Mifepristone is frequently used in large doses for management of Cushing’s syndrome. This is a case of a 35-year-old woman with Cushing’s syndrome, who presented with abdominal pain and jaundice. A month prior to admission, she had been started on a daily dose of 1,200 mg mifepristone. After evaluating for various other causes of liver injury, biopsy revealed cholestatic pattern of liver disease, likely associated with drug-induced hepatotoxicity. Mifepristone was discontinued and her symptoms resolved. We believe this is one of the first few reported cases of drug-induced liver injury (DILI) associated with mifepristone use.

INTRODUCTION: Gastric ischemia is a potentially lethal condition which can lead to necrosis, perforation, and overall increased mortality. To our knowledge, this is the first report of spontaneous vasogenic gastric necrosis. We present a patient with spontaneous idiopathic vasogenic gastric necrosis leading to a positive outcome. CASE DESCRIPTION/METHODS: 75-year-old female presented with a three day history of diffuse progressive abdominal pain, nausea, and bilious emesis. Physical exam was remarkable for diffuse abdominal tenderness, hyperactive bowel sounds and guarding. Labs revealed WBC 15.6 thousand/ul and Lactic Acid 2.9 mmol/L. CT abdomen showed gas in the gastric wall and portal vein (Figure 1). Upper endoscopy revealed diffuse necrotic gastric tissue without perforation (Figure 2). After noting this, the patient was taken to the OR where a total gastrectomy with roux-en-y esophagojejunostomy was performed. Pathology showed active chronic gastritis with ulceration and focal hemorrhagic necrosis, ruling out malignancy and H.pylori. The patient recovered well and was discharged to a short-term care facility. DISCUSSION: Spontaneous ischemic gastric necrosis is a rare and potentially life-threatening if improperly managed. Mortality rate is high for gastric ischemia (33-41%) and even higher for perforation (50-80%)3-4. 75% of cases are from local vascular causes, others being obstruction or hypoperfusion2. Commonly patients present with abdominal pain, GI bleeding and confusion4. The pathophysiology of acute idiopathic gastric mucosal damage is unclear. One hypothesis describes an overwhelming amount of gastric acid, bile salts and ischemia causing a marked decrease in mucosal blood flow to gastric tissue1,5. Given the acuity and rapid clinical progression, it's imperative to have a high degree of clinical suspicion when evaluating such patients. In this case, a prompt diagnosis and early management led to a positive outcome.

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