Benjamin S B, Ishak K G, Zimmerman H J, Grushka A
Hepatology. 1981 May-Jun;1(3):255-63. doi: 10.1002/hep.1840010311.
Phenylbutazone has been reported to produce several forms of hepatic injury. A clinical and histologic review of 23 well-substantiated cases in conjunction with review of 43 case reports in the literature was undertaken. Utilizing the histologic features and available clinical data, the injury was classified as moderate-marked hepatocellular injury, minor hepatocellular injury, and other injury. No sexual differences were noted. Most patients had used the drug for less than 6 weeks. Features of hypersensitivity were common. Granulomas on liver biopsy were seen mainly in association with clinical evidence of hypersensitivity nd with minor hepatocellular liver injury. The majority of deaths occurred in cases with significant hepatocellular injury or systemic vasculitis. Analysis of available data suggests that, although hypersensitivity appears to contribute to phenylbutazone-associated hepatic injury, the drug also appears to have intrinsic hepatotoxic potential. Speculation is offered regarding the relative role of these two mechanisms in the several forms of hepatic injury induced by phenylbutazone.
据报道,保泰松可引发多种形式的肝损伤。我们对23例充分证实的病例进行了临床和组织学回顾,并结合文献中43例病例报告进行了分析。根据组织学特征和现有的临床数据,将损伤分为中度至重度肝细胞损伤、轻度肝细胞损伤和其他损伤。未发现性别差异。大多数患者使用该药物的时间少于6周。过敏反应特征较为常见。肝活检中的肉芽肿主要见于伴有过敏反应临床证据和轻度肝细胞损伤的病例。大多数死亡病例发生在有严重肝细胞损伤或系统性血管炎的患者中。现有数据分析表明,虽然过敏反应似乎与保泰松相关的肝损伤有关,但该药物似乎也具有内在的肝毒性潜力。文中对这两种机制在保泰松所致多种肝损伤形式中的相对作用进行了推测。