Liver failure associated with benzbromarone: A case report and review of the literature

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 Because of hepatotoxicity, it has been withdrawn from the market in Europe.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.