Villari D, Rubino F, Corica F, Spinella S, Di Cesare E, Longo G, Raimondo G
Dipartimento di Patologia Umana, Università di Messina, Italy.
Virchows Arch. 1995;427(2):223-6. doi: 10.1007/BF00196529.
We report a case of ductopenia associated with cholestatic hepatitis in a 59-year-old woman treated for 41 years for temporal epilepsy. The patient developed jaundice, without any clinical or biochemical features of hypersensitivity, 10 months after the beginning of treatment with sulpiride. Liver biopsy showed ballooning and acidophilic degeneration of the hepatocytes, macrophages packed with lipofuscin, biliary pigment in Kupffer cells, some biliary plugs, confluent necrosis and absence of biliary ducts in all the portal tracts. These features and the presence of foci of cholangiolitis suggest a destructive cholangitis as the pathogenetic mechanism causing ductopenia. Other causes of ductopenia were excluded. Sulpiride is known to produce severe cholestatic jaundice, which we believe is due to ductopenia. The absence of hypersensitivity and the 10-month latency suggest that sulpiride may cause liver damage through a toxic mechanism in genetically susceptible subjects.
我们报告一例59岁女性患者，该患者因颞叶癫痫接受了41年治疗，出现了与胆汁淤积性肝炎相关的胆管减少症。患者在开始使用舒必利治疗10个月后出现黄疸，无任何超敏反应的临床或生化特征。肝活检显示肝细胞气球样变和嗜酸性变性、充满脂褐素的巨噬细胞、库普弗细胞内的胆色素、一些胆栓、融合性坏死以及所有门静脉区均无胆管。这些特征以及小胆管炎病灶的存在提示破坏性胆管炎是导致胆管减少的发病机制。其他导致胆管减少的原因已被排除。已知舒必利可导致严重的胆汁淤积性黄疸，我们认为这是由于胆管减少所致。无超敏反应以及10个月的潜伏期提示舒必利可能通过遗传易感个体的毒性机制导致肝损伤。
