Martínez P, González de Etxabarri S, Ereño C, López G, Hinojal C, Teira R
Servicio de Medicina Interna, Hospital de Basurto, Bilbao.
Rev Esp Enferm Dig. 1993 Aug;84(2):124-6.
Acute liver toxicity caused by carbamazepine is a well known though infrequent event. Severe toxicity with hepatocellular insufficiency is even more rare. A case is presented of a patient who suffered of partial epilepsy on treatment with valproate and carbamazepine, who was admitted because of severe acute liver insufficiency attributable to carbamazepine. He had started treatment with the latter drug two weeks earlier, when he developed fever, jaundice, rash and signs of encephalopathy in association with elevation in serum transaminases levels and a decrease in prothrombin index (24%). Discontinuation of both antiepileptic drugs, together with the usual supportive measures, was followed by a complete resolution. Valproate was restarted without complications. Liver biopsy suggested acute hepatitis of drug-related origin. Granulomas or steatosis were not found. The histologic picture together with the relation between carbamazepine administration and the development of hepatotoxicity allow us to dismiss valproate as the possible causal agent of this patient's disease. Therefore, we believe it was an acute hepatocellular failure secondary to carbamazepine.
卡马西平引起的急性肝毒性是一种已知的虽不常见但确有发生的事件。伴有肝细胞功能不全的严重毒性更为罕见。本文报告一例正在接受丙戊酸盐和卡马西平治疗的部分性癫痫患者，因卡马西平导致的严重急性肝功能不全而入院。他在两周前开始使用后一种药物治疗，当时出现发热、黄疸、皮疹和脑病症状，同时伴有血清转氨酶水平升高和凝血酶原指数下降（24%）。停用两种抗癫痫药物并采取常规支持措施后，症状完全缓解。重新开始使用丙戊酸盐未出现并发症。肝脏活检提示药物相关性急性肝炎。未发现肉芽肿或脂肪变性。组织学表现以及卡马西平给药与肝毒性发生之间的关系，使我们排除了丙戊酸盐作为该患者疾病可能病因的可能性。因此，我们认为这是卡马西平继发的急性肝细胞衰竭。
