Tranexamic Acid-Induced Acute Renal Cortical Necrosis in Post-Endoscopic Papillectomy Bleeding

Acute renal failure can be the result of acute renal cortical necrosis (RCN), which commonly occurs from complications occurring during pregnancy. RCN is rarely caused by medications, although tranexamic acid, which is used in patients with acute bleeding for its antifibrinolytic effects, reportedly causes acute RCN in rare cases. An 82-year-old woman experienced gastrointestinal bleeding after endoscopic papillectomy of an ampullary adenoma. The bleeding was controlled with tranexamic acid administration; however, 4 days later, her urine volume decreased and she developed pulmonary edema and dyspnea. Serum creatinine levels increased from 0.8 to 3.9 mg/dL and dialysis was performed. Abdominal pelvic computed tomography with contrast enhancement revealed bilateral RCN with no renal cortex enhancement. Renal dysfunction and oliguria persisted and hemodialysis was continued. Clinicians must be aware that acute RCN can occur after tranexamic acid administration to control bleeding

Delayed Severe Hemobilia after Endoscopic Biliary Plastic Stent Insertion

Hemobilia is a rare gastrointestinal bleeding, usually caused by injury to the bile duct. Hemobilia after endoscopic retrograde cholangiopancreatography (ERCP) is generally self-limiting and patients will spontaneously recover, but some severe and fatal hemorrhages have been reported. ERCP-related bowel or bile duct perforation should be managed promptly, according to the type of injury and the status of the patient. We recently experienced a case of late-onset severe hemobilia in which the patient recovered after endoscopic biliary stent insertion. The problem was attributable to ERCP-related bile duct perforation during stone removal, approximately 5 weeks prior to the hemorrhagic episode. The removal of the stent was performed 10 days before the onset of hemobilia. The bleeding was successfully treated by two sessions of transarterial coil embolization

Pancreatic tuberculosis masquerading as pancreatic serous cystadenoma

Solitary pancreatic involvement of tuberculosis is rare, especially in an immunocompetent individual, and it may be misdiagnosed as pancreatic cystic neoplasms. Pancreatic cystic neoplasms are being identified in increasing numbers, probably because of the frequent use of radiology and advances in endoscopic techniques. However, they are composed of a variety of neoplasms with a wide range of malignant potential, and it is often difficult to differentiate pancreatic tuberculosis mimicking cystic neoplasms from benign or malignant pancreatic cystic neoplasms. Non-surgical diagnosis of pancreatic tuberculosis is inconclusive and continues to be a challenge in many cases. If so, then laparotomy should be employed to establish the diagnosis. Therefore, pancreatic tuberculosis should be kept in mind during the differential diagnosis of solitary cystic masses in the pancreas. We report a patient who had solitary pancreatic tuberculosis masquerading as pancreatic serous cystadenoma