A 13-year-old girl presented with inability to weight bear on the left lower limb. 10 months back she had sustained fracture around the left hip following trivial fall and was confined to bed. 4 months after this fall, she underwent surgery of left hip (it could be verified from patient records that she had pathological fracture neck of femur secondary to the unicameral bone cyst and was treated by open reduction, subtrochanteric valgus osteotomy, and fixation with sliding hip screw). Following surgery, she continued non-weight bearing ambulation with crutches as any attempt to bear weight resulted in pain. Examination revealed the following ROM of the left hip: Flexion - 110°, extension - 5°, abduction - 30°, adduction - 20°, and internal and external rotations - 10° each. There was true supratrochanteric shortening by 2 cm. Radiographs revealed ununited transcervical fracture neck of the femur with sliding hip screw in situ and evidence of healed subtrochanteric osteotomy. There was no evidence of any focal bone pathology. Treatment given: Both cases were operated in the fracture table under general anesthesia. Hip joint was accessed through Watson Jones approach. All implants were removed. Cancellous bone graft harvested from ipsilateral iliac crest interposed at the pseudarthrosis site after freshening. Non-vascular fibular strut graft of appropriate length inserted through the sliding screw tract across the fracture site. Lateral based (1.5 cm) subtrochanteric wedge removed to valgise the femoral neck to a desirable extent (aimed at increasing the neck-shaft angle by 15°). Both the osteotomy and fracture fixed with contoured 4.5 narrow dynamic compression plate and screws. In Case 1, a cancellous screw could be passed into the neck across the pseudarthrosis. It was not possible in Case 2 as the neck was very narrow. Case 2 had an interfragmentary screw across the osteotomy site. Histopathological examination of the bone wedge removed revealed evidence of fibrous dysplasia in Case 1 and did not show any pathology in Case 2. Presumably, the cyst had healed though previous radiographs showing the cyst was not available. ROM exercises were started in the immediate post-operative period for both cases. They were made to walk non-weight bearing with axillary crutches for a period of 2 months after which they progressed to partial weight bearing as tolerated. Once evidence of full union was noted on the radiographs, they were progressively made to weight bear fully, and crutches were discarded. The fracture united uneventfully in both cases. The results and follow-up characteristics are summarized in ( and ).


A 54-year-old woman was brought to the emergency department after a syncope at home. The patient had been cleaning the barbecue in the garden when she felt ‘hard heart beats’ and passed out without further warning. The patient had no memory of the incident that had resulted in a mild head trauma.
Her past medical history was remarkable for deep vein thrombosis (∼10 years earlier), ankylosing spondylitis, depression, and a recent transient ischaemic attack (TIA). Approximately 5 years earlier the patient had undergone a coronary angiogram following an episode of chest pains. The angiogram had identified no atheromatosis. Cardiovascular risk factors encompassed hypertension, well-controlled hypercholesterolaemia, and depression. The patient had never smoked and did not have diabetes or a family history of heart disease or sudden premature death. The physical examination, including a cardiac and neurological examination, showed no abnormalities.
At admission, the patient was prescribed the following: citalopram 40 mg/day, adalimumab 40 mg subcutaneously/2 weeks (for ankylosing spondylitis), paracetamol p.n. 1 g max 4 times/day, enalapril 10 mg/day, atorvastatin 40 mg/day, and clopidogrel 75 mg/day.
A CT scan of the cerebrum showed no cerebral damage. The ECG showed sinus rhythm and QTc interval +600 ms (Figure ). Blood tests were largely normal [serum: potassium 3.4 mmol/L (ref 3.5–4.6 mmol/L) and magnesium, 1.01 mmol/L (ref 0.71–0.94 mmol/L)]. Haemoglobin, leucocytes, creatinine, sodium, alanine transaminase, basic phosphatase, and C reactive protein were within normal ranges. Also, troponin I and D-dimer were not elevated. A transthoracic echocardiography was performed, showing no abnormalities.
After 1 day of telemetry, an episode of self-terminating Torsade de Pointes (TdP) lasting 18 s was recorded (Figure ). The patient was conscious during the episode but reported feeling dizzy and that symptoms were similar to what she had felt before her syncope the previous day. Empirical treatment with 16 mmol intravenous magnesium and 3 g of potassium chloride was immediately given. Serum potassium increased to 3.8 mmol/L on the following day but the QTc interval remained prolonged (640 ms).
The case was conferred with a psychiatrist, and citalopram was tapered under simultaneous rapid titration of sertraline to 100 mg/day. Citalopram was completely discontinued from Day 5. At 1 week from admission, the QTc duration was within normal range (Figure , QTc 450 ms), but the QTc duration fluctuated and was found outside normal range at Day 9 (600 ms), before normalization at Day 15 (460 ms). Earlier ECGs were available for evaluation; previous recordings showed QTc between 440 and 580 ms (Figure ).
At this point, it was considered possible that the patient was afflicted with the congenital long QT syndrome; even though two known triggers of induced QTc prolongation were present, correction of these did not clearly normalize QTc duration. In addition, previous ECG recordings clearly documented intermittent, significant QTc prolongation over an extended time period. On Day 8 treatment with atenolol 25 mg was initialized. On Day 9, an implantable cardioverter-defibrillator (VVI-ICD) was implanted. Genetic testing was ordered and the proband was found to be heterozygote carrier of the KCNE1 D85N (c.253G>A) variant.
The patient was closely followed the first 6 months after the TdP episode and seen monthly in the out-patient clinic. Currently, the patient is scheduled for follow-up with her cardiologist yearly, her ICD is interrogated in clinic every 6 months and by remote monitoring every 4 months. In 18 months of follow-up, the ICD has not registered any arrhythmias.


A 69-year-old man presented to the emergency department with three days of right upper quadrant and epigastric pain, jaundice and nausea. He had no previous abdominal surgeries.
On examination he was found to be jaundiced, with right upper quadrant tenderness. He had a negative Murphy’s sign. Liver function tests demonstrated a bilirubin of 154 umol/L, with an alanine transaminase of 732 U/L, aspartate transaminase of 448 U/L, alkaline phosphatase of 244 U/L and gamma-glutamyl transferase of 636 U/L. He was placed on intravenous ceftriaxone and metronidazole while awaiting imaging.
Transabdominal ultrasound of the biliary tract was limited by bowel gas but reported an impression of multiple stones in the region of the gallbladder. The CBD was measured at 7 mm but was not entirely visualized and intrahepatic ducts were dilated up to 5 mm.
The patient then proceeded to have a magnetic resonance cholangiopancreatography (MRCP) scan for further assessment of the biliary tree. This demonstrated choledocholithiasis within the distal CBD measuring 5.9 mm. The gallbladder was reported as only seen on axial T2 weighted images (Fig. ). The impression was the patient may have chronic cholecystitis with a shrunken gallbladder. Given the experience of the hepatobiliary surgeon involved in the case, a decision was made to proceed to laparoscopic cholecystectomy.
On laparoscopy, the gallbladder could not be identified on exploration of the liver bed. The principle of safe dissection, above axis of the sulcus of Rouviere, was followed to identify landmarks. MRCP imaging was reviewed again intra-operatively to help guide the surgical team and avoid commencing the dissection too low, given that a gallbladder was not present in the fossa. A 2 cm cystic duct stump and cystic artery was identified (Fig. ). An intra-operative cholangiogram was performed, confirming a distal CBD filling defect (Fig. ). CBD clearance under direct vision with choledochoscopy was performed to extract a 7 mm stone. The cystic duct was then secured with two PDS Endoloop® Ligatures and sent for histology. A drain tube was placed along the liver bed.
The patient was discharged home Day 5 post-operatively following removal of his drain tube. He was reviewed in the general surgery outpatient clinic 2 weeks following discharge where he had made a good recovery. There were no symptoms or signs of post-operative complications and his pain had resolved. His bilirubin and liver function tests had returned to normal. He was subsequently discharged from clinic following this review.


A 61-year-old otherwise healthy elderly Indian male presented to our surgical outpatient department with a 4-year history of a painless, cutaneous lesion in the lower back which had shown a rapid increase in size for the past 6 months. On clinical examination, the supragluteal region showed a grey-brown color, large, cauliflower-like, polypoidal growth measuring approximately 6.5 × 4.5 × 2.5 cm with normal appearing surrounding skin and free from underlying structure []. There was no associated lymphadenopathy. Imaging evaluation with magnetic resonance imaging demonstrated a well-defined mushroom-shaped lesion appearing intermediate in signal intensity on T1 and T2, with hypointense stalk limited to superficial skin with no evidence of deep invasion. The lesion appeared hyperintense in fat-suppressed sequence. The routine laboratory investigations were unremarkable. Clinical and radiological findings were suggestive of a malignant cutaneous tumor. A wide local excision was performed []. Upon histopathological examination, cut surface of the specimen was friable, grey-white with cystic changes, and showed epidermis with papillomatosis with papillary projections extending and invaginating in a cystic space. These papillary invaginations were lined by glandular epithelium with apocrine differentiation, comprising two layers of epithelial cells: inner luminal surface columnar cells with decapitation secretions and basilar outer cuboidal cells []. The outer epidermis of the lesion extended into a growth showing hyperkeratosis, acanthosis with mild dysplasia and invasion in deep dermis by squamous nests, with surrounding dense mononuclear cell infiltrates and desmoplastic reaction, and evidence of keratin pearl formation []. The histopathological findings were consistent with well-differentiated SCC arising within SCAP. The surgical margins of the specimen were clear. There was no evidence of lymphovascular or perineural invasion. The postoperative recovery was uneventful. On follow-up at 3 years, the patient showed no evidence of local recurrence or metastasis.


A 72-year-old woman with a history of chronic renal insufficiency, hypothyroidism, peripheral neuropathy, hypercholesterolemia, anxiety, and tremor was referred from her primary care physician’s office to the emergency department for evaluation of pancytopenia. Her peripheral neuropathy had been managed with carbamazepine for several years. Bone marrow biopsy revealed infiltration and near-total replacement by cells filled with eosinophilic crystalloid material (, ). Hematopoietic cells were virtually undetectable, and extensive reticulin fibrosis was noted. CD138-positive, κ-restricted plasma cells () were highlighted to form collections and aggregates in the marrow, comprising at least 30% of total cellularity. No definitive IgG, IgA, or IgM was observed within the plasma cells. Histiocytes comprised the remainder of the cell population and were highlighted by CD68 () and CD163. κ expression () was also noted within the histiocytes. CD34 and CD117 failed to reveal a significant blast population. Other than occasional expressions, no significant myeloid population was highlighted by CD15. No CD1a expression was observed within histiocytes/macrophages. No metastatic carcinoma was revealed by cytokeratin. CD61 also failed to reveal the presence of megakaryocytes.
By polychromatic flow cytometry, approximately 58% of cells in the specimen displayed the phenotypic and light scatter properties of lymphocytes. Most of these were T cells, without specific phenotypic abnormalities, including CD4-positive and CD8-positive subsets (CD4:CD8 ratio of 2.5:1). B cells comprised approximately 12% of cells. No normal B-cell precursors (hematogones) were seen. Phenotypically mature B cells comprised a mixture of κ- and λ-bearing cells, without evidence of light chain restriction. Cells with the phenotypic and light scatter properties characteristic of plasma cells comprised 4% of cells, and included predominantly a cytoplasmic κ-restricted plasma cell population. No definitive expression for IgA, IgG, IgD, and IgM was noted within the plasma cells. CD34-positive myeloblasts comprised approximately < 1% of cells. Very few granulocytic cells were observed (17% of total cells), and 5% nucleated red blood cells were seen.
Further workup including serum protein and immuno-fixation electrophoresis showed hypogammaglobulinemia and markedly elevated monoclonal free κ light chains with a free κ:λ ratio of more than 700:1. These findings were most consistent with CSH associated with plasma cell myeloma. The patient was immediately placed on bortezomib and dexamethasone. Subsequent skeletal survey revealed no significant evidence of lytic lesions.
Formal written informed consent was not required with a waiver by the appropriate Institutional Review Board of Hartford Hospital (FWA00021932).


A 28-year-old man, who underwent live-related (Donor: father) renal transplant from outside hospital in 2015, on maintenance immunosuppression with tacrolimus, prednisolone and mycophenolate mofetil, presented with fever for 1.5 months, shortness of breath for 10 days, and hematochezia for a week. There was an associated rise in serum creatinine from a baseline of 1.3 to 11 mg/dl. A renal biopsy performed for allograft dysfunction was suggestive of polyomavirus infection. The patient was started on hemodialysis and referred to our unit for further management. The patient had a pulse rate, blood pressure and respiratory rate of 112/min, 100/60 mm of Hg, and 24/min, respectively. On examination, he had right-sided pleural effusion. Peripheral smear examination revealed microcytic hypochromic anemia with hemoglobin of 5.7 g/dl. Patient's general condition was stabilized with 3 units of packed red blood cell (RBC) transfusion. His HIV status was negative. Computed tomography angiography of the abdominal vessels, upper GI tract endoscopy, and the sigmoidoscopy were unremarkable. The pleural fluid revealed a total count of 400 cells/uL (90% polymorphs), protein of 1.5 g/dl, sugar 102 mg/dl (corresponding blood sugar 180 mg/dl), adenosine deaminase of 40.67 IU, and the gene Xpert was positive for Mycobacterium tuberculosis (MTB). The patient was subsequently started on anti-TB therapy and alternate day hemodialysis for anuria. After 3 days, patient developed hematochezia with subsequent shock. The patient was stabilized with fluids, and blood transfusion and an urgent upper GI endoscopy followed by sigmoidoscopy was performed, which were normal. A 99m technetium labeled RBC scan was done, which showed evidence of active GI bleed, likely site being the terminal ileum and caecum. In view of life-threatening LGI bleed, emergency laparotomy along with intraoperative enteroscopy [] was performed and showed multiple ulcers in terminal ileum, caecum, and proximal ascending colon along with multiple sessile polyps in the ileum []. Intraoperatively, there were multiple adhesions with thickened mesentery, and a mural thickening of 3 cm length at 2.5 feet proximal to ileocecal (IC) junction was observed. A right hemicolectomy followed by end ileostomy was performed. The biopsy unveiled necrotizing epithelioid cell granulomas with multinucleated giant cells cuffed by lymphocytes; stain for acid-fast bacilli (AFB) showed many AFBs (gene Xpert was positive for MTB) and a diagnosis of ulcero-constrictive TB of the intestine was made. During the hospital stay, the patient developed wound infection followed by wound gaping, swab culture, and sensitivity showed growth of Acinetobacter baumannii and was started on intravenous colistin in renal modified dose. However, his sepsis further worsened, and the patient succumbed to his illness.


A 76-year-old man with a history of type 2 diabetes mellitus, hypertension, old cerebrovascular accident, and spinal stenosis. He presented with anemia and tarry stool initially. Upper gastrointestinal (UGI) panendoscopy and abdominal computed tomography (CT) revealed a submucosal tumor, consistent with gastrointestinal stromal tumor, so he was regularly followed up at the gastrointestinal outpatient department. However, stool occult blood positive with anemia was still found 3 months later, but no tarry stool, poor appetite, nausea, vomiting, abdominal pain, or body weight loss was found. Owing to the aforementioned, UGI panendoscopy was performed again, which showed a hyperemic area at the posterior wall of the high body to the cardia and a submucosal mass, approximately 1.8 cm, with tiny erosions at the lesser curvature side of the antrum. In addition, no preoperative hiatal hernia was found (). The biopsy of the high body showed a poorly cohesive carcinoma. Then, an abdominal CT scan disclosed a gastric polypoid tumor, approximately 1.5 cm, with penetrating subserosal connective tissue without invasion of the visceral peritoneum or adjacent structures, cT3N0M0, stage IIA. Thus, preoperative peripheral parenteral nutrition support was provided, and then laparoscopic total gastrectomy with Roux-en-Y anastomosis in the ante-colic route and D2 lymphadenectomy were performed. An extra 1-cm esophagectomy above the gastroesophageal junction was also performed for the equivocal frozen pathology without mediastinal lymph node dissection. No intraoperative complications were observed, and the hiatus was not opened wide during the surgery, in which the crus muscle was transected by dividing the phrenoesophageal membrane only for creating enough space for the side-to-side esophagojejunostomy (EJS) anastomosis using a linear stapler(Endo-cuter J&J, 45–3.5; ). The common entry hole was then closed using an intracorporeal continuous suture of 3-0 V-Loc, and the final pathological report was poorly cohesive carcinoma, pT4aN1M0, stage IIIA, with a clear surgical margin.
Five days later, follow-up chest radiography demonstrated a hiatal hernia over the left chest (). As the postoperative course was uneventful, the hiatal hernia was followed up with observation. The patient gradually started water intake, a liquid diet, and a soft diet. However, 8 days after the operation, he presented with poor appetite and abdominal fullness, which progressed to vomiting, dyspnea, and high fever (39.5°C). A laboratory examination revealed a white blood cell count of 20,300/μL and C-reactive protein level of 19.2 mg/dL. The chest-to-abdominal CT scan demonstrated a disruption of the left-side diaphragm, with a severely distended small bowel herniation into the left pleural space and massive pleural effusion (). A diagnosis of incarcerated hiatal hernia was made, and emergent exploratory laparotomy was performed. Intraoperative findings revealed the herniated Roux limb through the defect on the diaphragmatic hiatus into the left pleural cavity with massive pleural effusion and food material (). The incarcerated intestine was drawn back into the abdominal cavity safely. A transient ischemic change of the Roux limb was observed, which improved after reduction. Unfortunately, EJS leakage and perforation of the small intestine, 20 cm above the jejunojejunal anastomosis, were also found. The perforated intestine was repaired using a linear stapler (Endo-cuter J&J, 45–3.5), the EJS anastomosis was reinforced for poor healing with a 3-0 silk suture, the crus was approximated with 2 figure-8 sutures, and the diaphragm was repaired with 1-0 Prolene suture (). Feeding jejunostomy was performed for nutrition support. Moreover, for the left pyothorax and EJS leakage, thoracoscopic decortication of the left chest and esophagostomy with T-tube diversion were performed. Then, the patient was transferred to the intensive care unit for postoperative monitoring.
Enteral nutrition via a jejunostomy tube begun on postoperative day 1. Bacteremia and fungemia were found later, but after antibiotic treatment and intensive care, he recovered well except for a mild residual empyema. In addition, the esophagogram showed no anastomotic leakage and no recurrent hiatal hernia (), so oral intake was started. Then, he was discharged after 92 days of hospitalization under a stable condition.
At the latest follow-up, the patient had a fall event that caused an intracranial hemorrhage and sudden-onset desaturation several days later, which caused his death.


The patient is an 18-year-old woman. When she was 13 years old, she visited a doctor because of primary amenorrhea. Chromosome analysis revealed 46, XY karyotype (), and she had an artificial menstrual cycle for 2 years. On June 1, 2016, the then 16-year-old woman visited the emergency room following a complaint of acute abdominal pain. A computed tomography (CT) scan revealed a pelvic mass, and the initial AFP level was >3,000 ng/mL. Laparoscopic pelvic tumor resection was performed at a local hospital. Intraoperative observation showed that the patient had typical female external genitalia with sparse pubic hair and a normal clitoris. The mass was approximately 10 cm in diameter and was not connected to the vagina, and the fallopian tubes were discovered on the side of the mass. No other tumors were observed after a comprehensive intraoperative exploration was performed. The mass was completely resected, and the pathology report confirmed that the histological type of the gonadal tumor was YST without other GCT or SM components after extensive sampling. Smooth muscle tissue lined with the endometrium was also observed from certain sections, which indicated that both the uterus and pelvic tumor had been resected. After the surgery, seven cycles of chemotherapy were performed: four cycles with PEB and three cycles with PE. The AFP level was within the normal limits after the second cycle. However, a CT scan after the seventh cycle revealed abdominal and pelvic metastases including liver metastases. Furthermore, continuous vaginal bleeding occurred after the surgery. Hysteroscopic exploration was performed to search for the cause of vaginal bleeding. According to the local operation recording, a 3 cm neoplasm in the vagina, which was not connected to the pelvic cavity, was noted. The symptom of vaginal bleeding was still observed after the surgery, and she received hemostatic drugs as the symptomatic treatment.
After almost 1 year since the last chemotherapy was performed, the patient was referred to our hospital because of vaginal bleeding and abdominal distension. A whole-body tomography-computed tomography (PET-CT) scan revealed multiple metastases in the abdominal wall and pelvic cavity, and on the surface of the liver and intestine. All tumor markers including AFP were within normal ranges. Consultant pathology reports revealed YST in the first surgery, but SMs derived from YST for the second surgery.
Owing to the different pathology reports and continuous vaginal bleeding, we performed laparoscopic exploration and examination under anesthesia. Intraoperative findings included the following: 1,500 mL bloody ascitic fluid, multiple gray solid tumor nodules on the omentum majus and liver surface, and an approximately 3 cm bleeding nodule on the anterior abdominal wall (). There was a bleeding neoplasm in the vagina, and after its resection, ulcer tissues could be seen at the deep end of the vagina. After exploratory surgery, the platelet level gradually declined for an unknown reason and decreased to 30×109/L on the third day after the surgery. The patient presented with symptoms of hemorrhagic shock, and we had to perform emergency exploratory laparotomy on that day owing to acute intraperitoneal hemorrhage. The operation (right streak gonad resection, omentectomy, and tumor resection) was performed after obtaining informed consent from the patient. The primary purpose of the second surgery in our hospital was hemostasis, and it was impossible to perform satisfactory tumor reduction at that time (remaining tumor >1 cm).
The pathology report confirmed SMs derived from YST, and the specific histological type of SM was sarcoma. His-topathological analysis of liver metastatic tumors revealed a lacunar, microcystic, or reticular pattern. Irregular or fusiform tumor cells were variably sized with severe nuclear atypia. Mitotic figures were observed. Pleomorphic tumor giant cells could be seen and had a scattered distribution. The stroma was edematous with multifocal hemorrhage (). IHC staining showed that tumor cells were focally positive for AE1/AE3 (), but negative for GPC3 and Sal-like protein 4 (SALL4) (), and the Ki-67 labeling index was approximately 10% (). Histopathological analysis of the vaginal tumor revealed the same pattern (). IHC staining showed that tumor cells were negative for AE1/AE3, GPC3, and SALL4 (). Histopathological analysis from the right gonad sections revealed fibrous tissue with no germ cells, which indicated PGD (), and IHC staining was negative for octamer-binding transcription factor 3/4 (OCT3/4) (). All micrographs were taken using an Olympus Camera U-TV0.5×C.
Considering the sarcomatous components of the tumor, we performed three cycles of PEI (cisplatin, etoposide and ifosfamide) chemotherapy. However, pelvic ultrasound revealed that the pelvic residual lesions did not reduce and vaginal bleeding was still observed, while all the tumor markers were within normal ranges. We also performed whole exome sequencing, and the germline mutation results demonstrated copy-number variations of FGF9 gene (chr13:21948488-25914325)×1 and frameshift mutation of MAP3K1 gene c.2822_2827delCAACAA (p.Thr941_943del); somatic gene mutation of samples from the primary gonadal tumor and metastatic tumors revealed a non-synonymous mutation of KRAS (c.182A>G). There was no indication for currently targeted drugs.
After communicating with the patient, she refused to undergo further treatment. At the time of this writing this report, the patient has been alive with the disease 7 months after the final PEI chemotherapy was administered.


A 66-year-old female patient had experienced intermittent right epigastric pain for almost 2 mo.
A 66-year-old Chinese female presented to our hospital with intermittent right epigastric pain for 6 mo. An enhanced computed tomography (CT) scan of the abdomen revealed a solid lesion with a size of 2.3 cm × 2.3 cm in the junction of the left lateral lobe of the liver. Contrast-enhanced ultrasound suggested the presence of hepatocellular carcinoma. Subsequently, a radical partial hepatectomy was performed and the operation went smoothly. Except for regular follow-up examinations, the patient did not receive adjuvant chemotherapy or radiotherapy. However, enhanced CT of the abdomen and fluorine-18-fluorodeoxyglucose positron emission tomography/CT (PET/CT) suggested lymph node metastases. She was unsuitable for surgery because of the location and number of metastatic lymph nodes. The patient was admitted to our department for further evaluation and treatment.
She had a 16-year history of chronic hepatitis B virus infection.
Unremarkable.
Vital signs, such as respiration, pulse, temperature, and blood pressure, were within the normal range. There were no other positive signs with the exception of mild tenderness in the right upper abdomen.
The initial laboratory examinations included a complete blood count which showed a normal white blood cell count, haemoglobin, and platelet count. Liver enzymes were elevated: alanine transaminase, 26 IU/L; aspartate transaminase, 23 IU/L; and serum albumin, 27.3 g/L. Quantitative analysis of hepatitis B markers revealed that the level of hepatitis B virus surface antigen was 829.9 IU/mL. She was negative for hepatitis B surface antibody and hepatitis B virus e antigen, but positive for hepatitis B e antibody and hepatitis B core antibody.
Contrast-enhanced CT of the abdomen revealed enlarged lymph nodes in the portacaval space and the zone of the pancreatic head and ligamentum hepatogas-tricum. PET/CT confirmed metastases according to the history of hepatic FDCS (Figure ).


A 53-year-old man with no history of specific disease presented with abdominal pain. He visited another hospital and underwent laboratory tests and abdominal computed tomography. He was diagnosed with chronic hepatitis B and liver cirrhosis (LC) associated with hepatocellular carcinoma (HCC) and was referred to our hospital for further work-up and suitable treatment.
At the time of admission, the patient’s blood pressure and pulse rate were 140/90 mm Hg and 90 beats per minute, respectively. Further, his breathing rate and body temperature were 22 breaths per minute and 36.4°C, respectively. Abdominal distension and shifting dullness were observed, whereas no palpable mass, tenderness, or rebound tenderness was detected in the abdomen. The results of complete blood cell count were as follows: white blood cell count, 5,630/mm3; hemoglobin, 9.7 g/dL; hematocrit, 28.5%; and blood platelet count, 73,000/mm3. Moreover, the results of serum biochemical test were as follows: total protein, 6.0 g/dL; albumin, 1.8 g/dL; total bilirubin, 1.53 mg/dL; aspartate aminotransferase, 95 IU/L; alanine aminotransferase, 15 IU/L; alkaline phosphatase, 697 IU/L; gamma-glutamyltranspeptidase, 166 IU/L; blood urea nitrogen, 19.4 mg/dL; and creatinine, 1.0 mg/dL. Prothrombin time and activated partial thromboplastin time were within normal limits.
Abdominal ultrasonography, dynamic magnetic resonance imaging, and esophagogastroduodenoscopy (EGD) were performed, and ultimately, the patient was diagnosed with LC, HCC infiltrating both the liver lobes with portal vein thrombosis, grade 2 esophageal varices with red color sign, and type 2 gastroesophageal varices (GOV2). On day 4 of hospitalization, he underwent prophylactic endoscopic variceal ligation (EVL) and transarterial chemoembolization in accordance with the Barcelona Clinic Liver Cancer guidelines for HCC. Despite appropriate management, the patient’s liver function gradually deteriorated, and esophageal variceal bleeding (EVB) and hepatic encephalopathy recurred during admission.
On day 12 of hospitalization, he presented with hematemesis (400 mL of blood) resulting from EVB and was immediately transferred to the intensive care unit. EGD and therapeutic EVL, along with aggressive blood volume resuscitation and intravenous administration of terlipressin, were performed to control EVB but failed because of unstable vital signs and massive bleeding. SB tube insertion (All Silicone Sengstaken–Blakemore Tube®; Create Medic Co., Yokohama, Japan) was performed as subsequent treatment, and medical therapy including administration of terlipressin was continued. On day 13 of hospitalization, grade 2 hepatic encephalopathy developed, and the SB tube was abruptly cut off because of the patient’s irritability.
Emergency EGD showed esophageal and gastric balloon transection from the SB tube, which remained fully inflated and impacted. We attempted to deflate the balloon using various methods based on previous reports. Endoscopic injection needle (WS-2416PN2504; Omnimed Ltd., England, UK) and endoscopic cutter (FS-5L-1; Olympus, Tokyo, Japan) were initially used, but the balloon, having thick elastic walls, was not easily punctured. We subsequently used endoscopic hot biopsy forceps (FD-1U-1; Olympus) and employed argon plasma coagulation, which proved unsuccessful as the balloon, which was made of silicone, had excellent electrical insulating and heat-resistant properties. On the presumption that a sharper and more rigid instrument could cut the balloon, we finally chose and used endoscopic scissors (FS-3L-1; Olympus) to perforate the balloon (), and the deflated balloon was gently removed using an endoscopic snare (SD-210U-10; Olympus) without any complication ().


A 50-year-old woman came to the hospital with chief complaints of abdominal discomfort and pain. Abdominal examination revealed mild ascites. Computed tomography showed a well-defined heterogeneous poorly enhancing mass measuring 5.5 cm × 4.5 cm × 4.3 cm in the right ovary and mild ascites. Serum CA125 levels were within normal limits. Clinically, a diagnosis of malignant ovarian epithelial malignancy was considered, following which total abdominal hysterectomy with bilateral salpingo-oophorectomy was performed, and the specimen was sent for histopathological examination. Grossly, the right ovary showed a well-demarcated solid and spongy tan lesion with focal hemorrhagic specks measuring 3 cm × 2.5 cm × 1.5 cm. The residual ovary showed cystic change with yellowish discoloration []. Microscopically, sections from the right ovary showed a vaguely lobular lesion composed of closely packed capillary sized blood vessels lined by bland endothelial cells with hobnail appearance, arranged in anastomosing or sinusoidal pattern in a hyalinized and edematous stroma. Few capillaries showed fibrin thrombi. Scattered mononuclear cells were seen within the capillaries and stroma. The residual ovarian stroma showed stromal luteinization [ and ]. Immunohistochemically, the endothelial cells showed strong positivity for CD31 [] and CD34 confirming the vascular origin of the lesion. The stromal cells were negative for these markers.


A 31-year-old woman was seen in the Rheumatology Clinic due to a history of 6-month onset of pain and swelling in the hands. Furthermore, in the last year, she presented with frequent nasal ulcers. She had no fever or deterioration in her general health status. Diagnosed with epilepsy at the age of 12, with partial seizures, she has been on CBZ treatment (300 mg twice daily) for 18 years, with good clinical control. Fifteen years ago, an attempt was made to withdraw the antiepileptic medication, but with the appearance of new seizures, it was decided to maintain the treatment. The cardiac-pulmonary auscultation was normal in the physical examination, with arthritis being observed in the carpal, metacarpophalangeal, and proximal interphalangeal joints. No skin lesions, enlarged organs, or swollen lymph glands were observed. The complete blood count results showed a hemoglobin of 11.5 g/dL, with a hematocrit of 32.5%. The white cells were normal, as well as their differential count and number of platelets. The liver and kidney function tests were normal, as well as the thyroid hormones and the hepatitis B and C serology. The rheumatoid factor was negative, and the antinuclear antibodies (ANA) were positive to a titer of 1/1280 (homogeneous pattern), and positive anti-nucleosome antibodies. The rest of the antibodies were negative, including anti-dsDNA, anti-histones, anti-Sm, anti-RNP, anti-Scl70, anti-PMScl, anti-Ro/SSA, anti-La/SSB, anti-Jo1, anti-centromere, anti-PCNA, anti-ribosomal P, anti-neutrophil cytoplasmic antibodies (ANCA), and anticardiolipin IgM/IgGs. The complement levels were low, with a C3 of 62 mg/dL (normal: 90–180) and a C4 of 6 mg/dL (normal: 10–40).
The patient was diagnosed with probable lupus induced by CBZ, and treatment with hydroxychloroquine (200 mg/day) was started. The Neurology Department was consulted on the withdrawal or change of anticonvulsant treatment. An EEG was performed, in which the presence of irritative activity was observed in the left anterior temporal region, for which treatment was initiated with levetiracetam (1000 mg twice daily), with the gradual withdrawal of CBZ. The clinical symptoms of the patient disappeared after the CBZ withdrawal. The hydroxychloroquine was discontinued as well, and the lupus clinical symptoms did not reappear during the 1-year follow-up. The ANA remained positive to a lower titer (1/640) during that same period, with negativization of anti-nucleosome antibodies.
In addition to the case presented, reports of CBZ-DILE were identified using the PubMed/Medline database. The following combined two groups of keywords were used: (lupus, systemic lupus erythematosus, SLE, lupus-like, SLE-like, drug induced lupus) and (carbamazepine, Tegretol, anticonvulsant). Reports of CBZ-DILE from databases were included if clinical information was available. The search was conducted in February 2018.
Three series (, , ), with a majority of coincident cases and several isolated cases (, , , , –) of CBZ-DILE, have been published with clinical information on patients taking CBZ, up to a total of 27 cases, including our patient (). Two cases of CBZ-induced cutaneous lupus were also found (, ), as well as 2 cases of DILE in patients taking the drug analogue oxcarbazepine (, ).
Of the 27 CBZ-DILE cases described, 20 occurred in women and 7 in men. The mean age when the DILE symptoms appeared was 30.2 years±12.4 (range 9–63), with 26 of the 27 cases younger than 50 years. The mean time between the start of treatment with CBZ and the appearance of the clinical picture of DILE was 36.5±60.2 months (range 1–240), being greater than 1 year in 12 of the cases. The CBZ dose used was 200 mg/day in 2 cases, 400–800 mg/day in 17 cases, and 1000–1600 mg/day in 4 cases, with no data being available on the other 4 patients. The symptoms that led to the use of CBZ were epilepsy in 22 cases, psychiatric alterations in 4 cases, and facial pain in 1 case. The most frequent signs of DILE were arthralgia/arthritis in 19/27 (70.4%), rash in 16/27 (59.2%), fever/malaise in 8/27 (29.6%), pleuritis/pericarditis in 6/27 (22.2%), swollen lymph nodes in 4/27 (14.8%), oral or nasal ulcers in 3/27 (11.1%), photosensitivity in 2/27 (7.4%), myositis in 2/27 (7.4%), and alopecia, Raynaud, splenomegaly, and obliterative bronchiolitis in 1 case each. No renal or neurological changes associated with lupus were observed.
Considering the changes in the laboratory tests, hematological anomalies (anemia, leucopenia, lymphopenia, thrombopenia) were mentioned in 12 (44.4%) cases. ANA were positive in all cases, except in the first 2 cases described, as there were no data available. Anti-dsDNA were positive in 10 out the 21 cases (47.6%) in which this determination was performed, as well as the anti-histone antibodies in 12 of the 16 cases (75%) in which they were analyzed. LE cells were positive in 4 cases, anti-Sm/RNP antibodies in 2 cases, and anti-SSA, anti-nucleosomes, and anticardiolipin, in 1 case each. A low complement was observed in 6 cases. The HLA profile was reported in 6 patients. HLA-DR4 was present in 3 cases and the HLA-DR2, A1, A3, and B7 in 2 cases each. One patient had both HLA-DR2 and HLA-DR4.
In all cases, it was observed that all the clinical symptoms were resolved after the CBZ withdrawal, except in 3 cases (, , ) in which the outcomes were not completely clear. As well as the CBZ discontinuation, treatment with corticosteroids was required in 12 cases, with antimalarial drugs in 5 cases, and with immunosuppressants in 2 cases. The clinical resolution occurred between 1 week and 18 months after the CBZ withdrawal. The recurrence of symptoms was observed in 1 case after the reintroduction of CBZ, and in another case the ANA became positive, with no clinical reactivation, after reintroducing CBZ. Although there are also descriptions of DILE with oxcarbazepine (, ), in 1 case, the signs and symptoms were resolved after changing the CBZ for oxcarbazepine (). In 1 patient, the appearance of lupus symptoms was mentioned in association with other anticonvulsants (). In 7 of the 19 cases with data available, the ANA had returned to being negative between 3 and 30 months, whilst in the other 12 of the 19 (63.1%), the ANA remained positive during the variable time of the follow-up, although usually at lower titers and some specificities becoming negative. There were no deaths.


A 77-year-old woman with past medical history significant for diabetes mellitus, hypertension, Hypercholesterolemia, recent deep venous thrombosis; presented the emergency room with a 5-day history of worsening shortness of breath, nausea, vomiting, and minimal urine output. She was found to have hypothermia and hypotension and she quickly decompensated requiring endotracheal intubation and vasopressors. Significant laboratory study results showed a total bilirubin level of 2.0 mg/dL, alkaline phosphatase of 900 U/L, aspartate aminotransferase and alanine aminotransferase levels of 45 and 94 U/L, respectively, white blood counts of 23 K/μL, potassium of 7.8 mmol/L, creatinine of 14.35 mg/dL and urea nitrogen of 116 mg/dL. Continuous renal replacement therapy was initiated, and Computed tomography scan of the abdomen and pelvis was obtained which demonstrated distention of the gallbladder with gallstones and mild thickening of the wall concerning for acute cholecystitis (Fig. ). The patient was started on broad spectrum antibiotics to treat sepsis from biliary source. She underwent percutaneous cholecystotomy followed by endoscopic retrograde cholangio-pancreatography with balloon sweep since the tube was poorly draining (Fig. ). She was taken to the operating room for laparoscopic cholecystectomy. Histopathology of the resected gallbladder demonstrated cholecystitis and plasmacytoma (Fig. ). Further laboratory and imaging studies confirmed the diagnosis of multiple myeloma.


A 52-year-old female with past medical history significant for triple negative high grade invasive ductal carcinoma of breast treated last year with mastectomy and chemotherapy with no residual disease; presented the emergency room with a 1-week history of right upper abdominal pain which radiates to the back. Pain was associated with nausea and vomiting and would come on about an hour after eating. Laboratory study results showed a total bilirubin level of 5.5 mg/dL, alkaline phosphatase of 340 U/L, aspartate aminotransferase and alanine aminotransferase levels of 305 and 442 U/L, respectively, and white blood counts of 5.4 K/μL. Computed tomography scan and magnetic resonance imaging of the abdomen demonstrated metastatic disease to the liver and bones, Gallbladder wall edema, and Periportal edema within the liver concerning for cholangitis (Fig. ). The patient was taken to the operating room for laparoscopic cholecystectomy and intraoperative cholangiogram. Histopathology of the resected gallbladder demonstrated metastatic poorly differentiated adenocarcinoma from the breast (Fig. ). The patient continued to deteriorate and she passed away in the next several days.


A 55-year-old female with a large mass was admitted to our hospital. She had no traumatic episode. Magnetic resonance imaging (MRI) revealed a well-defined and gadolinium-enhanced mass (5.5 × 4.9 cm) in her right thigh. MRI also revealed a mass extending into the vastus intermedius muscle beyond the intermuscular septum (red square and arrows in Figs and , and original schema in Fig. ). A needle biopsy from the mass confirmed the histological diagnosis of synovial sarcoma which was positive for SS-18 break apart by fluorescence in situ hybridization (FISH). After 2 cycles of neo-adjuvant chemotherapy, a wide resection of the tumor was performed. A histopathological examination (red square in Fig. ) showed that the tumor had direct invasion into the intermuscular septum (Fig. ). Five months after the surgery, the patient has shown no sign of recurrence.


A 63-year-old man presented to the Emergency Department (ED) with complaints of sore throat for the past 5 days. He also reported symptoms of dysphagia to solids only and intermittent hiccups during meals for two months. He denied any history of abdominal pain, constipation, diarrhea, weight loss, nausea, vomiting, fever or night sweats. He had no significant prior medical or surgical history and also denied taking any medications. He did not smoke cigarettes, drink alcohol, or use illicit drugs. Family history is insignificant for any malignancy. On examination, his vital signs were normal and systemic examination was unremarkable. He underwent a computed tomography (CT) Neck Soft Tissue without contrast which did not show any acute findings. He recently underwent screening colonoscopy, which was significant for low grade tubular adenoma. He was scheduled for an esophagogastroduodenoscopy (EGD) which showed lower esophageal stenosis at the distal esophagus, which could not be traversed with a regular scope. Ultrathin upper endoscope was used to pass the stenosed esophageal area and further examination showed a large, infiltrative, ulcerated, circumferential mass at the gastro esophageal junction and cardia (see Fig. and ). Subsequent biopsy revealed diffuse large B cell lymphoma (DLBCL) of the gastro esophageal junction and cardia (Fig. and ). On immunohistochemical stain, the tumor cells were positive for leukocyte common antigen (LCA), CD20 (CD; cluster of differentiation), CD79 and were negative for cytokeratin AE1/AE3, CD3, CD5, CD10, CD43, CYCLIN-D1, B- cell lymphoma 2 antibodies and B cell lymphoma 6 antibodies (see Fig. and ). The Ki 67 index was reportedly very high.
Further workup for tumor staging was performed. Computed tomography (CT) of the abdomen and Pelvis with contrast, showed a mass like thickening of the distal esophagus and proximal stomach with probable nodal involvement. PET Scan showed abnormal activity in distal esophagus, gastric fundus and nodes above and below the diaphragm. Table shows laboratory parameters. The diagnosis of Stage IV (esophagus and gastric involvement) DLBCL was made and the patient was started on R-CHOP chemotherapy regimen (RCHOP; rituximab, cyclophosphamide, hydroxydaunorubicin, oncovin (vincristine), and prednisone). Table showed laboratory parameters.


A 73-year-old woman was referred to our hospital for abdominal swelling and vomiting, which had persisted for 2 days. She was receiving chemotherapy with FOLFOX (fluorouracil plus leucovorin and oxaliplatin) for pancreatic cancer. Her abdomen was swollen but soft, and she had mild tenderness at the lower abdomen. Her vital signs were stable without a high fever. Laboratory data revealed an elevated white blood cell count (17 480/μL; range 3500–9100) and C-reactive protein (38.61 mg/dl; range < 0.30).
Contrast-enhanced abdominal computed tomography (CT) revealed a 48 × 28 mm mass in the pancreatic head that had invaded the whole circumference of the SMA. The SMA was occluded by the invasion of pancreatic cancer, and almost all of the small intestine was dilated with a very thin wall that was not enhanced (Figs 1 and ). We diagnosed the patient with peritonitis and extensive necrosis of the small intestine due to SMA occlusion by the invasion of pancreatic cancer.
On emergency laparotomy, a large amount of intestine was ischemic and necrotic, as seen on CT. Fortunately, there was no obvious perforation of the dilated small intestine (Fig. a). The small intestine was ischemic between the jejunum (15 cm on the anal side from the ligament of Treitz) and ileum (120 cm on the oral side from the terminal ileum). However, the arterial flow of the vasa recta and marginal artery of the visually non-ischemic jejunum and ileum were not palpable. We therefore confirmed the arterial flow of the visually non-ischemic jejunum and ileum by indocyanine green (ICG) fluorescent imaging (Fig. b and ). ICG fluorescent imaging revealed that the blood flow was decreased between the jejunum (10 cm on the anal side from the ligament of Treitz) and ileum (100 cm on the oral side from the terminal ileum). We therefore resected the parts of the small intestine in which a decreased blood flow had been confirmed by ICG fluorescent imaging (Fig. a). The whole colon, the blood flow of which was supplied by the inferior mesenteric artery, was also preserved, as the blood flow of the colon was maintained. The dilated jejunal stump that had been preserved was closed, and an external drainage tube was inserted into the jejunum end via the stomach; gastroileostomy was then performed (Fig. b). The patient was discharged uneventfully on postoperative day 24. She spent approximately two months at home; however, she was readmitted to hospital with small bowel obstruction caused by the progression of pancreatic cancer on postoperative day 78 and is currently receiving palliative care.


A 34-year-old pregnant woman (G3P2L2) was admitted with reduced vision preceded by 2 weeks of hyperemesis and decreased food intake. She had no history of seizures, loss of consciousness, headache, or fever. She was conscious and afebrile. Her pulse rate was 92/min and blood pressure was 110/60 mmHg. Her gait was ataxic, and ocular examination revealed gaze-evoked nystagmus. Her vision was light perception (right eye) and finger counting (left eye). There was no neck stiffness. Examination of fundus showed features consistent with papillitis in both eyes (hyperemia and swelling of the disc with blurred disc margins and distended veins). Magnetic resonance imaging (MRI) showed T2WI, FLAIR, and diffusion-weighted imaging MR images showing hyperintensity in dorsomedial thalami and periaqueductal grey matter with diffusion restriction []. The diagnosis of WE was made based on her clinical presentation and radiological findings. She was treated with high-dose intravenous thiamine injection (500 mg 8 hourly). Her vision improved within 3 days and nystagmus was resolved. At the time of discharge, she was much better, but ataxia persisted.


A 69-year-old woman presented to our hospital with a gradual reduction in vision of the left eye 1 year after uncomplicated cataract surgery of that eye. On examination, her best-corrected visual acuity (BCVA) was 6/18 in the right eye and 6/24 in the left eye, and the slit-lamp examination (SLE) revealed a very mild ocular surface disease in both eyes and PCO in the left eye. The patient was not using any topical or systemic treatment.
Nd:YAG laser capsulotomy using a Zeiss Visulas YAG II 532 s device (total energy of 30–35 mJ, and the inverted D method) was performed on the left eye. The procedure was done without the use of a contact lens.
Following the non-eventful procedure, an optically clear visual axis with a clear cornea was observed, and the IOP was 17 mm Hg. Standard treatment with dexamethasone drops four times a day for 4 days was initiated, she was referred for follow-up 1 week later.
The patient returned to our clinic 2 weeks later complaining of pain and decreased vision in her left eye. Upon further questioning, she reported using topical steroids liberally to relieve pain. On examination, her BCVA was 1/120 in the left eye, and the SLE revealed a central full-thickness corneal perforation measuring 0.5 × 0.5 mm with a shallow anterior chamber and a positive Seidel test. Anterior segment optical coherence tomography demonstrated a disrupted corneal perforation with a full-thickness central gap (Fig. ). We prescribed topical ocular antibiotics, cycloplegics, and hypotensive medications and bandaged the eye with a soft therapeutic contact lens. At the follow-up visit 1 week later, her BCVA had improved to 6/36 in the left eye. The SLE revealed that the corneal perforation had decreased in size and that the anterior chamber had deepened. A passive positive Seidel sign was still present. She received additional treatment with oral doxycycline, vitamin C and topical ocular serum drops. At the final follow-up 12 weeks after her left eye capsulotomy, the patient was pain free, her BCVA was 6/18, and she had a paracentral corneal scar, a normal depth anterior chamber and a negative Seidel sign. A repeated anterior segment optical coherence tomography demonstrated a deep stromal scar with bridging continuous superficial stromal and epithelial layers (Fig. ).


A male, 59 years old, complained blackish stool in the last 2 weeks. His abdomen had slowly enlarged over the previous 4 years, and he felt pain especially in the middle of the stomach. He denied consuming alcohol drink, smoking, or history of other diseases, such as hepatitis and congenital disorder of the blood. The patient’s condition gets weaker, but he can still eat and drink, and no vomiting. There is no swelling in the extremities.
Physical examination revealed pale of the eyelid, no icteric, no hepatomegaly, splenomegaly, and ascites. Rectal examination was positive of blackish stool, no fresh blood, and no palpable mass. Laboratory finding was anemia (hemoglobin 6.88 g/dL and haematocrit 22.02%), normal leukocyte and thrombocyte, hypoalbuminemia (albumin 2.8 g/dL), normal liver function (AST 14.7 U/L and ALT 11.1 U/L), and normal renal function (BUN 22.8 mg/dL and serum creatinine 0.79 mg/dL). Hemostatic test slightly elevated with APTT 30.9 s, PPT 16.7 s, and INR 1.43. We also found non-reactive at HBsAg and anti-HCV test, normal bilirubin serum (total 0.78 mg/dL, direct 0.31 mg/dL, and indirect 0.47 mg/dL), normal alkaline phosphatase (60 U/L), and normal gamma-GT (39 U/L), but high CRP count 23.39 mg/L (normal 0–5 mg/L).
The abdominal Doppler ultrasonography presented noncirrhotic liver with average size (13 cm), splenomegaly (13.9 cm), dilatation of portal vein (1.27 cm), low portal vein peak velocity (19.4 cm/s), and ascites (). This finding was confirmed with contrast-enhanced abdominal computed tomography (CT) scan, which revealed dilatation of portal vein with thrombus, normal liver parenchymal, normal biliary tract, splenomegaly with dilatation of splenic vein, and ascites (). He was examined used esophagogastroduodenoscopy, which revealed esophageal varices grade 3 with the positive red color sign and stomach varices ().
We transfused packed red cell two bags each day to improve hemoglobin level, but it cannot achieve until hemoglobin level was 10 g/dL. Every day he got melena, so it is indicated ongoing upper gastrointestinal bleeding. We decided to do Sugiura technique surgery with his baseline hemoglobin 5.29 g/dL. We performed the modified Sugiura technique through left subcostal incision () and proximal splenorenal shunt.
We performed splenectomy first () followed by devascularization of the distal esophagus using harmonic scalpel through hiatus of diaphragm. We made a small anterior gastrostomy. Then, we made a transection and end-to-end anastomosis of the lower esophagus () using a CDH29A stapling device (Ethicon curved intraluminal stapler). We performed separate Lembert suture to reinforce of the esophageal anastomosis and stitched the gastrostomy. We performed devascularization of the upper 2/3 of the lesser and major gastric curvature () and then pyloroplasty to facilitate gastric emptying (). The last procedure we anastomosed end-to-side of the splenic vein to left renal vein ().
His condition improved after surgery and overwhelming post-splenectomy infection (OPSI) did not occur. He can eat and normally drink, no pale, no fatigue, and no melena. He consumed medicine propranolol 60 mg per day to prevent portal hypertension and warfarin 5 mg per day to release the thrombus. Two months after surgery, we examined esophagogastroduodenoscopy and revealed esophageal varices grade 2 with the negative red color sign, cardia stomach edema, no gastric varices, and gastric snakeskin (). We evaluated esophagogastroduodenoscopy 6 months after surgery, the results were the same as the previous examination, but there was no edema in the gaster. One-year follow-up after surgery, his physical condition was better and no sign of complications.


A 45-year-old male patient was referred to the prosthodontics clinic to complete the restoration of a dental implant (3.7 mm×11 mm, Zimmer implant, Standard Plus, regular neck, Zimmer Dental, Carlsbad, CA, USA), at the site of tooth #21. The dentist had placed an implant 3 months previously and then started the construction process of a cement-retained crown for restoring implant #21 and fabricated a gold customized implant abutment. Before completion of the implant restoration, the patient was referred to our clinic to continue the treatment.
During the first visit, patient medical and dental history was reviewed. According to the American Society of Anesthesiologists (ASA) physical status classification system, the patient is ASA1. The patient's chief complaint was to continue the treatment of his anterior teeth. Upon smiling, the patient has a low to average smile line. The apparent teeth have a homogenous shade that the patient was satisfied with. Intraoral examination revealed adequate periodontal health, tooth #11 had a provisional crown, and tooth #21 is an implant with a healing abutment. The patient has thin gingival biotype. Radiographic examination displayed the current process of external root resorption for tooth #11. The patient was provided with complete information regarding treatment options to make a decision for tooth extraction and implant placement of #11 (). The patient signed an informed consent to proceed with the treatment plan.
The cone-beam computed tomography (CBCT) image for the patient displayed sufficient sound buccal, lingual, and apical alveolar bone around tooth #11. A surgical guide was developed as a duplicate for the prior master cast for the prosthodontist with self-cure acrylic resin. The surgeon was guided through predetermined mesiodistal and buccolingual center channel for tooth extraction #11 in the patient’s mouth. The implant mount attachment was facilitated with the help of an acrylic transfer jig to assure the cast fabrication for quick succession to fabricate the fixed dental prosthesis after placing an implant. In addition, the vacuum-formed template for provisional restoration fabrication was used for fabricating a 1.5 mm thermoplastic material.
The surgical process was performed by the periodontist by giving local anesthesia to the patient. Tooth #11 was removed by performing flapless and atraumatic extraction, followed by normal socket saline rinsing, debridement, and curettage. In addition, during implant drilling, the mouth of the patient was secured through the teeth-supported surgical guide. By using the standard protocols for the Zimmer system, implant placement and bone preparation were performed in the patient’s mouth. The placement and torquing of a Zimmer implant were ensured at 40 N cm (). In contrast, there was no essential requirement made by the dentist toward soft tissue suturing.
After the implant placement, the transfer jig was secured on the adjacent teeth and the implant mount was carefully connected to the jig by adding autopolymerizing acrylic resin. The implant mount was retrieved from the patient mouth with the attached jig, screwed to an implant lab analog and then transferred to the cast. Two implant temporary abutments from Zimmer (Zimmer Dental, Carlsbad, Calif) were placed on the cast and prepared using the clear vacuum-formed shell template ().
The implant supported fixed provisional restoration was constructed to develop the preferred emergence profile using acrylic resin. The provisional fixed dental prostheses were appropriately finished and polished.
The temporary abutments were screwed to the implants in the patient’s mouth, and Teflon tape was used to block both temporary abutments’ access holes. Afterward, the minimum amount of non-eugenol temporary cement was used to cement the provisional restoration and excess cement was safely removed. Occlusion was adjusted to ensure minimal contacts during eccentric and centric occlusion ().
Post-operative instruction was given to the patient and recall visits were done after 7 days, 4 weeks, 8 weeks, 12 weeks, and 16 weeks. On each follow-up appointment, the healing was assessed with no signs of inflammation or infection. Also, the development of the soft tissue emergence profile around the implant was monitored and the provisional restoration was adjusted if required. Esthetics and phonetics were evaluated and the patient displayed a complete satisfaction with the outcome ().
A definitive open tray impression was done by using Impergum Penta-Soft after 4 months of healing (). The customization of impression copings was based on the transference of the emergency profile of the soft tissue. The soft tissue emergence profile was transferred to the mastercast using light body polyvinyl siloxane material ().
Full contour wax up was made for crowns #11 and 21 on the master cast. The clear vacuum-formed shell template was used to adjust the old gold custom abutment of implant #21. Afterward, mounted master casts, gold abutment #21, and the clear template were sent to Astra Tech (Mölndal, Sweden) to design and fabricate a customized milled CAD/CAM Atlantis abutment. Abutment design of implant #11 was requested to match the design of gold abutment #21 except in material. The abutment designed for implant #11 was fabricated from zirconia for comparison purposes. An approval from the prosthodontists was taken via email for the abutment design (). A one-piece customized abutment which consisted entirely of zirconia was milled and shipped to the clinic.
Upon arrival, both abutments were checked on the cast for exact duplication. Full contour acrylic resin crowns were constructed on both abutments to confirm the equal thickness of both crowns on all sections. Thickness evaluation was made using a polygauge and all the readings were equal on both crowns in all sections ().
Next, crowns with porcelain fused to zirconia were constructed for implant abutments #11 and #21. Again, the buccal thicknesses of the final crowns were measured and compared using a polygauge. All readings were comparable for both crowns (). Afterward, abutments were screwed to both implants and final crowns were checked in the patient’s mouth to evaluate esthetics and phonetics. Shade evaluation of both crowns was carried out by the treating prosthodontist on their buccal surfaces (incisor, middle, and cervical thirds) using VITA Easyshade Advance System (VITA Zahnfabrik, H. Rauter GmbH & Co. KG, Bad Säckingen, Germany). All readings were comparable in relation to CIE L*a*b* color space, Classical Vita Shade Guide and 3D Master Shade Guide. The shades of both crowns were comparable and rated clinically satisfactory by the treating prosthodontist and patient. Finally, customized abutments were torqued to 30 N cm, access hale were blocked with Teflon tape, and the final crowns were cemented with non-eugenol temporary cement (Temp Bond NE, Kerr; Orange, CA, USA) ().
Two experts in fixed prosthodontics who had not taken part in the patients’ treatment performed the clinical evaluation. Both observers had good eyesight that will assist in comparing the esthetic appearance of both implants supported all-ceramic crowns with gold and zirconia abutment side by side. Variations were detected using artificial diffuse light and the Vita 3D Master shade guide by standing 50 cm from the mouth of the patient where the head of the patient was positioned upright. There was no difference observed in the color aspect by prosthodontics.
The recall visits were done after 2 weeks, 1 month, 3 months, and 1 year from delivery of final restorations. Both implants and their restorations were assessed. The patient was satisfied with the esthetics and functional outcome of the final restorations, as was the prosthodontist (). A written informed consent has been provided by the patient to have the case details and accompanying images published. The institution allows
publication
of the patient’s treatment and images for scientific purposes.


A 46-year-old African lady presented with decreased vision, floaters, and flashes in the right eye of 6 months duration. She was diagnosed as right eye choroidal hemangioma elsewhere and treated with 5 monthly intravitreal anti-VEGF injections elsewhere. On examination, best-corrected visual acuity (BCVA) in the right eye was finger counting at 50 cm. Anterior segment examination was bilaterally normal. Right eye fundus examination showed an orange-red choroidal mass at the posterior pole, with subretinal fluid (SRF) []. Left eye visual acuity was 6/6 and fundus examination was normal. Right eye ultrasound (USG) showed a solitary tumor abutting the optic nerve head with high surface reflectivity and non-homogeneous, moderate-to-high internal reflectivity [], measuring 8.4 mm (horizontal basal) × 10.6 mm (vertical basal) × 5.3 mm (height). Magnetic resonance imaging (MRI) on T2-weighted image revealed ovoid-shaped heterogeneous mass predominantly hyperintense []. Optical coherence tomography (OCT) of the right eye showed choroidal tumor with overlying retinoschisis and SRF [Fig. and ]. Right eye fundus fluoroscein and indocyanine green angiography showed early hyperfluoroscence with staining in the last phase [Fig. and ]. Treatment options of PDT (gold standard), TTT, low-dose EBRT, and CyberKnife were discussed, and the patient chose CyberKnife radiation therapy. She was treated with single fraction radiation of 12 Gy (gray) dose given over 30 min. At 10 months follow-up (which was the last follow-up), the right eye vision improved to 3/60 and fundus examination showed subretinal pigmentary changes at the treated area []. Post-treatment ultrasound dimensions were: 8.4 mm (horizontal basal) × 10.4 mm (vertical basal) × 2.8 mm (height) []. OCT showed complete resolution of retinochisis and SRF with foveal thinning []. MRI revealed mass enchancing homogeneously, decreased in size as compared to previous scan []. No evidence of treatment-related side effects like dry eye, cataract, radiation retinopathy, or optic neuropathy were noted till the last follow-up.


An 81-year-old man never-smoker was referred to our hospital due to cough, sputum and fever continuing for over 2 weeks on Sept 1, 2016. In all the patient’s medical history, he had only suffered from hyperlipidemia and gallbladder stones, and had received surgical treatment for cervical dislocation 5 years ago. He denied previous diseases, including cancer or malignant tumors, and had never received any radiation or chemotherapy, and had never been exposed to any particular substance, such as arsenic. There are only occasional small amounts of alcohol in his life and no history of heavy drinking or alcoholism. Because of the distance of time and the poor medical conditions of many years ago, the patient was unable to account for the cause of death and illness of his parents and family members. Computed tomography (CT) of this patient’s chest showed an abnormal mass shadow in his left lower lung, mediastinal lymph node enlargement. The serum concentration of the serum carcinoembryonic antigen (CEA) was 53.32 ng/mL, and prostate specific antigen (PSA) was >100ng/mL. Abnormal signal foci in the central region of prostate magnetic resonance imaging, the bladder is poorly filled, with several prominent shadow-like sacs on the left side wall. The whole body bone imaging examination showed abnormal bone metabolism, consistent with the signs of multiple bone metastases (). The histopathologic findings revealed hypodifferentiated adenocarcinoma after a biopsy specimen obtained by fiber-optic bronchofiberscopy (). After the same detailed understanding of the process of prostate puncture and cystoscopy, the painful experience of bronchoscopy made the patient firmly refuse further invasive examination, because both prostatic puncture and cystoscopy are invasive examination. According to the rules, the clinician must obtain the patient’s consent for invasive examination, otherwise it can not be carried out.
Then, the EGFR mutation status of the specimens obtained by bronchoscopy was investigated, and the result showed both exon 19 deletions and an L858R point in exon 21. Then icotinib (125 mg) (patent number WO2003082830; Zhejiang Bata Pharma Ltd., Hangzhou, People’s Republic of China) was orally administered three times a day after the result was EGFR mutation-positive.
The patient had mild diarrhea after taking icotinib, and obvious relief of cough and chest discomfort, so he did not follow the doctor’s advice to review the chest CT until 3 months later. CT results showed a marked reduction in tumor size ().
After 6 months, the patient came back to see the doctor again because the frequency of urination affected his nighttime sleep. The difference is that this time the patient is in good spirits and believes that the doctor can solve his discomfort in urination. The results of urological magnetic resonance imaging (MRI) examination showed irregular enlargement of prostate and abnormal signal (), which considered prostate cancer, not excluding left seminal vesicle gland involvement, while the left bladder wall occupied space (), pelvic lymph node enlargement. Echocardiographic display of pericardial effusion. The serum concentration of the serum CEA was 3.62 ng/mL, and PSA was >100 ng/mL. The whole body bone imaging examination showed that abnormal bone metabolism was progressive. Urologists again recommend prostate puncture or cystoscopy. Patients refuse invasive examination, hoping to receive minimal suffering treatment according to the expected diagnosis.
Hormonal therapy is recommended in urology. Bicalutamide tablets (Casodex, AstraZeneca GmbH) 50 mg is taken orally once a day and Leuprorelin acetate microspheres sustained release for injection (Beijing Biote Pharmaceutical Co. Ltd) 3.75 mg is given subcutaneously every 4 weeks, strontium dichloride for bone metastasis. Later, the patient’s symptoms improved according to the doctor’s instructions. The patient was not admitted to hospital until September 3, 2017 (4 months after receiving prostate treatment and 11 months after lung cancer targeted treatment) due to frequent urination and increased pain in the lower abdomen. Blood reexamination showed CEA 2.8 ng/mL, PSA 1.18 ng/mL, CT examination showed that the prostate gland is full, with uneven density and calcification, which is consistent with the changes after endocrine therapy. The left side wall of the bladder is significantly irregularly thickened and involves the lower end of the left ureter, and the left renal pelvis and ureteral dilatation and hydrocele. CT also showed partial nodules decreased in both lungs (considering the metastasis of prostate cancer in the lungs) (), new nodules appeared, and pericardial effusion did not change significantly. The whole body bone imaging examination showed abnormal bone metabolism was significantly alleviated (). Then, the patient underwent transurethral electric resection of bladder lesions. Postoperative pathology showed invasive urothelial carcinoma (). Nine days after surgery, the patient developed hematuria, bladder irrigation was given and catheterization was retained for 3 weeks. Targeted therapy for lung cancer and treatment for prostate cancer remained unchanged. On April 4, 2018, he was admitted to hospital again because of hematuria and urine urgency. Considering the diagnosis of recurrence of bladder cancer and the patient’s intolerance to surgery, he was given bilateral internal iliac artery angiography plus superselective embolization, and gemcitabine 1,000 mg was applied during the operation. On May 16, 2018, the patient was admitted to the hospital again due to urination urgency, urination pain and fever for 2 days. After anti-infection and improvement of the general condition, the patient’s symptoms improved. After that, the original treatment was maintained. On May 22, serum creatinine rose to 182.97 µmol/L, and the patient refused further treatment. Due to dizziness and head swelling for 10 days, aggravated nausea and vomiting for 1 day, he was re-admitted to the hospital on June 27, 2018. Since then, the patient had stopped taking all oral medications, including icotinib. The blood test results showed that blood creatinine 887.14 µmol/L, BUN 51.08 mmol/L, blood potassium 5.9 mmol/L, hemoglobin 58 g/L, CEA 16.7 ng/mL, PSA 0.063 ng/mL, and arterial blood gas analysis showed pH 7.34. The results of ultrasonography showed hydronephrosis with bilateral ureteral dilatation, irregular thickening of bladder wall with solid nodules and intraluminal sediment. Diagnosis: renal failure, hydronephrosis, metabolic acidosis, electrolyte disturbance. The patient and his family members refused the treatment of hemofiltration, hemodialysis and nephrostomy. The patient died suddenly at home on July 25, 2018, and his family refused to perform the autopsy. Written informed consent has been provided by the patient’s next-of-kin to have the case details and any accompanying images published.


A 68-year-old male presented to an outside hospital with sudden onset left-sided chest and back pain accompanied by left leg numbness and weakness. His symptoms started suddenly after strenuous physical activity. The patient was taking warfarin by alternating daily doses (1.5 mg and 5 mg) for atrial fibrillation. On admission, he had left leg plegia (motor power 0/5) and reduced sensation to touch from T4 level bilaterally. Coagulation panel showed elevated international normalized ratio (INR) of 4.25 (normal range: 0.9–1.2), prolonged activated partial thromboplastin time of 40.9 (normal range: 28–38), and reduced prothrombin time (Stago Prothrombin Assay) activity 11% (normal range: 70–130%). The patient was admitted for diagnostic work-up and was continued on warfarin. Noncontrast head computed tomography (CT) was within normal limits. Three days after admission, the patient's neurological function deteriorated and he developed right leg paresis and bladder retention. These symptoms prompted noncontrast spinal CT that demonstrated nonhomogenous hyperdense intradural mass lesion extending from T2 to T6 levels [Figure and ]. The patient was transferred to the neurosurgery department for further management.
Upon admission to our department the patient had grade C myelitis based on the American Spinal Injury Association (ASIA) Classification from T4 level. He had left leg plegia (power 0/5) and right leg paresis (power 0–1/5 hip/knee flexors/extensors and 2/5 plantar flexors/extensors). Based on the Autonomic Standards Assessment Form, the patients’ general autonomic function assessment was normal, and he had loss of urinary, anal sphincter, and erectile functions. Spinal MRI showed heterogeneous mass lesion extending from T3 to T6 levels on the left side of the spinal canal. The lesion was hyperintense on T2-weighted sequences and heterogeneous intensity on T1-weighted sequences, which was suggestive of acute-to-subacute subdural blood clot, with dislocation of the spinal cord by the hematoma and signs of myelopathy [Figure –]. The patient was administered 2000 International Units of human prothrombin complex concentrate (PCC) for coagulopathy and underwent emergent surgery that was performed 3 days after his initial symptoms and within 24 hours of neurological deterioration. Left side hemilaminectomy extending from T3 to T6 levels was performed. The dural sac was tense and nonpulsatile with bluish discoloration. The dura was opened longitudinally. The clot was 5–6 mm thick and was located in the left posterolateral portion of the dural sac, partially organized, gently adhesive to the spinal cord, and encasing thoracic nerve roots. The clot was gently dissected from the spinal cord and nerve rootlets using dissector, suction, and bipolar cautery. Clot remnants were rinsed from the subdural space with isotonic saline. Pulsation of the spinal cord was evident after the clot was removed. Bleeding source was not identified. After complete hemostasis, the dura was closed in water-tight fashion. Drainage was left in the epidural space and the wound was approximated in layers.
Postoperative period was uneventful. Warfarin was replaced with fraxiparin and reinstituted on postoperative day 7. MRI at day 1 after the surgery demonstrated completely removed hematoma. There was T2-weighted hyperintense signal in the central portion of the spinal cord suggestive of myelopathy and edema extending from T1 to T8 levels, as well as nonhomogenous hypointense areas on T2-weighted sequences extending from T1 to T6 levels [Figure –]. Epidural drainage was removed on day 2. At discharge to the inpatient rehabilitation unit 2 weeks after the surgery, the patient reported improved sensations and right leg strength (power 3/5 hip/knee flexors/extensors and 1/5 plantar flexors/extensors) with remaining left leg plegia and altered urinary and bowel functions.
Three months after the surgery, leg motor strength (power: left leg 2/5 and right leg 5/5 plantar flexors/extensors) and bladder function were improved. The patient was able to stand with support and was ambulatory with wheelchair. He had reduced sensation to touch below the T8 level. MRI was suggestive of myelopathy extending from T3 to T6 levels with deviation of the spinal cord to the left [Figure –].


A 56-year-old male patient sustained road traffic accident and presented to our emergency department with a history of pain in the thoracic spine and progressive weakness of both the lower limbs for 3 days. On examination, the thoracic spine was kyphotic and tender at the mid-thoracic region. The patient had spinal cord injury with ASIA–C neurological deficit. Patients’ medical records show that he had a history of spinal tuberculosis 25 years ago, which was treated conservatively by 9 months of anti tuberculosis chemotherapy (INH, rifampicin, ethambutol, and pyrazinamide) and bed rest. The patient had good recovery of symptoms and attained favorable status at 4 months of conservative treatment but had asymptomatic kyphotic deformity since then.
Radiographic evaluation [Figures and ] of the patient revealed kyphosis of thoracic spine and fracture of the solidly fused thoracic fusion mass involving all three columns. The kyphotic fusion mass was extending from T7 to L1 with apex of kyphosis at T12. The fracture was noticed between vertebral segments between T10 and T11, and there was a gap in the fusion mass with breach in the anterior cortex with translation of the fractured ends of fusion mass. Magnetic resonance imaging showed the absence of intervertebral discs and complete fusion from D8 to L1 vertebral bodies. There was a hyperintense fluid collection at the ends of fractured fusion mass and separation of fractured ends. There was no significant cord compression resulting from internal gibbus deformity. The angle of global kyphosis was 57°, and local kyphosis at fracture site was 63° []. Kyphosis angles were calculated using Surgimap 2.2.7 version. The pattern favors that of traumatic fracture in view of sharp fracture margins without any adjacent sclerosis and symptoms being strongly associated with a history of trauma.
The patient was managed by stabilization of the fracture with posterior spinal instrumentation using pedicle screws and rods construct. Circumferential decompression of the spinal cord was done by posterior laminectomy and transpedicular approach. The anterior deficit between the fractured ends of fusion mass was freshened and 7-mm titanium interbody cage filled with bone grafts was inserted and compressed. No attempt was made to correct the deformity []. Postoperative period was uneventful, and the patient noticed a significant improvement in the neurological status and became ambulant within 4 months after surgery. The patient was pain free with thoracic kyphosis similar to his preinjury state. At 2 years’ followup, radiological images showed complete bony fusion at the fracture site [].


A 50-year-old woman nonsmoker presented with left-sided chest pain for 12 months, cough for 6 months, and loss of appetite for 6 months. On examination of the respiratory system, dullness on percussion and decreased breath sounds on auscultation were found on the left interscapular region with no features of mediastinal shift. It was suggestive of a space-occupying lesion. The clinical examination of the rest of the system revealed no abnormality. Routine blood investigations were within normal limits. For confirming the clinical findings and further evaluation, chest X-ray was done which was suggestive of left-sided homogeneous opacity in the upper zone probably an intrathoracic mass lesion. On further investigation, contrast-enhanced computed tomography (CECT) scan of the thorax [] revealed that the lesion was seen encasing branches of the arch of the aorta completely and the arch of the aorta partially and seen abutting them with ill-defined fat plane. Transthoracic fine-needle aspiration cytology and tru-cut biopsy of the left lung mass were done for histopathology and immunohistochemistry. Histopathology revealed tissue infiltration by a tumor disposed in nests and trabeculae. The tumor cells are polygonal with moderately pleomorphic nuclei, granular chromatin, and moderate amount of eosinophilic cytoplasm. Mitotic figures (3/10 high-power fields [HPFs]) and apoptotic bodies are evident []. Immunohistochemistry [] was positive for chromogranin, and Ki-67 proliferation index was 5%. It was negative for cytokeratin-7 (CK-7), thyroid transcription factor-1, and CK-5/6. These findings were consistent with AC.


A 67-year-old female underwent a laparoscopic cholecystectomy complicated by injury to the CBD at an outside hospital. The proximal bile duct was cannulated with a 12 French red Robinson catheter, which was brought out through the right lateral abdominal wall. The patient was transferred to our facility for management of the CBD injury.
The patient was afebrile and hemodynamically stable. On physical exam her abdomen was soft, appropriately tender, non-distended and no rebound or guarding. A complete metabolic panel (CMP) and complete blood count (CBC) were within normal limits. A total bilirubin of 0.8 mg/dL was normal (reference normal 0.0–1.4 mg/dL). An abdominal computed tomography (CT) scan revealed a CBD injury 2 cm below the confluence of the right and left hepatic ducts, and a drain in the proximal CBD. There was also evidence of a right hepatic artery (RHA) injury. Due to the RHA injury, a definitive surgery was to be delayed for approximately six weeks to allow for collateralization of the CBD.
The patient noted that the biliary drain produced approximately 100 mL of daily bilious output since her discharge. However, she returned 1 month after her discharge noting that there was no biliary drain output for two weeks. She had no systemic complaints. She was anicteric and her abdomen was soft, non-tender and non-distended with no rebound or guarding. The patient was admitted to the hospital for evaluation of drain patency.
The labs on admission revealed a normal CMP and CBC, a slightly elevated alkaline phosphatase of 171 U/L (reference normal 34–104 U/L), normal aspartate transaminase and alanine transaminase levels, and a normal direct and total bilirubin of 0.2 and 0.5 mg/dL, respectively. A CT of the patient’s abdomen showed the external biliary drain within the CBD and no intra-abdominal fluid collections or intrahepatic biliary dilations. A cholangiogram showed a fistulous connection between the proximal CBD and the duodenum (Fig. ). An elective choledochoduodenal fistula takedown and Roux-en-Y hepaticojejunostomy were performed.


A 12-year-old male patient reported to the Department of Paediatric and Preventive Dentistry in SDM College of Dental Sciences and Hospital, Dharwad, Karnataka, with a chief complaint of swelling in the upper front region of the jaw since 2 months. The patient gave a history of trauma 2 months back while playing. Extraorally a diffused swelling was present on the left side of the face extending from the left infraorbital margin to the corner of the mouth and left ala of the nose []. Intraoral examination revealed a solitary swelling of 5 × 4 cm with diffused margins in anterior one-third of the palate. Anteroposterior extent was from the palatal aspect of 11 to the distal aspect of 25. Mediolateral extent was from the region of midpalatal suture involving the palatal gingival margin of 21–25 []. The swelling was firm during the palpation, bony hard in uniformity, whereas, it was not at all tender and pulsatile when there was no discharge. Grade I mobility was present with 21–25. The involved teeth when subjected to cold test and electronic pulp testing were found to be vital.
Orthopantomogram (OPG), maxillary occlusal radiograph and digital volumetric tomography (DVT) were performed. The orthopantomography revealed a unilocular radiolucency of 3 × 4 cm with well-defined borders, prolonging since, and mesial feature of 11 toward the distal feature of 25. Authoritatively lengthening up to the nasal cavity and maxillary sinus and inferiorly extending up to the middle third of roots of 21–25. The radiolucency revealed the presence of an impacted supernumerary tooth. Similar findings were observed with DVT [ and ].
Fine-needle aspiration cytology was done, and 2 ml of blood tinged and sticky fluid was withdrawn. The cytosmear revealed a mixed inflammatory lesion predominantly of chronic inflammatory cells. Based on clinical, radiographic and cytologic features a provisional diagnosis of infected dentigerous cyst was made. Endodontic treatment was done for the involved teeth followed by their semi-rigid splinting. Due to the close proximity of the lesion to vital structures, enucleation and curettage were done under general anaesthesia. Complete excision of the lesion was done. Apicectomy was done for the involved teeth followed by placement of platelet-rich fibrin. The gross excised tissue was brown in color and 2.5 × 2.7 cm in size with a supernumerary tooth attached to the specimen [].
Histopathologically, on processing specimens from different areas of the excised lesion the cystic lining consisting of non-keratinized stratified squamous epithelium with flat interface [] showed predominant uniform thickness with focal luminal proliferation called as epithelial plaque [], through a plane epithelial, connective tissue boundary without palisading the basal cell. Vacuolated/clear cells in the basal/spinous layer and periodic acid-Schiff (PAS)-positive metaplastic numerous mucous goblet cells with occasional ciliated cells in the superficial cell layer were also present in the cystic lining []. Based on the histopathologic findings a final diagnosis of GOC was confirmed.
So far, on 1 year follow-up no recurrence was observed and OPG revealed new bone formation at the site of the cystic lesion []. A long-term follow-up of 5 years is advised.


The first case study was a 65 year old male with diminution of vision in the right eye (RE). The patient had a history of viral keratits in his RE within the past year. Upon examination, it was found that the patient had visual acuity of perception of light and an adherent leukoma with dry ocular surface in the RE. PK was performed in the RE with cataract extraction and posterior chamber intraocular lens (IOL) implantation under peribulbar anesthesia by using an 8 mm donor graft.
On the first postoperative day, the graft had mild edema with subtotal epithelial defect. The anterior chamber was formed with mild cellular reaction and IOL was in place. The patient was started on ciprofloxacin-dexamethasone combination drops (Ciplox-D, Cipla Ltd) six times a day, carboxymethyl cellulose 1% (Relub-DS with stabilized Oxychloro Complex as preservative from Centaur pharmaceuticals) drops ten times a day, and hypromellose 2% (Lacrigel from Sunways India Pvt. Ltd.) gel at bedtime. During the first weeks follow up, the patient complained of blurred vision and white discoloration of the cornea. On examination, there was a whitish granular deposition in the subepithelial region in the inferior half of the cornea corresponding to the site of the previously present epithelial defect (). The patient did not complain of pain or irritation. However, it was suspected that ciprofloxacin deposition was present, and the patient’s treatment was therefore switched to prednisolone acetate 1% (Predmet, Sun Pharmaceuticals) drops four times and tobramycin 0.3% (Toba, Sun Pharmaceuticals) drops four times a day, along with lubrication. The graft cleared leaving a persistent epithelial defect (PED) after 4 weeks of treatment. After 2 weeks the graft developed recurrent viral keratitis and the graft eventually failed despite all efforts.


A 45 year old male with bullous keratopathy in the RE in a case of presumed posterior polymorphous corneal dystrophy was scheduled to undergo PK. The patient suffered from intermittent pain and redness of his eye in the past 4 years. On examination, it was found that his RE had visual acuity of hand movement and mild circumciliary congestion with hazy cornea. There was epithelial micro- and macrobullae with diffuse stromal edema. The anterior chamber had an irregular depth and 360° posterior synechiae with a cataract. Posterior segment could not be visualized. IOP was 12 mmHg in the RE, as measured by an airpuff tonometer.
The patient underwent PK in the RE with cataract extraction and posterior chamber IOL implantation under peribulbar anesthesia using an 8 mm donor graft. Postoperatively, the graft had mild edema with Descemet folds and a central epithelial defect. The anterior chamber was formed with moderate cellular reaction and fibrinous exudates. The patient was started on ciprofloxacin-dexamethasone combination drops (Ciplox-D, Cipla Ltd) eight times a day, carboxymethyl cellulose 1% drops (Relub-DS with stabilized Oxychloro Complex as preservative from Centaur pharmaceuticals) six times a day, and atropine 1% (N-pin, National Healthcare) drops three times a day, and followed-up after 7 days.
A presence of whitish granular subepithelial deposition in the central cornea () was found when the patient presented on the 10th postoperative day. Suspecting ciprofloxacin deposition, the medications were changed and the patient was started on prednisolone acetate 1% (Predmet, Sun Pharmaceuticals) eyedrops six times a day, tobramycin 0.3% (Toba, Sun Pharmaceuticals) drops four times a day, and carboxymethylcellulose (Relub-DS with stabilized Oxychloro Complex as preservative from Centaur pharmaceuticals) drops eight times a day.
The deposits completely cleared after 20 days and the epithelium healed leaving behind a faint opacity in the area of the drug deposition, probably due to delayed epithelialization of the cornea. On the next follow-up after a month, the graft had developed features of acute graft reaction and the graft failed despite medical management.


A 42 year old male was scheduled for a triple procedure for adherent leukoma following perforated corneal ulcer in the RE. Visual acuity was hand motion in the RE and 6/6 in the left eye. The IOP was 31.8 mmHg in RE and 12.2 mmHg measured with a Schiotz tonometer. After intravenous mannitol (5 mL/kg), the patient underwent PK with lens extraction under peribulbar anesthesia. Intraoperatively, there was high vitreous pressure, and the posterior chamber IOL was not stable. While removing the IOL, there was a tear in the posterior capsule, and an anterior vitrectomy was performed. Postoperatively, the graft host junction was well apposed and an epithelial defect was present. The graft had moderate edema with descemet folds and there was a fibrinous exudate in the anterior chamber. The patient was started on prednisolone acetate 1% (Predmet, Sun Pharmaceuticals) eyedrops ten times a day, ofloxacin 0.3% (Ocucin, Sun Pharmaceuticals) drops eight times a day, carboxymethylcellulose drops (Relub-DS with stabilized Oxychloro Complex as preservative from Centaur pharmaceuticals), six times a day, and timolol-brimonidine combination drops (Brimopress-T, Centaur pharmaceuticals) 2 twice a day. The patient was followed-up after 20 days. The epithelial defect was healing but there was whitish granular deposition in the subepithelial layer beneath the healed epithelium with central epithelial defect (). Ofloxacin eyedrops were stopped and the frequency of tear substitutes was increased. The cornea cleared gradually over the next 4 weeks.


Patient 1 is an 80-year-old woman with stage 3B chronic kidney disease (CKD) who received an inadvertent dose of denosumab 1 month after her regularly scheduled dose. Eighteen days following the second dose, the patient presented to the emergency department with severe weakness that prevented her from getting out of bed. She denied seizures, syncope, chest pain, or palpitations. Neurological exam revealed 4/5 strength in all extremities. Chvostek sign was absent. Chemistries revealed a serum total calcium of 4.2 mg/dL, magnesium 1.2 mg/dL, phosphorous 2.4 mg/dL, ionized calcium 0.56 mmol/L (normal 1.11–1.3 mmol/L), 25-hydroxy vitamin D 11.0 ng/mL (normal 30–100 ng/mL), and intact PTH was >3,639 pg/mL (normal 14–60 pg/mL). Her eGFR on admission was 31 mL/min/1.72m2, and her serum creatinine was 1.9 mg/dL (baseline between 1.5 and 2 mg/dL). Two months prior to admission she had a serum calcium of 9.2 mg/dL. ECG revealed prolonged QT interval of 479 ms and prominent T waves. These two changes caused the automated interpretation of the ECG to indicate a heart rate 133/min, while her clinicians interpreted the heart rate to be 75 (Fig. ).


Patient 2 is a 66-year-old woman with a history of Crohn's disease and an ileostomy. She presented to the emergency department with profound, debilitating weakness 22 days following her regularly scheduled dose of denosumab. She had received biannual treatments for 5 years at this point. Neurological exam revealed 5-/5 strength in all extremities. She exhibited mild psychomotor slowing. Chvostek sign was absent. Serum chemistries demonstrated a serum total calcium of 4.5 mg/dL, magnesium 1.6 mg/dL, phosphorous of <1.0 mg/dL, ionized calcium 0.89 mmol/L and intact PTH 2,356 pg/mL. 25-hydroxy vitamin D was 4 ng/mL. The last prior vitamin D measurement in our records was 2 years prior and measured <4.0 ng/mL. This measurement was drawn 2 weeks after a dose of denosumab was administered, and the importance of supplementation was reinforced to the patient at that time. This patient had no evidence of CKD with an eGFR of 101 mL/min/1.72m2 and a serum creatinine of 0.7 mg/dL. It should be noted that patient 2 had a history of mild, asymptomatic hypocalcemia (with values ranging from 6.0 to 10.4 mg/dL) in the year prior to admission with an intact PTH ranging between 300 and 500 pg/mL and mildly low serum phosphorous levels. Vitamin D deficiency limiting intestinal phosphorous absorption and denosumab-induced elevated PTH levels causing phosphaturia would account for hypophosphatemia. Patients with vitamin D deficiency in the absence of denosumab treatment typically have mildly elevated PTH levels, though generally no higher than 110 pg/mL []. The laboratory findings upon admission of both patients are presented in Table .


A 61-year-old Korean man who was incidentally diagnosed with suspected adenocarcinoma in his health screening test was referred to the gastroenterology unit of our institution. Although the patient had diabetes mellitus and variant angina, he had been treated with standard medication, and he had been relatively healthy until recently. He had also no significant symptoms, such as weight loss, abdominal pain, poor oral intake, and abdominal discomfort. Physical examination showed no signs of fever, chills, diarrhea, and abnormal bowel movements or sound. Preliminary laboratory test results were within normal limits, but the liver function test showed mild elevated levels: aspartate aminotransferase, 40 U/L; alanine aminotransferase, 72 U/L; and gamma glutamyl transpeptidase, 54 U/L. Esophagogastroduodenoscopy revealed a mucosal erosive lesion with a well-visible underlying vascular pattern, suggestive of type 0–IIc early gastric cancer at the anterior wall of the distal body of the stomach (Fig. ). Histopathologic examination of the endoscopic biopsy specimen showed moderately differentiated adenocarcinoma. The results of the Helicobacter pylori urease test (Campylobacter-like organism test; HALYARD Health, Yokohama, Japan) were negative. An abdominal computed tomography scan indicated no definite mass or wall thickening of the stomach and revealed neither lymph node enlargement nor distant metastasis (Fig. ). Subsequently, the patient underwent endoscopic submucosal dissection (ESD) and achieved en bloc resection with negative margins (Fig. ). The resected gastric ESD specimen was carefully examined by serial sections at 2-mm intervals and produced mapping. Microscopically, the tumor, measuring 1.6 × 0.8 cm, comprised both 60% adenocarcinoma and 40% squamous cell carcinoma (SqCC) components. Adenocarcinoma components showed irregular glandular structures with a tubular type and were moderately differentiated (Fig. ). The SqCC components were located adjacent to the adenocarcinoma components, and 2 individual lesions collided in the center of the tumor. The SqCC components exhibited a large solid nest of squamous cells with intercellular bridges and keratinization (Fig. ). Both individual components had invaded into the submucosal layer (800 μm) (Fig. ) accompanied with extensive lymphoid follicles. Lymphovascular invasion was also found (Fig. ). Notably, a few cells with mucin production were infrequently found within some areas of the SqCC component (Fig. ). As expected, immunohistochemistry (IHC) for p40 was positive in the SqCC components but negative in the adenocarcinoma components (Fig. ). In contrast, IHC for CK7 was negative in the SqCC components but positive in the adenocarcinoma components (Fig. ). Interestingly, IHC for carcinoembryonic antigen (CEA) was positive in some areas of both components (Fig. ). To identify molecular characteristics, microsatellite instability testing was performed by comparing the allelic profiles of the 5 microsatellite markers (BAT-26, BAT-25, D5S346, D17S250, and D2S123) in formalin-fixed paraffin-embedded tumor and normal tissues. The polymerase chain reaction products were determined using a DNA autosequence (ABI 3500xL genetic analyzer; Applied Biosystems, Foster City, CA, USA) according to the instructions. The results of microsatellite instability testing were microsatellite stable in both the adenocarcinoma and SqCC components. In contrast, few tumor cells in the adenocarcinoma components were positive in the Epstein-Barr virus-encoded RNA in situ hybridization.
Additional gastrectomy was recommended for the patient, but the patient refused all procedures and treatments and was transferred to another hospital. Subsequently, the patient was lost to follow-up.