Rhabdomyolysis due to lamivudine re-administration in a patient with HBV-related hepatic failure caused by interruption of lamivudine and adefovir.

A 47-year-old man with chronic hepatitis B was admitted to Kobe Asahi Hospital on January 26, 2014 presenting with hepatic failure. Laboratory examinations revealed the following: total bilirubin, 3.39mg/dl; aminotransferases, AST, 2,700U/l; ALT, 1,800U/l; prothrombin time 40.8%; HBeAg(+); HBeAb(-) and HBV DNA, 9.1 log IU/ml (Real-time detection PCR test, LSI Medience Corporation, Tokyo). Under the diagnosis of chronic hepatitis B (stage F3), lamivudine (100mg once daily) had been administered since September 2004. Liver function worsened in September 2005, and YIDD mutation was detected. IFN-α 300MU/mg three times a week was administered from October 2005 to August 2006. In September 2006, IFN treatment was replaced by adefovir (10mg once daily). Liver function and virological markers improved steadily from April 2007 to October 2013. Laboratory examinations in June 2013 revealed the following: AST, 28U/l; ALT, 9U/l; HBeAg (-); HBeAb (-); HBV DNA was not detectable. The therapy with lamivudine and adefovir was suspended by the patient in November 2013. On January 26, 2014 when he developed hepatic failure, administration of lamivudine and adefovir was resumed together with entecavir. On February 19, the level of creatine phosphokinase (CPK) was high (4,195 IU/l), and the levels of blood and urine myoglobin reached 648 ng/ml (normal <100 ng/ml) and 570 ng/ml (<8.5 ng/ml), respectively. Troponin T was negative and the isozyme pattern of CPK was type MM. No evidence of muscle trauma, infection, or other metabolic signs were present, and the patient demonstrated no specific symptoms. The drugs administered at the time of increased serum CPK were ursodeoxycholic acid, pitavastatin calcium, lamivudine, adefovir, and entecavir. Under the suspicion of drug-induced rhabdomyolysis, pitavastatin calcium intake was discontinued LETTERS TO THE EDITOR