Mihas A A, Holley P, Koff R S, Hirschowitz B I
Gastroenterology. 1976 May;70(5 PT.1):770-4.
Fulminant hepatic failure developed in a 24-year-old black woman who had been treated with propylthiouracil and propranolol for hyperthyroidism. Clinical and biochemical recovery followed discontinuation of drug therapy. Liver biopsy disclosed submassive hepatic necrosis. During the acute phase of the disease, lymphocyte transformation studies revealed sensitization of the patient's lymphocytes to propylthiouracil but not to propranolol. Sensitization remained demonstrable 2 months after cessation of the former drug. Lymphocytes obtained from a hyperthyroid patient treated with propylthiouracil without complications failed to show evidence of sensitization. These observations indicate that submassive hepatic necrosis may result from treatment with propylthiouracil and are consistent with the notion that sensitization mechanisms may be responsible for the hepatic injury induced by this drug.
一名24岁的黑人女性因甲状腺功能亢进接受丙硫氧嘧啶和普萘洛尔治疗后发生暴发性肝衰竭。停用药物治疗后临床和生化指标恢复。肝活检显示亚大块肝坏死。在疾病急性期，淋巴细胞转化研究显示患者淋巴细胞对丙硫氧嘧啶敏感，但对普萘洛尔不敏感。停用前一种药物2个月后仍可检测到敏感性。从无并发症的丙硫氧嘧啶治疗的甲状腺功能亢进患者获得的淋巴细胞未显示致敏证据。这些观察结果表明，亚大块肝坏死可能由丙硫氧嘧啶治疗引起，并且与致敏机制可能是该药物所致肝损伤原因的观点一致。
