall of trachea and a widened carina with constricted right main bronchus []. Bronchoscopic biopsy from the mass showed inflammatory granulation tissue with proliferation of capillaries and infiltration of a large number of inflammatory cells. Gomori's methenamine silver stain showed fungal spores morphologically resembling Histoplasma capsulatum []. Bronchoalveolar lavage (BAL) and transbronchial needle aspiration (TBNA) from subcarinal lymph node also showed the presence of capsulated round microorganism on a background of inflammatory exudates compatible with Histoplasma capsulatum. Post-bronchoscopic sputum for fungal culture showed a growth of Histoplasma capsulatum. The patient did not have any past history suggestive of exposure to Histoplasma capsulatum. The patient was treated with intravenous amphotericin B 50 mg/day for 1 week followed by oral itraconazole 200 mg twice daily. Significant clinical improvement was noticed by 7 days and follow-up chest X-ray after one month showed a significant radiological resolution [].


A 70-year-old male presented with shortness of breath for 3 days. There was associated mild non-productive cough. Patient had a past history of episodes of cough with expectoration and fever on several occasion. However, the patient had never suffered such a severe respiratory embarrassment in the past. On examination, there was tachycardia (heart rate of 100 bpm), tachypnea (respiratory rate was 25/min) with SpO2 85% and FiO2 50%. Patient was afebrile and blood pressure was within normal range (measured on at least three occasions). On general physical examination, the patient had pallor. However, there was no cyanosis, clubbing or pedal edema. Cardiorespiratory examination was significant for bilateral crepitations and occasional bronchial breath sounds. The heart sounds were normal. Hemogram revealed mild anemia (hemoglobin 11.5 g%). However, the total and differential leukocyte counts as well as platelet counts were normal. Routine biochemical tests including renal and liver function tests were normal. Chest radiograph (CXR) revealed patchy areas of bronchiectasis in both lungs. In addition, there were fibrotic opacities, more on the right side []. Echocardiography revealed dilatation of the right atrium (RA) and ventricle (RV). Associated findings included decreased contractility of RV and moderate tricuspid regurgitation. A diagnosis of acute pulmonary thromboembolism (PTE) was suggested. Doppler ultrasound evaluation of bilateral lower limbs was negative for deep venous thrombosis. Well's pre-test probability score was 4.5 (pulmonary embolism more likely than alternate diagnosis and heart rate more than 100). CT pulmonary angiography (CTPA) was subsequently performed to establish the diagnosis. CTPA excluded the diagnosis of acute PTE; however, high resolution CT reconstructions revealed massive enlargement of trachea (maximum diameter of 33 mm) and right main bronchus (maximum diameter of 25 mm) with evidence of tracheal and bronchial diverticula. There was extensive bronchiectasis involving the right upper lobe with peripheral fibrotic opacities suggestive of parenchymal scarring [Figures and ]. The main pulmonary artery was dilated. Further, the echocardiography findings of dilatation of RA and RV were confirmed. The pulmonary artery hypertension (PAH) was explained to be due to extensive parenchymal disease. Retrospective evaluation of a CXR done 1 year back revealed tracheabronchomegaly. The lung fields were unremarkable. Thus, a diagnosis of tracheabronchomegaly with bronchiectasis and PAH was made and patient was put on oxygen therapy and chest physiotherapy.


A 34 year old female patient reported to Department of Oral Medicine and Radiology, with a chief complaint of swelling of the lower jaw since six years. She stated that a small swelling on the left side of jaw was noticed six years ago, measuring about 1cm in diameter, which gradually increased to the present size, involving both sides of the face. There were no subjective symptoms, except for difficulty in chewing food.
Gross facial asymmetry was noticed due to a swelling involving the middle and lower one third region of the face []. Bilaterally fullness of the cheeks and lower lip with obliteration of the mentolabial sulcus and nasolabial fold was noticed. A well demarcated swelling was noticed over the left cheek region and a diffuse swelling over the right side, which extended from the left ramus of the mandible to the right body of the mandible with obliteration of inferior border of the mandible. Swelling on the left side was roughly ovoid in shape, measuring about 8 × 6 × 5 cm[]. Skin over the swelling was stretched. On palpation the swelling is hard in consistency, lobulated and nontender; with no accompanying cervical lymphadenopathy.
On intraoral examination [], a diffuse swelling was seen extending from the left to right retromolar region. Bilaterally, vestibular obliteration was noticed due to buccal labial and lingual cortical plate expansion with normal appearing mucosa. Swelling was hard, lobulated and nontender. Correlating the history and clinical findings, a provisional diagnosis of benign fibro-osseous lesion of mandible was given and differential diagnosis of fibrous dysplasia, ossifying/cementifying fibroma and central giant cell granuloma (non- aggressive lesion) was given. Patient was further subjected to hematological, radiological and histopathological investigations. Routine hematological examination, serum protein, calcium, phosphorus and alkaline phophatase levels were estimated and the values obtained were within the normal range.
Panoramic radiograph [] revealed a well defined mixed radiopaque and radiolucent lesion, extending from left ramus region to the right angle of the mandible, measuring about 11 × 7 cms. Internal architecture exhibited a cotton-wool pattern of calcification. Centrifugal growth fashion is appreciable, which causes a ball-like circular lesion and bowing of the inferior border of mandible. The inferior cortex is parallel to the tumor mass above with no evidence of erosion. Occlusal radiograph [], revealed irregular expansion of both bucco-lingual cortical plates and lingual displacement of involved teeth. Posterior-Anterior (PA) mandible view [] revealed a mixed radiopaque, radiolucent lesion involving the left ramus region and extending up to the right angle of the mandible.
Plain axial view and 3D-CT scan [Figures and ] revealed a large expansile lesion within the mandible, which involves right and left body and left ramus of mandible, which exhibits mixed sclerotic and lucent areas measuring 11.8 × 7.0 × 7.3 cm.[]
An incisional biopsy was performed and the tissue was sent for histopathological evaluation [] which irregularly shaped bony trabaculae interspersed in connective tissue stroma which is fibrocellular. Trabaculae contains osteocytes in lacunae within them. Several spherical masses of a cellular calcified material resembling cementum were seen through the fibrous tissue. Fibroblasts in the stroma are numerous and spindle shaped with prominent nuclei which were suggestive of cemento- ossifying fibroma. Based on clinical, radiographic and histopathological findings a final diagnosis of giant cemento-ossifying fibroma of the mandible was made.


A 30-year-old, nulliparous woman with a twin pregnancy was referred to our hospital during the 15th gestational week for a routine prenatal check. She had suffered from primary infertility secondary to bilateral salpingectomy, and underwent in vitro fertilization. She had conceived triplets and had chosen selective embryo reduction during the 8th gestational week. The couple was healthy, and neither the history of teratogenic exposure nor the family history were remarkable. Initial ultrasonographic examination (Accuvix XQ, Medison Co. Ltd., Seoul, Korea) with a 2-6-MHz transabdominal probe) during the 15th gestational week revealed a thick dividing membrane and two separated placentas, indicating dichorionic placentation. The amount of amniotic fluid of both fetuses was appropriate for gestational age. Whereas twin A showed normal growth, in twin B, all of the long bones appeared to be abnormally short (the long bone measurements with the femur measuring 11.6 mm, tibia 7.2 mm, humerus 11.5 mm, radius 7.9 mm, all compatible with <5th percentile). Curved femurs with a telephone-receiver-like appearance, short ribs, and a narrow thorax with prominent abdomen were also observed (). The femur length (FL)/abdominal circumference (AC) ratio was 0.12. The vertebral and skull ossification patterns were normal. No overt cloverleaf skull deformity was observed. The nasal bone was not visible but there are no other abnormalities in fetal face.
The couple was counseled about the increased risk of chromosomal abnormality or lethal TD. Thereafter, they decided to undergo an assessment of specific FGFR3 mutations by routine cytogenetic analysis. Amniocentesis of the twins performed during the 15th gestational week showed normal karyotypes (46, XY and 46, XY) for both babies. However, nucleotide sequence analysis of cDNA during the screen for mutations in FGFR3 for twin B revealed a C to T transition at nucleotide 742 (C742T) within exon 6. This heterozygous 742C->T (R248C) mutation in the FGFR3 causes an Arg248Cys (CGC->TGC) substitution. Molecular analysis of the same locus in twin A showed normal finding ().
We counseled the couple extensively, and explained that this genetic condition causes type-1 TD. Thereafter, they decided to proceed with selective fetal termination with the hope of proceeding with a normal singleton pregnancy. At the 19th gestational week, selective fetal termination was performed under ultrasonographic guidance using a 20-gauge needle and injection of potassium chloride into the fetal heart. The remainder of the pregnancy was uneventful and the patient delivered a healthy male infant weighing 3,575 g and a mummified, macerated fetus weighing 91 g during the 39th gestational week by Cesarean section due to persistent occiput posterior position.


Having the first intervention done at another health center, a 38-year-old male patient engaged in mining, presented to our emergency department (ED) with an isolated crush injury of the left leg 18 hours after lateral and medial sides of his left knee was temporarily squeezed at a high speed between a tree and an operative machine. The patient’s history revealed that he presented to the hospital 5 hours after the injury as the skin did not have a laceration. Investigation of the epicrisis reports and hospital records revealed that the patient underwent Doppler ultrasonography at the sixth hour. The Doppler examination revealed the presence of a probable thrombus\in the popliteal area. An embolectomy was attempted with a Fogarty catheter, but was unsuccessful as the catheter did not pass through the distal area. The patient presented to our ED at the 18th hour of the injury. In the immediate physical examination of the patient, the left knee level showed signs of paleness, coldness, anesthesia, hemorrhagic bullae, and ecchymosis posterior to the knee (). Tibialis posterior, dorsalis pedis, and popliteal arterial pulses were not felt. There was no motor function of the ankle and the toes. Successive tendon examination did not show any signs indicating a possible tendon injury. Radiographs of the leg did not show any bone pathology. The previously performed angiography revealed that the popliteal artery was totally occluded and there was no pathway to distal flow (). The patient was transfused 2 units of blood for hematocrit <27%, and as his general condition deteriorated an above-knee amputation was undertaken.
Under spinal anesthesia, the patient was placed in the supine position in a sterile field. Knee tendon examinations did not reveal any pathological finding under anesthesia.
A fish-mouth incision was performed over the skin and the fascia. The bone was shortened 10 cm proximal to the femoral condyle. The popliteal artery and the vein were identified, tied, and cut. The proximal sciatic nerve was dissected, tied, and cut. The adductor magnus muscle was attached to the distal femur rudiment with ticron sutures. The amputation stump was sutured (). Following surgery, when the amputation was investigated, 3 cm of intimal damage to the popliteal artery was detected and necrosis of the muscle, tendon, and neurovascular structures was present at this level. During the post-operational period, no complications developed in the wound and the patient was followed-up on for 2 years.


A 48-year-old male was referred to the endocrinology clinic complaining of generalized edema, increased blood pressure and blood glucose levels. The patient was on medication due to hypertension that was diagnosed 1 year ago. Recently, the blood pressure was not well-controlled, the blood glucose level was high and generalized edema developed.
The patient was diagnosed with MTC 14 years ago; total thyroidectomy with right cervical lymph node dissection was performed and I-131 metaiodobenzylguanidine (MIBG) 200 mCi was administered. He was treated with tumor resection for recurred MTC on a mediastinal lymph node 13 years ago. Nine years ago, MTC recurred on the left cervical and left parahilar lymph nodes and was treated with I-131 MIBG 200 mCi after surgery. Two years ago, MTC recurred thirdly on the cervical and mediastinal lymph nodes and lung and was treated with cervical and mediastinal lymph node dissection and the left upper lobe wedge resection of the lung. Since then, the patient has not shown any signs or symptoms of recurrence.
The patient's height was 172 cm and weight was 84 kg, 2 kg over his usual weight. His blood pressure was 185/110 mm Hg with a pulse rate of 90 beats per minute and a breathing rate of 18 breaths per minute. The patient's body temperature was 37℃. Moon face and facial flushing were observed. Buffalo hump and purple striae were absent. Mild pitting edema was observed on the anterior tibia and slight skin pigmentation was present.
Peripheral blood examination showed a white blood cell count of 14,450 cells/µL, hemoglobin of 15.3 g/dL, and platelet count of 358,000 cells/µL. On serum biochemical examination, total cholesterol was 252 mg/dL with total protein of 6.5 g/dL, albumin of 4.1 g/dL, total bilirubin of 1.1 mg/dL, alkaline phosphatase of 101 U/L, aspartate aminotransferase of 17 U/L, alanine aminotransferase of 62 U/L, blood urea nitrogen of 10.3 mg/dL, and creatinine of 0.6 mg/dL. On serum electrolyte examination, sodium was 145 mmol/L with potassium of 2.8 mmol/L, chloride of 94 mmol/L, and bicarbonate of 40.4 mmol/L. Fasting plasma glucose level was 168 mg/dL with glycated hemoglobin of 8.6%. Hormone examination showed total T4 of 12.75 µg/dL (range, 5 to 13) and thyroid stimulating hormone of 0.07 µIU/mL (range, 0.15 to 5.0). Serum calcitonin was 127.86 pg/mL (<10.0) and carcinoembryonic antigen was 29.46 ng/mL (<5). Plasma ACTH concentration was measured with immunoradiometric assay (ELSA-ACTH kit, CisBio, Belford, MA, USA), and was 203.9 pg/mL (range, 6.0 to 60.0). Serum cortisol concentration was 36.0 µg/dL (range, 5 to 25.0) with a 24-hour urine cortisol of 2,237.1 µg/day (range, 20 to 90). On the low dose dexamethasone suppression test, inhibited serum cortisol was 32.50 µg/dL. The 24-hour urine examination results were as follows: metanephrine 14.46 µg/day (range, 52 to 341), normetanephrine 28.21 µg/day (range, 88 to 444), epinephrine 6.57 µg/day (<40), norepinephrine 26.43 µg/day (<80), and vanillylmandelic acid 3.51 mg/day (<8). To validate the RET gene mutation, peripheral blood was collected from the patient and white blood cells were separated by centrifugation to extract genomic DNA. For polymerase chain reaction, BIGDYE version 3.1 cycles sequencing kit (Applied Biosystems, Foster, CA, USA) reagent was utilized and 3,730 automated sequencer (Applied Biosystems) was used to analyze DNA sequence. The DNA sequencing showed no RET gene mutation.
Chest and abdomen computed tomography revealed recurred lesions on the mediastinal lymph nodes, lungs, and liver (), but no abnormal findings in adrenal glands (). Sellar magnetic resonance imaging showed no abnormality in the pituitary gland (). Gastroscopy, colonoscopy, and positron emission tomography did not identify suspicious primary lesions in other regions.
Calcitonin and chromogranin A staining was positive on resected tissues on the third recurrence 2 years ago, which is indicative of MTC. ACTH immunohistochemistry staining was negative ().
Because curative resection of the MTC lesions was difficult on the fourth recurrence, close follow-up with further chemotherapy was considered. To control the ectopic ACTH syndrome, the patient was administered ketoconazole. The dosage was gradually increased over 3 months up to the maximum dosage (1,200 mg/day), but the serum cortisol concentration level did not decrease. Therefore, bilateral adrenalectomy was performed. After surgery, ACTH remained above 200 pg/mL, but plasma glucose and blood pressure levels were improved sufficiently and the oral antidiabetic agent and antihypertensive medication were discontinued. The patient has been living in good condition until 6 months after the surgery without any medication other than glucocorticoid and mineralocorticoid agents.


The present case is about a 26-year-old male patient who presented to our emergency department with 3 days history of abdominal pain, distention and bilious vomiting. He had no previous surgery and did not recollect similar episodes in the past. On examination, he was afebrile and hemodynamically stable. Blood counts and biochemical values were within the normal limits. On clinical examination, abdomen was distended with visible intestinal peristalsis, but without any guarding. There were no surgical scars and hernial orifices were free. Plain X-ray abdomen showed dilated small bowel loops with multiple air fluid levels []. Ultrasound abdomen suggested the possibility of an appendicular mucocele. He was taken up for urgent laparotomy with a clinical diagnosis of acute intestinal obstruction. Intra-operatively there was minimal hemorrhagic fluid localized in right iliac fossa and small bowel loops were dilated. A MD was seen attached to the mesentery of nonadjacent small bowel by a peritoneal band, which was arising from its tip. The diverticulum was axially torted and gangrenous. In addition there was compression of ileum by the peritoneal band resulting in intestinal obstruction, which was relieved on dividing the band []. Resection and anastomosis of the small bowel including the MD was performed. Recovery was quick and uneventful and patient was discharged within a week.


A 43-year-old chronic alcoholic male patient presented in emergency with complaints of severe diffuse pain abdomen associated with vomiting of 2 h duration with a history of mild upper abdominal pain for last 15 days. He was not a known diabetic or hypertensive. On clinical examination, the patient had diffuse tenderness and distension of abdomen and no guarding or rebound tenderness. Laboratory investigations revealed leucocytosis with counts of 16,500, raised serum amylase and lipase with normal liver enzymes and alkaline phosphatase and random blood sugar was raised. X-ray chest and abdomen showed raised left hemidiaphragm and no air fluid levels or free gas under diaphragm. Ultrasonography of the abdomen did not reveal any significant abnormality. Diagnosis of acute pancreatitis was made and patient was managed conservatively and responded well to treatment but his blood sugar level remained high for which he was given insulin. Contrast enhanced computed tomography (CECT) of abdomen was performed after 6 days of admission, which showed intrapancreatic pseudocyst in the head of pancreas with dorsal agenesis of pancreas and eventration of left hemidiaphragm ( and ). Patient was discharged in stable condition after 9 days of admission on oral antibiotics and insulin.


A 28-year-old female was admitted in our department because of a large right-sided intracerebral hemorrhage as a result of a ruptured arteriovenous malformation. She underwent neurosurgical and endovascular treatment. Due to a post hemorrhagic hydrocephalus external ventricular drain was performed. During the intensive care treatment she unfortunately developed meningitis. After antibiotic treatment, the meningitis was cured and a ventriculo peritoneal shunt was performed. However, the follow up imaging, revealed an isolated enlarged fourth ventricle despite shunting of the lateral ventricles. Therefore a shunting of the fourth ventricle has been done as well. Nearly 22 months later the patient presented again with secondary walking and coordination impairment.
Neurological examination showed increasing ataxia and eye movement disorder beside the known left-sided hemiparesis. Cranial computed tomography (CT) demonstrated remarkable dilation of fourth ventricle indicating a shunt dysfunction. Furthermore syringomyelia without tonsil herniation has occurred, which was identified through cervical magnetic resonance imaging (MRI) extending from C2 to C7. The complete replacement of the dysfunctional shunt system was immediately performed. Postoperatively, the syringomyelia resolved within 6 months and the associated neurological deficits improved as well. An entire resolution of the trapped fourth ventricle was confirmed on CT scan ().


A 28-year-old female presented to emergency department with complaints of generalized abdominal pain, non-passage of feces and flatus, and multiple episodes of vomiting of 4 days duration. There was no history of surgery and no comorbidities. On examination, there was tachycardia, hypotension, and signs of dehydration. Abdomen examination revealed generalized distension, diffuse tenderness, guarding and absent bowel sounds. Hematological and biochemical investigations revealed leukocytosis with neutrophilia, raised blood urea and serum creatinine. X-ray chest and abdomen showed no free gas under diaphragm, there were multiple air fluid levels, and dilated small bowel loops. Ultrasonography of abdomen showed dilated small bowel loops with moderate amount of interbowel fluid. As there were signs of septic shock, and strangulation, and renal function tests were deranged, contrast enhanced computed tomography (CECT) was not performed. With the diagnosis of small bowel obstruction and a possibility of strangulation, after nasogastric decompression, aggressive preoperative fluid replacement, and correction of electrolyte disturbances, emergency exploratory laparotomy was done. On exploration, small bowel loops were dilated, and a long segment of small bowel were infarcted. The mid, distal jejunum and proximal ileal loops were found to pass through a defect in the proximal jejunal mesentery () with compression of vascularization of herniated bowel loops (). Rest of the small bowel, colon and stomach were normal. After reduction of herniated bowel loops, resection of the gangrenous loops with end to end anastomosis between proximal jejunum and mid ileum was performed and mesenteric defect was closed properly. Postoperative period was uneventful and patient was discharged on postoperative day 8.


A 16-year old male presented with non-bilious emesis. His emesis began 5 days earlier, upon discharge from the hospital after posterior spinal fusion for scoliosis. Born in Korea, he was adopted and brought to the United States as a baby. His birth history and biological family medical history are unknown. He underwent left congenital diaphragmatic hernia repair soon after birth, orchiopexy for undescended testis at age 5 years, Ladd procedure for small bowel malrotation and obstruction at age 6 years, and additional laparotomy for small bowel volvulus with lysis of peritoneal adhesions and appendectomy at age 14 years. His medical history also included left lung hypoplasia, ostium secundum atrial septal defect (ASD), left pulmonary vein stenosis, and chronic asthma, for which he took fluticasone proprionate/salmeterol and trimethoprim/sulfamethoxazole. He had no known history of renal disease, vesicoureteral reflux, urinary tract infection (UTI), or embolic disease. He was a junior in high school, taking advanced placement courses.
The patient’s height and weight were 170 cm (between 25th and 50th percentiles for age) and 35.9 kg (below 5th percentile for age). He had an oral temperature of 36.1°C, blood pressure of 127/76 mmHg, and heart rate of 81 beats per minute. His precordium was hyperdynamic, and a II/VI systolic murmur was heard. He had a midline abdominal wall scar, normal bowel sounds and no rebound tenderness or guarding. Scoliosis and a healing incision from recent spine fusion were apparent. Micrognathia was also present, but no other orofacial, ocular, aural, or limb deformities were noted. Laboratory results obtained in evaluation of emesis included normal serum electrolytes, amylase and lipase.
Chest and abdomen radiographs showed mixed bubbly lucencies and curvilinear opacities in the left lower hemithorax, and the possibility of a recurrent diaphragmatic hernia with bowel migration into the chest was raised. Due to complexity of the patient’s anatomy and his past surgical history, abdominopelvic CT with oral and intravenous contrast was pursued in lieu of ultrasound for further evaluation of the diaphragm and bowel. CT revealed evidence of prior left diaphragmatic hernia repair and Ladd procedure with bowel malrotation. No recurrent diaphragmatic hernia was seen; pleuroparenchymal scarring and atelectasis at the left lung base, alternating with areas of relatively well-aerated lung, explained the plain radiographic abnormalities. There were no CT findings of bowel obstruction, mass, or inflammation. However, renal craniocaudal dimensions of 7.5 cm on the right and 8.7 cm on the left were below the 5th percentile for age. In addition, both kidneys were abnormal in appearance (), providing impetus for further investigation into the patient’s renal status.
Serum creatinine was 1.2 mg/dL (reference range: 0.6-1.1 mg/dL), and blood urea nitrogen was 13 mg/dL (reference range: 6-20 mg/dL). Estimated creatinine clearance was 99.2 mL/min/1.73 m2 [calculated by the original Schwartz equation, before isotope dilution mass spectrometry (IDMS)-traceable standardization of creatinine calibration]. Hemoglobin (12.7 g/dL) and hematocrit (36%) were normal. Although urine dip testing showed no protein seven days prior to the CT scan, protein was present in urine (30 mg/dL) on repeat dip testing done the day after CT scanning.
Open surgical biopsy of the right kidney was performed. The surgeon did not report any visible scarring on the exposed surface of the kidney. Histopathological examination of the biopsy specimen revealed findings consistent with oligomeganephronia, namely normal parenchymal organization but hypertrophy of glomeruli and tubules (). There were very few globally sclerotic glomeruli, but many tufts contained segmental zones of perihilar sclerosis. These changes were accompanied by streaks of fibrosis, tubular atrophy, and chronic inflammation. There was no evidence of renal dysplasia, medullary nephronophthisismedullary cystic disease complex or polycystic kidney disease. Electron microscopy demonstrated minimal foot process effacement and was negative for glomerular basement membrane changes of hereditary nephritis. Liver biopsy, performed in conjunction with renal biopsy, was normal.
The patient’s emesis was attributed to postoperative ileus and narcotic effect. Symptoms resolved as narcotics were weaned. With improvement in nutrition, along with sodium, potassium, and phosphorus restriction, the patient gained ten pounds in five months. Lowdose lisinopril was initiated for mild hypertension and proteinuria. In addition, vitamin D3 therapy was begun. With time, serum creatinine increased (), and the patient became progressively fatigued. Prior to renal transplantation for renal failure at age 20 years, serum creatinine was 5.4 mg/dL and creatinine clearance was 13.6 mL/min/1.73 m2 (calculated for an adult using the IDMS-traceable modification of diet in renal disease study equation). Urine protein:creatinine ratio peaked at 1.9 (reference range: <0.2).
Ultrasound of the native kidneys () was first performed after renal transplantation and showed small, echogenic kidneys with poor corticomedullary differentiation, in keeping with presence of chronic renal parenchymal disease. The sonographic appearance had no specific features to indicate etiology of the renal disease. No renal cysts or calcifications were seen.


In April 2013, a 71-year-old female with no significant past medical history presented to our institution with painful bowel movements for the last 3 months. The patient also noticed blood-streaked stools and reported a 16-lb unintentional weight loss over a 1-year period. The review of her systems was negative otherwise. On examination: the woman was 5′ 7.5′ (1.715 m) tall, weight was 172 lb (78.019 kg), with a BMI of 26.54, and her vital signs were normal. Digital examination of the rectum revealed two small hemorrhoids at the 6 o'clock position and a firm, nonobstructing mass near the anal verge. The patient underwent a colonoscopy in September 2013 which revealed a nonobstructing, ulcerated anal mass, approximately 1 cm from the anal verge. A biopsy of the mass demonstrated an invasive, poorly differentiated carcinoma (fig. ). Stains for CK5/6 and P63 were positive, likely suggesting a primary squamous cell carcinoma of the anus. Tumor markers including CEA, CA 15–3 and CA 27–29 were negative. A CT of the abdomen and pelvis demonstrated an abnormal mass at the anorectal junction, with no evidence of lymph nodes or liver metastases in September 2013 (fig. ). PET combined with a CT scan demonstrated marked metabolic activity in the primary anal mass and a 1-cm perirectal lymph node near the coccyx, suggesting a node-positive disease in October 2013 (fig. ). An MRI of the pelvis confirmed the PET/CT findings (fig. ). The patient's tumor was sent to an outside institution for a second opinion, and the report was concluded as the tumor may in fact be a malignant melanoma. The patient subsequently underwent an exploratory laparotomy with an APR and left-end colostomy in October 2013. The patient tolerated the surgical procedure without any complications. The pathologic specimen confirmed a malignant melanoma arising in the anal skin and extending into the rectum, involving the anal and perirectal soft tissue and 6 regional lymph nodes (fig. ). The tumor was classified as grade 3, poorly differentiated, stage IIIA, T2N1M0 according to the tumor-node-metastasis classification of colorectal cancer []. Immunohistochemical analysis results were positive for the expression of the S-100 protein, HMB-45 and vimentin, whereas negative for the expression of cytokeratin and SMA (fig. ). The patient agreed to the plan of starting chemotherapy with mitomycin and 5-fluorouracil (for the anorectal melanoma).


A 51-year-old woman with a history of bipolar affective disorder was presented to our hospital with an 8-h history of nausea and epigastric pain radiating caudally. Three months prior to admission, an elevated serum triglyceride level (408 mg/dL) was noted, but the patient didn't receive any lipid-lowering agents. Two months before presentation, she was treated for bipolar effective disorder with valproic acid 500 mg twice daily, quetiapine 600 mg at bedtime, and flurazepam 30 mg at bedtime. One month prior to admission, valproic acid was tapered and stopped, and quetiapine dose had been increased to 800 mg at bedtime. At current presentation, she was taking both quetiapine 800 mg and flurazepam 30 mg at bedtime. There was no history of alcohol abuse, recent abdominal trauma or surgery, preceding viral syndromes, or cholelithiasis, and no other concomitant medications were being used.
The initial physical examination indicated a diffuse abdominal tenderness without muscle guarding or rebound tenderness, and hypoactive bowel sounds were auscultated. Laboratory studies showed a leukocyte count of 9.9×109/L, with a differential count of 68% neutrophils and 24% lymphocytes. Serum electrolytes and liver function tests were within normal limits. Other pertinent laboratory values included a serum amylase of 352 IU/L (normal, 30-110 IU/L), serum lipase of 1210 IU/L (normal, 23-300 IU/L), triglyceride of 1508 mg/dL (normal, 35-150 mg/dL), and a total cholesterol level of 450 mg/dL (normal, 130-200 mg/dL). Abdominal ultrasound showed no evidence of gallbladder disease or dilatation of the bile ducts. Abdominal computed tomography showed a blurring contour from pancreatic head to tail, with minimal fluid collection at the pancreatic head region. A diagnosis of acute pancreatitis was made.
Then the patient was treated symptomatically with volume repletion and meperidine for pain relief. Quetiapine was suspected as the cause of severe hypertriglyceridemia, and was immediately withdrawn. In addition, treatment with oral fenofibrate 160 mg daily was commenced for reducing serum triglycerides. Ten days later, the patient was free of abdominal pain, the serum amylase and lipase values were normal, and the triglyceride level was reduced to 337 mg/dL. The patient was discharged on the following medications: aripiprazole 5 mg at bedtime, flurazepam 60 mg at bedtime, and fenofibrate 160 mg once daily. The patient was discharged with appointments for follow-up with the endocrinology and psychiatry services. She was asymptomatic at the 3-month follow-up.


A 40-year-old male presented with confusion, short-term memory loss, and unsteady gait for one month. He also complained of intermittent right facial numbness, diplopia, bilateral lower extremity numbness and weakness, and severe choking spells while coughing. The patient mentioned that when he had visited Ohio four weeks ago, a dead bird was found with West Nile virus infection. On examination, he was drowsy, but oriented to time, place, and person with mild maculopapular rash on his upper back, chest, and face. Cranial nerve examination revealed a subtle downbeating nystagmus. His motor strength, sensory exam, and deep tendon reflexes were normal. The cerebrospinal fluid (CSF) showed lymphocytic pleocytosis, while the remaining results were normal. The patient was started on empirical antibiotics, while the culture results were awaited. Magnetic resonance imaging (MRI) of the brain and complete spine were unremarkable. The patient had pronounced bilateral subconjunctival hemorrhage with progressive drowsiness the next day. West Nile IgM in the CSF was noted to be positive, while his mental status deteriorated and he required intubation within the next 24 hours. Electroencephalography (EEG) showed mild bicentral slowing, with no evidence of epileptiform discharges. An ophthalmology examination showed acute hemorrhagic conjunctivitis, conjunctival chemosis, and periorbital edema, with no chorioretinitis on fundoscopy (). Supportive management was continued with gradual improvement of his mental status.


A 29-year-old African-American male was admitted to our hospital because of headache associated with nausea, vomiting, and blurred vision. Intermittent headaches over the preceding 4 years were ascribed to CM1. In the month prior to admission, the patient's headaches had increased in frequency and in severity. He described the headaches as pounding and rated the intensity of the pain as 10 on a scale of 0 to 10, where 10 is the most severe. The pain began in the occipital region and extended to the forehead unrelated to coughing or straining. A few days before admission, nausea, vomiting, and blurred vision accompanied some of the episodes of headache. As the patient's headaches continued to worsen, he was admitted to an outside hospital. Magnetic resonance imaging (MRI) of the brain showed an 18 mm cerebellar tonsillar herniation and a disproportionately large communicating fourth ventricle with dilated but stable ventricular system, and no change from previous studies []. Cervical spine MRI was normal. In light of the patient's worsening symptoms, he was transferred to the University Hospital of Brooklyn for surgical intervention. The patient did not report limb weakness, paresthesia, or breathing difficulty, nor a history of cardiac arrhythmia, hypoglycemia, alcohol abuse, or epilepsy. The patient had no family history of neurologic or cardiac disease. Preadmission medications included variable amounts of acetaminophen, hydrocodone, and ibuprofen for headache control.
On evaluation, the patient's vital signs were normal, the lungs were clear and no bradycardia or cardiac pauses were observed. He was alert and oriented. There was no nuchal rigidity to passive flexion of the neck. The pupils were equal and reactive to light. The optic disc margins were sharp and the visual fields were normal. The remainders of the physical and neurological examinations were normal except for mild bilateral horizontal gaze-evoked nystagmus and a slightly unsteady gait. Laboratory studies, including complete blood count, serum electrolytes, blood glucose, urine specimen, and the results of the blood pressure and heart rate monitoring were normal. The patient was considered in stable condition because of a stable ventricular size with stable vital signs, relative preservation of motor and sensory pathways, and no respiratory stress during alertness. In light of his presumed stable condition, medical management of the patient's acute cephalodynia rather than urgent surgery became the priority. He was disconnected from the vital signs monitor and admitted to the neurosurgical ward for surgery to be scheduled after presurgical risk assessment testing, including routine laboratory studies, chest X-ray, and electrocardiogram. Medical management of the patient's pain during the first 24 hours of admission, starting in the emergency room and continuing in the neurosurgical ward, included 60 mg of codeine by mouth, 650 mg of acetaminophen by mouth, 10 mg of intravenous (IV) morphine sulfate (2, 4, and 4 mg at 4-hour intervals), 4 mg of IV hydromorphone, and 10 mg of IV metoclopramide. At 4:10 am on the second day of hospitalization, about 26 hours after admission, the patient complained of severe headache. Upon rising from bed, he became incontinent of urine. After the patient was placed in bed, hydromorphone 4 mg and metoclopramide 10 mg were given IV. At 8:00 am, the patient was found cold and pulseless in bed with no recordable blood pressure or cardiac activity on electrocardiogram and was pronounced dead. A complete postmortem examination revealed a CM1 with mild hydrocephalus without uncal herniation or syringomyelia. Toxicological screening was negative. The cause of death was not identified, but myocardial infarction, cardiac conduction defect, and suffocation due to vomiting or choking were convincingly excluded.


A 75-year-old right-handed female patient was admitted to our hospital for the evaluation of recurrent fevers. She had been well until 3 weeks before admission, when fever and fatigue developed. She had a history of cholecystectomy, spinal compression fracture, and an old cerebral infarction of the left middle cerebral artery. After the brain infarction, she developed aphasia and right hemiplegia and became dependent on a wheelchair. She showed paroxysmal atrial fibrillation, and warfarin was prescribed to prevent a second stroke.
On examination, her blood pressure was 150/70 mm Hg, her pulse 90 beats per minute, and her body temperature was 37.5°C. There was a small decubitus ulcer on the sacrum and a nonpitting edema in both legs. No lymph node swelling was noted. Neurological examination revealed aphasia and right hemiplegia. The rest of the examination was normal. Her white blood cell count was 11,000/mm3 (reference range 3,500–8,000/mm3). Her blood levels of lactate dehydrogenase (LDH), C-reactive protein, and soluble interleukin-2 receptor (sIL-2R) were high at 458 IU/l (normal <229 IU/l), 16.8 mg/dl (normal <0.8 mg/dl), and 3,458 U/ml (normal <515 U/ml), respectively. Her blood levels of electrolytes, glucose, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, amylase, brain natriuretic protein, and vitamin B1 were normal, as were her renal and thyroid function. Lumbar puncture was performed; there was no pleocytosis in the cerebrospinal fluid, but the protein and IgG levels were increased to 85 mg/dl (normal <50 mg/dl) and 17 mg/dl (normal <4 mg/dl), respectively. A urine culture showed no growth. Blood specimens were sent for cultures of bacteria, mycobacterium, and fungi. All results were negative. A contrast-enhanced CT of the chest, abdomen, and pelvis failed to reveal any abnormal lesions that could have caused the fever. No adrenal gland mass was noted. A brain MRI obtained 3 weeks after admission showed an old infarction but was otherwise normal. Tests for antibodies to hepatitis B, hepatitis C, human immunodeficiency virus, human T-lymphotropic virus, and the Treponema pallidum were negative. Antibiotic treatments including ciprofloxacin at 600 mg/day, panipenem/betamipron at 1 g/day, and ceftazidime at 2 g/day combined with arbekacin at 200 mg/day were undertaken, but all were ineffective. 67Ga scintigraphy showed no abnormal uptake. The fever continued for more than 3 weeks and fulfilled the criteria for FUO. Because the serum levels of LDH and sIL-2R remained high, we suspected a hematogenous tumor such as myeloma, and bone marrow puncture was performed, but the result was normal. Although there were no skin lesions, we strongly suspected IVL and thus performed a random skin biopsy. The biopsy was obtained from 1 lesion of the purpura on the abdomen and 2 regions of the skin with a normal appearance on the abdomen and left thigh. Histological examination revealed atypical cells lodged in the intravascular lumens in the subcutaneous tissue of the normally appearing left thigh region (fig. ). Higher magnification revealed vessels filled with large malignant lymphoid cells and eosinophilic nucleoli (fig. ); the cells were stained with CD20 antibodies but not with CD3 (fig. ). The patient was thus diagnosed with IVL (intravascular large B-cell lymphoma). Her consciousness deteriorated 6 weeks after admission. An MRI obtained 7 weeks after admission showed a mass lesion involving the right basal ganglia, thalamus, corona radiata, uncus, and crus cerebri (fig. ). The mass was isointense on a T1-weighted image, hyperintense on a T2-weighted image, and exhibited mild restricted diffusion on a diffusion-weighted image (DWI). The mass was homogeneously enhanced (fig. ). No definite ischemic lesions were noted. All radiological findings were compatible with those of PCNSL. The patient's status was too poor for chemotherapy. An MRI obtained 9 weeks after admission showed an enlargement of the mass (fig. ). She died 11 weeks after admission. Permission for a postmortem examination was not obtained.


A 28-year-old female presented with complaint of pain and swelling in her left inguinal region since 1 month. Swelling was insidious in onset, with a slight increase in the size of the swelling since its occurrence. There was no history of vomiting, bowel and bladder dysfunction. On examination, an oval, approximately 4 × 3 cm in size, tender, cystic and fluctuant swelling was present in the left inguinal region. Transillumination test was negative. Swelling was irreducible against manual pressure. There was no expansible cough impulse, peristaltic activity or abnormal vascularity-associated with the swelling. Signs of inflammation were absent. Lymph nodal examination was normal. Ultrasonography revealed left inguinal hernia, with well-defined, oval, anechoic cystic swelling within the inguinal canal measuring 4 × 3 cm []. Patient underwent laparoscopic excision of cyst of canal of Nuck with left inguinal hernioplasty. Peritoneum was opened and hernia defect was identified []. Round ligament was identified along with the hydrocele of the canal of Nuck. Cyst of canal of nuck was separated from the round ligament and excision of the cyst of canal of Nuck was carried out []. A 15 × 10 cm polypropylene (Prolene, Ethicon, Mumbai, India) mesh was placed to cover the hernia defect []. Peritoneal flaps were approximated. Post-operative period was uneventful and patient recovered satisfactorily. Histopathologic examination confirmed it as Hydrocoele of canal of Nuck. Patient is asymptomatic on follow up.


The present case report is about a 22-year-old male patient who presented with enlarged right cervical lymph node. Biopsy revealed-Hodgkin's lymphoma (mixed cellularity). 18F-FDG PET/CECT performed for staging revealed metabolically active lymph nodes on either side of the diaphragm [, broken arrows], enlarged spleen with multiple hypodense hypermetabolic, lesions [, arrow] (SUVmax= 9.4; Spleen SUVmax/liver SUVmax ratio = 3.76) and bone lesion. He was then given 6 cycles of chemotherapy and 18F-FDG PET/CECT was done for response evaluation. PET/CT showed complete metabolic response, with normal spleen uptake [, arrow] (Spleen SUVmax= 2.5, Liver SUVmax= 2.6 S/L ratio = 0.96). At 1-year later routine follow-up the patient complained of mild fever, lethargy and listlessness. In view of previous history of Hodgkin's lymphoma, relapse was suspected and 18F-FDG PET/CECT was advised. PET/CT revealed enlarged spleen with diffusely increased FDG uptake [Figure –, arrow] (SUVmax= 5.3; Liver SUVmax= 2.3 S/L ratio = 2.30). The first differential in the given clinical scenario was splenic relapse of lymphoma, however, a second differential diagnosis of some infective/inflammatory process was considered. On further evaluation, peripheral smear showed evidence of malaria parasite infection (Plasmodium vivax). The patient was then started on anti-malarials with complete clinical improvement. Follow-up PET/CT after 7 months revealed normalization of size and 18F-FDG uptake of spleen [, arrow] (SUVmax= 3.0; Liver SUVmax= 2.7 S/L ratio = 1.1). This clinical case can be easily misinterpreted as lymphoma relapse. Hence, malaria and other relevant (endemic) infective possibilities (Kala-Azar etc.) should be considered and further investigation, if warranted, should be advised.


A 41-year-old woman presented with recurrent, metastatic, ER-positive invasive ductal carcinoma. The patient had initially presented 10 years prior with a palpable breast lesion. Pathology at the time of initial diagnosis was remarkable for a 7-cm invasive ductal carcinoma with lymphovascular invasion, as well as positive metastatic lymph nodes with evidence of extracapsular extension. Immunohistochemistry demonstrated the tumor to be ER-positive (70%), progesterone receptor-negative, and HER2-positive.