BackgroundEdoxaban is an orally administered anticoagulant treatment that is used in patients with cerebral infarction, venous thrombosis, or other conditions, with a reported incidence of gastrointestinal hemorrhage at approximately 1%. We encountered the rare case of a patient who developed a gallbladder hemorrhage after the administration of edoxaban.Case presentationAn 86-year-old Japanese woman visited our gastrointestinal department due to the chief complaint of melena lasting for a week. Her medical history included hypertension and embolic cerebral infarction, and she was taking orally administered carvedilol (5 mg/day) and edoxaban (30 mg/day). Her palpebral conjunctiva was pale during a physical examination, indicating the possibility of anemia. Her blood test results confirmed severe anemia with red blood cells at 1.7 × 106/μL and hemoglobin at 4.7 g/dL. An upper gastrointestinal endoscopy revealed bile and fresh blood on the duodenal bulb and in more distal regions; hemobilia was suspected. A computed tomography scan on the ninth hospitalization day confirmed the hemobilia with a gallbladder fundus high-density signal. She was discharged on the 30th day of hospitalization with only fluid therapy and no progression of anemia. Moreover, she underwent a laparoscopic cholecystectomy 1 month after discharge, but the pathologist did not identify false aneurysms or neoplastic lesions. She has not been shown to develop anemia for 5 months after surgery.ConclusionsOur case suggests that gallbladder hemorrhage needs to be considered a possible complication for patients on direct oral anticoagulants.

Background Yellow nail syndrome is a rare condition associated with a triad of symptoms: yellow nails, lung lesions, and lymphedema. We report a case of yellow nail syndrome caused by titanium exposure from multiple artificial joint replacements. Case presentation A 78-year-old Asian woman presented to our outpatient department with chief complaints of cough, fever, and nausea. The patient was hospitalized for observation because of the presence of hypoxemia and bilateral pleural effusion. Her medical history included knee joint replacement and two spinal fusion surgeries. Her physical examination conducted following hospitalization revealed yellow nails on both hands and feet. This finding, combined with the observation of bilateral pleural effusion, raised suspicion for yellow nail syndrome. Blood analysis yielded negative results, as did the tests for sputum culture, interferon liberation, pleural effusion culture, and pleural effusion cytology. Pleural histopathological analysis and imaging yielded negative results. Considering the possibility of titanium exposure from artificial joints based on the patient’s medical history, we examined a chest radiograph obtained before the second spinal fusion surgery; however, no pleural effusion was observed. Pleural effusion was observed, however, following the surgery. On the basis of these findings, the patient was diagnosed with yellow nail syndrome due to titanium exposure. Conclusions Clinicians should examine the nails of patients with unexplained pleural effusion. Moreover, they should inquire about titanium exposure when obtaining the patient’s medical history.

Background Encapsulating peritoneal sclerosis (EPS) is a rare condition in which the small intestine is covered by an inflammatory fibrocollagenous membrane; the exact etiology of EPS is unclear. Herein, we report the case of our patient who underwent hemodialysis and cell-free and concentrated ascites reinfusion therapy (CART) and was diagnosed with EPS. Case presentation A 64-year-old Japanese man visited our emergency department with a chief complaint of abdominal pain. He had a medical history of cirrhosis due to hepatitis C for 25 years. He had undergone partial resection of the small intestine 2 years earlier for an incarcerated hernia. One year earlier, he experienced renal failure due to hepatorenal syndrome and started hemodialysis three times a week and CART twice a month. Physical examination of the abdominal wall revealed a lack of peristalsis of the intestinal tract and strong tenderness on palpation. Because hernia of the small intestine was found on computed tomography, we suspected strangulation ileus, requiring emergency operation. When the abdomen was opened, the entire small intestine was found to be wrapped in a fibrous membrane and constricted by it. The patient was diagnosed with EPS; hence, during surgery, the fibrous membrane was excised, resulting in decompression of the intestinal tract and subsequent recovery. Conclusions EPS is thought to be related to various elements, but no case of EPS induced by CART has been reported to date. EPS should be considered in the differential diagnosis of small bowel obstruction in patients undergoing CART for refractory ascites.

Background Systemic lupus erythematous that causes various organ damage is rarely associated with pancreatic lesion. To the best of our knowledge, no cases presenting with hemorrhage shock caused by gastric penetration of pancreatic pseudocyst due to lupus pancreatitis have been reported. Herein, we report a case of hemorrhage shock caused by gastric penetration of pancreatic pseudocyst due to lupus pancreatitis. Case presentation A 53-year-old Japanese man with a history of systemic lupus erythematous, pancreatic pseudocyst, and chronic pancreatitis complained of epigastric pain and had hematemesis. He visited our emergency room and was admitted in our hospital. Upper endoscopy showed that hemostasis was obtained; however, computed tomography scan was performed since he was suspected to have gastric penetration into hollow viscera. The computed tomography revealed accumulation of fluid around the pancreas and gastric penetration of pancreatic cyst. Blood test showed increased serum amylase level. These results suggest that the exacerbation of chronic pancreatitis causes the penetration. Surgery was considered; however, we took a wait-and-see approach since hemostasis was obtained. After that, he was in stable condition, although he suffered from fever and accumulation of left pleural effusion was observed by computed tomography. However, he had massive hematemesis and melena 9 days after hospitalization and died in spite of several treatments including blood transfusion. Autopsy revealed that he actually had pleural thickening, which is not caused by accumulation of left pleural effusion but by severe pleural inflammation. We therefore performed additional blood and urinary tests on the same day. The test results showed that he had a high titer of anti-double-stranded deoxyribonucleic acid (DNA) antibody, hypocomplementemia, and erythrocyturia, indicating that he had systemic lupus erythematous with high disease activity considering his fever and pleural inflammation. Conclusions Patients who have systemic lupus erythematous with high disease activity have the potential to develop fatal complications due to pancreatitis, so appropriate treatments are required for such patients.