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.