S4855 Atypical Hyperbilirubinemia in a Pregnant Patient: Infliximab-Induced Hepatocellular Injury

Introduction: Crohn’s disease is a highly variable form of inflammatory bowel disease commonly presenting with fever, abdominal pain, diarrhea, nausea, vomiting, weight loss, and fatigue. First-line therapy for severe phenotypes of this disease includes anti- tumor necrosis factor a agents, such as Infliximab. This medication is generally well tolerated, yet cases of severe hepatotoxicity have been reported in patients on active treatment. We present a case of a patient who developed severe hepatocellular injury 5 months after initiating Infliximab therapy for Crohn’s disease. Case Description/Methods: A 27-year-old pregnant woman at 21 weeks gestation with a history of fistulizing Crohn’s disease, presented for evaluation of 1-day history of generalized pruritus. She had started on Infliximab approximately 5 months prior to presentation of these symptoms. Baseline labs revealed hemoglobin 11.5, platelet count 244, AST 701, ALT 809, total bilirubin 2.6, and elevated total bile acids. Autoimmune workup yielded positive ANA (1:320), IgG levels were WNL, whereas viral hepatitis serology and serum toxicology were negative. Right upper quadrant ultrasound showed cholelithiasis with a normal biliary duct diameter, confirmed via magnetic resonance cholangiopancreatography. Over the course of her 2-day admission, she showed only marginal improvement in her symptoms and hepatic function. Twelve days later, she presented back with significantly worsening hepatocellular injury with AST 1154, ALT 1300, Alk Phos 164, total bilirubin 13.4, and direct bilirubin 11.5, along with normal hemoglobin and platelet counts. Liver biopsy was pursued revealing acute panlobular hepatitis comprised of neutrophils, lymphocytes, plasma cells, and eosinophils. Hepatocyte and canalicular bile plugs were also present. These findings were suggestive of drug-induced liver injury. Infliximab was discontinued, and she was treated with prednisone taper resulting in normalized liver function. Discussion: Infliximab-induced hepatitis is a rare, but serious complication which occurs via an autoimmune or direct hepatotoxic effect. Our case appears to be consistent with hepatocellular liver injury from Infliximab therapy that is probably autoimmune-mediated. Furthermore, our patient had a full recovery of liver function following discontinuation of Infliximab therapy along with a course of steroids, which bolsters our hypothesis of infliximab-induced liver injury.