Reinhardt M, Machnik G, Krombholz B, Jahn G
Dtsch Z Verdau Stoffwechselkr. 1985;45(6):283-94.
Liver injuries following application of dihydralazine in 14 patients, ten of them with the typical pattern of perivenous liver cell necrosis, are reported. The other 4 patients, all having been exposed to additional hepatotoxic substances, histologically showed mixed patterns of tissue injury in liver biopsy. Moreover, in 6 of 14 patients there were diseases in the upper abdomen and/or metabolic disorders as well as an exposition to chemical hepatotoxic substances, or an additional application of potential hepatotoxic drugs. 9 of 14 patients had been treated with propranolol and dihydralazine simultaneously. One female patient showed the typical morphologic pattern of 'dihydralazine-damage' after application of propranolol only. In 3 cases with reexposition of dihydralazine merely one of them developed the typical histological behaviour documented in the literature. Distinct fibrosis of the liver remained in 2 cases. Consequently, to the hitherto existing pathogenetic concept of dihydralazine-caused liver injury as a metabolic-toxic-allergic one, there is to be added the new aspect of summing up of the actions of various additional noxious agents.
报告了14例应用双肼屈嗪后出现肝损伤的病例,其中10例具有典型的肝小叶中央静脉周围肝细胞坏死模式。另外4例患者均接触过其他肝毒性物质,肝活检组织学显示为混合性组织损伤模式。此外,14例患者中有6例存在上腹部疾病和/或代谢紊乱,同时接触过化学性肝毒性物质,或额外应用了潜在的肝毒性药物。14例患者中有9例同时接受了普萘洛尔和双肼屈嗪治疗。1例女性患者仅在应用普萘洛尔后出现了典型的“双肼屈嗪损伤”形态学模式。在3例再次接触双肼屈嗪的病例中,只有1例出现了文献中记载的典型组织学表现。2例患者肝脏出现明显纤维化。因此,在迄今已有的将双肼屈嗪所致肝损伤视为代谢-毒性-过敏性损伤的发病机制概念基础上,还应增加一个新的方面,即各种其他有害因素作用的叠加。