Abstract
The patient was a 66-year-old male with a 24-year history of dialysis for chronic renal failure due to chronic glomerulonephritis. He also demonstrated hypertension, hyperuricemia and moderate hepatic dysfunction due to chronic alcohol abuse prior to starting cinacalcet HCl. His medical history included surgery for bilateral carpal tunnel syndrome. During follow-up, the intact-PTH level increased to 371 pg/dL. Despite the fact that active vitamin D3 was administered orally, the intact-PTH level remained elevated. Therefore, cinacalcet HCl was initiated at 25 mg/day. On the 4th day after initiating administration, liver escape enzymes were significantly elevated (AST 1,709 IU/L, ALT 561 IU/L, LDH 1,602 IU/L). Abdominal computed tomography showed hepatomegaly and a gallstone, but did not identify any dilatation of the intrahepatic or common bile duct or structural abnormalities of the hepatic parenchyma. Acute exacerbation of alcoholic liver injury was considered a possible cause, but cinacalcet HCl-induced liver injury was the most likely cause ; therefore, cinacalcet HCl was discontinued immediately. The liver escape enzyme levels decreased significantly 1 week after discontinuation (AST 49 IU/L, ALT 61 IU/L, LDH 172 IU/L). The diagnostic scale for drug-induced liver injury at the workshop in Digestive Disease Week-Japan 2004 (DDW-J 2004) showed a score of 7 in this case. The disease was considered the hepatocellular type based on the interval from first administration to onset, eosinophilia, and data after discontinuation, which indicated that the patient had cinacalcet HCl-induced liver injury. The liver escape enzyme levels returned to normal 2 weeks after discontinuation. There have been very few previous reports of cinacalcet HCl-induced liver injury. In such rare cases, the increase in the liver escape enzyme levels might not be more than 1%. Herein, we report our unique case in which the liver escape enzyme levels were suddenly elevated, immediately after the initiation of cinacalcet HCl and returned to normal only when the drug was discontinued or liver protective agents were administered.
