LAUSR

BACKGROUND Benzbromarone is a uricosuric agent that reduces proximal tubular reabsorption of uric acid. Because of hepatotoxicity, it has been withdrawn from the market in Europe. Recently, some benefit-risk assessments of benzbromarone suggest that benzbromarone has greater benefits than risks, and the application of benzbromarone in the treatment of gout and hyperuricemia is still under debate. CASE SUMMARY A 39-year-old man was admitted to the hospital for icterus and nausea, and he was treated with benzbromarone (100 mg/d) for 4 mo because of hyperuricemia. He had a 10-year history of beer drinking (alcohol: about 28 g/d). Laboratory data showed severe liver injury and serious coagulation dysfunction; tests for autoimmune antibodies, viral hepatitis, and human immunodeficiency virus were negative. Despite administration of liver function-protecting drugs and efficient supportive treatment, the patient deteriorated quickly after hospitalization and developed grade II encephalopathy within a few days. The patient accepted continuous plasma exchange six times; however, his condition did not improve. Based on suggestions from multidisciplinary consultation, the patient underwent liver transplantation 26 d after admission. Liver specimen pathology results showed massive necrosis consistent with drug-induced liver injury, supporting the diagnosis of acute liver failure associated with benzbromarone. The patient recovered quickly thereafter. CONCLUSION This case highlights that clinicians should be on the alert for the severe hepatotoxicity of benzbromarone. Before prescribing benzbromarone, physicians should evaluate the high-risk factors that may lead to liver injury and provide suggestions for monitoring benzbromarone's hepatotoxicity during treatment.