Abstract

Acipimox, a niacin derivative, is a lipid-lowering drug that is widely used to treat hyperthyroidism. It is generally well tolerated and causes fewer adverse effects than niacin. Acipimox has been reported to induce mild adverse effects, mainly pruritus and flushing. Concerning hepatotoxicity induced by acipimox, only limited information is available regarding the symptoms and therapeutic schedule. In this study, we report the case of a 40-year-old man with hyperlipidemia who developed liver injury after treatment with acipimox. After treatment discontinuation, his liver function gradually improved. After obtaining negative results in tests for hepatitis, infectious mononucleosis, and rheumatologic diseases, in addition to ultrasonographic findings, acipimox administration was resumed, and his liver enzyme levels again remarkably increased. In the absence of any biliary obstruction or other obvious causes of hepatic injury, acipimox-induced hepatocellular injury was strongly suspected in accordance with the Roussel-Uclaf Causality Assessment Method. Acipimox was again discontinued, and magnesium isoglycyrrhizinate was introduced. The patient's liver function tests gradually improved over 3 days and displayed marked improvement after 1 week. On the basis of the recorded findings, drug-induced liver injury was highly suspected, and rechallenge and the exclusion of other obvious factors were required to establish the diagnosis of acipimox-induced hepatic injury. Furthermore, the importance of evaluating hepatotoxicity using the Roussel-Uclaf Causality Assessment Method and the effectiveness of magnesium isoglycyrrhizinate for treating liver cell injury were demonstrated.