2345 Do You Wish to Have a Liver Transplant? A Case of Testosterone Booster-Induced Toxic Hepatitis

Abstract

INTRODUCTION: Drug-induced hepatitis is inflammation of the liver that is caused by a toxic amount of certain medicines, vitamins, herbal or food supplements. We present a case of a young adult male with testosterone booster induced acute hepatitis, abnormally high liver enzymes but otherwise relatively asymptomatic presentation. CASE DESCRIPTION/METHODS: 35 year old man, who presented to the hospital with flu like symptoms for 3 days. Gastroenterology was consulted for urgent evaluation of new onset nausea, vomiting and fatigue, associated with a >60-fold increase in his transaminases and alkaline phosphatase. His liver function was: AST U/L 2450, ALT 3300 U/L, Alkaline Phosphatase 200 U/L, LDH 1660 U/L, GGT 750 U/L, Indirect bilirubinemia, with abnormally high ferritin levels of >6000 ng/ml. His further workup including viral serology of HSV, Hepatitis, EBV, CMV, Influenza; Urine toxicology; ANA; Anti Smooth Muscle Antibody, Ceruloplasmin, Alpha-1 Antitrypsin was negative. Liver function including protein and PT/INR was normal. With an unremarkable spleen and portal vein ultrasound, he also underwent CT abdomen and pelvis without contrast on day 3 of admission which was not rewarding. With uptrending liver enzymes, liver biopsy was done and pathology showed findings consistent with drug-induced hepatitis- collapsed portal tracts with inflammation comprising of histiocytes, lymphocytes, scattered eosinophils with few plasma cells. On detailed questioning, he reported endorsing high dose testosterone booster orally, to improve his muscle mass. The medication was stopped. Liver enzymes started down trending over a period of 1 week. He was eventually discharged on oral steroids. Patient was thereafter lost to follow up outpatient. DISCUSSION: Drug induced liver injury (DILI) is mostly a diagnosis of exclusion with supporting liver biopsy findings. DILI has several clinical manifestations ranging from asymptomatic elevations in liver enzymes to fulminant liver failure culminating in death or liver transplantation. DILI may be predictable and dose-dependent, or may be idiosyncratic. Rapid and severe recurrence may occur with re-exposure and stopping the drug or supplement is of utmost importance. Our patient had mixed hepatocellular-cholestatic injury. General guidelines involve giving gluccocorticoids to patients with hypersensitivity reactions who have progressive cholestasis or no significant improvement despite withdrawal of causative agent. Patient counselling for avoidance is of utmost importance.