The incidence of drug-induced hepatic injury has been increasing as a result of more widespread use of workout supplements containing anabolic steroids to increase muscle mass. Synthetic androgenic steroids are shown to cause cholestatic liver injury, but the exact mechanism of injury is not completely understood. We present a case of a healthy, young, active duty Army male soldier who developed pruritis and jaundice shortly after starting to take a body-building supplement containing anabolic steroids, and was subsequently found to have significant biopsy proven drug-induced liver injury.

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Burkitt's lymphoma is a very aggressive type of B-cell NHL with replication approaching 100%. Primary gastrointestinal lymphoma is rare. In our case, a 24-year-old male initially presented with symptomatic anemia. He was initially evaluated with colonoscopy and EGD, both of which were unremarkable. A capsule endoscopy was then performed to further evaluate his significant anemia which revealed friable inflamed ulcerated mass in the jejunum. A push enteroscopy was then performed to obtain tissue from the jejunal mass. Biopsy results and immunohistochemical stains were consistent with Burkitt's lymphoma. PET/CT scan revealed only jejunal involvement. Treatment consisted of bowel resection prior to chemotherapy due to concern for perforation with chemotherapy. Patient achieved complete remission after the treatment.

Discussion: Adverse effects related to GES use include disruption of lead placement, erosion in the submucosa or mucosa, and obstruction, with generator site infection as the most common issue. Studies have shown that lead penetration into the gastric lumen occurs in 3% of patients, with 16% of patients requiring a corrective surgical procedure. This patient's presentation demonstrates a rare event after GES placement. Typically, leads are placed in the muscularis propria of the greater gastric curvature. Lead displacement can be detected either on imaging or if impedance values are outside the normal range; however, neither of those occurred in this patient. Abnormal presentations demonstrated by patients with GES should be evaluated thoroughly, with suspicion for hardware malposition. Diagnostic work-up with endoscopy can guide further management.[3586] Figure 1. A: Upper endoscopy revealing linear, subepithelial protrusions at the greater curvature of the antrum, located approximately 10 cm from the pylorus, consistent with typical gastric stimulator leads Figure B: Abdominal x-ray showing an anterior view of gastric pacer generator and lead placement.

INTRODUCTION: Gastric leaks following laparoscopic sleeve gastrectomy (LSG) are a feared complication, occurring in 2.4 % of cases in the proximal portion ( >90%). LSG is more prone to a leak due to a long staple line and high intraluminal pressure, sealed between an intact pylorus and lower esophageal sphincter and less likely to close spontaneously. There are no standardized guidelines for management of this or other forms of anastomotic leaks. We present a case that failed to respond to initial attempt to close with a luminal stenting, which led to multiple techniques to include endoscopic vacuum therapy (EVT), pneumatic dilation of the sleeve, and pylori Botox injection that ultimately achieved success. CASE DESCRIPTION/METHODS: 51 year old female with a recent history of laparoscopic sleeve gastrectomy complicated by a proximal leak detected 4 weeks post op. She initially underwent endoscopic closure with an Ovesco placement over the defect of the sleeve leak and stent placement across the sleeve. UGI immediately following the procedure revealed no leak. Subsequent imaging two weeks following the procedure revealed a leak, requiring the stent removal. The endoscopic exam revealed a large proximal sleeve defect leading to a large purulent cavity (3 × 4 cm) with multiple sinus openings. She underwent endoscopic vacuum therapy (14 sessions) every 3-4 days, leading to the complete sealing of the cavity and reduction of the cavity. There was a 1 × 1 cm persistent sealed cavity with diffuse granulation tissue, requiring a placement of a double pigtail stent. After functional stenosis was noted under fluoroscopy, not allowing contrast to freely flow downstream, Botox injection of the pylorus and pneumatic dilation of the sleeve (to 30 mm, 3 sessions) were performed, to relieve the pressure gradient. UGI series confirmed the completely sealed nature of the cavity and smooth contrast flow distally to the small intestine. Pigtail stent was left indefinitely to allow natural healing. DISCUSSION: Multiple endoscopic techniques have been implemented to close LSG leaks. The new paradigm has focused on optimizing pressure gradients to allow internal drainage with closure of the cavity by secondary intention. Our case described an initial failed closure that ultimately achieved success with a variety of techniques to include internal drain placement and Botox and dilation. This subject would benefit from further study to determine optimal initial or stepwise approach.