Question: A 51-year-old Asian man has a known history of AIDS on antiretroviral therapy with dolutegravir and emtricitabine/tenofovir. He presented with a 1-month history of proctalgia, abdominal pain, and bloody diarrhea with urgency 11 times per day. He was previously treated for PCP pneumonia and otherwise he has no significant past medical history. He was first evaluated by a gastroenterologist at an outside clinic for his symptoms. Routine stool studies did not reveal an infectious cause of diarrhea. A computed tomography scan of the abdomen and pelvis showed rectal wall thickening, perirectal fat stranding, and lymphadenopathy. Colonoscopy revealed severe erythema, edema, friability, and granularity in the rectum 15 cm, confirming severe proctitis. He had acute and chronic inflammation with necrosis on histopathology. Upper endoscopy showed hiatal hernia and pyloric ulcers that tested negative for Helicobacter pylori. The patient was presumptively diagnosed with Crohn's disease and treated with rectal budesonide and metronidazole for 21 days with no improvement. He had progressive proctalgia, diarrhea, and a weight loss of 41 lbs over the following 2 months. He presented to our hospital for a second opinion. His CD4 count 1 month earlier was 700 cells/mL and the current CD4 count was 330 cells/mL. Repeat colonoscopy showed multiple rectal ulcers sparing the colon and terminal ileum (Figure A). Histopathology showed chronic active proctitis with ulcerated mucosa suggestive of inflammatory bowel disease (IBD). The examination was negative for dysplasia, and immunohistochemistry for cytomegalovirus and herpes simplex virus infection was negative. Given that the patient experienced poor response to previous treatment with steroids, further workup was initiated. What is the diagnosis? And what is the best next step? Look on page 1547 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.
transplants have yet been reported. Given the serious implications of this disease and the number of vaccines against COVID-19 given world-wide, further research is needed to better understand this entity and its pathophysiology.
Bilirubin 9.3 mg/dL (Direct 4.3 mg/dL, Indirect 3.5 mg/dL). CT scan of the abdomen and pelvis showed hepatomegaly with a normal biliary tree. The EBV viral capsid antigen (VCA) IgM was positive at .160 u/ML. Patient underwent a liver biopsy on hospital day 3 which showed sinusoidal patterns of inflammation and an in-situ hybridization study confirmed the diagnosis of EBV hepatitis. She was started on Solumedrol 1 mg/kg with improvement of symptoms and resolution of hepatic and hemolytic anemia lab abnormalities. Discussion: Hepatic involvement due to Epstein-Barr virus infection can be common but is typically subclinical or mild in presentation with only 5% of patients presenting with jaundice. The pathological manifestations can be extensive, as patients can also present with hemolytic anemia, specifically cold agglutinin autoimmune hemolytic anemia. The pathogenesis is believed to be due to EBV IgM antibodies cross reacting with RBC antigens. The pathogenesis of cholestasis in EBV hepatitis involves direct damage of hepatic cells by autoantibody free radical activation and the inflammation of bile ducts. The majority of cases are self-resolving; however, antivirals such as ganciclovir in conjunction with corticosteroids can provide benefit in severe cases. Due to the high global prevalence of Epstein-Barr virus, healthcare professionals should be aware of the diagnosis, management and complications of hepatic manifestations. Introduction:We present a case of acute on chronic liver failure in a patient on chronic Augmentin and total parenteral nutrition (TPN). We highlight the mechanisms and key findings of liver injury associated with intestinal failure and Augmentin, which are relevant for evaluating the risks and benefits of such therapies. Case Description/Methods: A 49-year-old woman with a history of cervical cancer treated with chemoradiation complicated by vaginal stenosis with reconstructive surgery complicated by short gut syndrome with chronic TPN dependency and chronic pelvic infections on Augmentin suppression therapy presented with hyperbilirubinemia and acute renal failure. Initial laboratory results include bilirubin 29.4 (predominantly direct), mildly elevated liver enzymes, normal alkaline phosphatase, INR 1.6, and creatinine 3.64. Her TPN and Augmentin were held. Evaluation for autoimmune markers and acute viral hepatitis serologies were negative. Genetic testing showed heterozygous C282Y mutation. Urinary copper was high with low serum ceruloplasmin, however ophthalmology exam was not concerning for Wilson's disease. Abdominopelvic non-contrast CT showed new abdominopelvic ascites. Liver biopsy revealed cholestatic hepatitis and cirrhosis. Her presentation was likely secondary to acute Augmentin hepatotoxicity in the setting of chronic intestinal-failure associated liver disease (IFALD). The patient ultimately expired due to septic shock. Discussion: Augmentin is a known cause of DILI, with clavulanic acid established as the causative agent. Onset occurs days to months following use and liver...
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