Kamijo Yoshito, Soma Kazui, Kokuto Mikio, Ohbu Makoto, Fuke Chiaki, Ohwada Takashi
Department of Emergency and Critical Care Medicine, Kitasato University, School of Medicine, Sagamihara Kanagawa, Japan. yk119kitasato-u.ac.jp
Arch Pathol Lab Med. 2003 Mar;127(3):364-6. doi: 10.5858/2003-127-0364-HIWHAC.
A 42-year-old man attempted suicide by ingesting about 150 mL of a saponated cresol solution containing about 50% cresol. His serum aminotransferase concentrations were elevated, and a coagulopathy was present at the time of admission, 15 hours after ingestion. The hyperaminotransferasemia and coagulopathy worsened on the second day, but resolved thereafter with supportive therapy. Histologic examination of a biopsy specimen obtained on the 14th day demonstrated focal dropout of hepatocytes (which were replaced by reticulin and collagen fibers), ballooning or hydropic degeneration of hepatocytes, and rapid regeneration with small hepatocytes in the periportal zones as well as in the centrilobular zones. A rapid onset of illness with periportal hepatocellular injury is inconsistent with damage due to a hepatotoxic metabolite of p-cresol produced by cytochrome P450, which has been suggested by studies in vitro. A direct transient noxious effect mediated via the portal or arterial circulation may be involved in hepatic injury after cresol ingestion.
一名42岁男性摄入约150毫升含约50%甲酚的皂化甲酚溶液企图自杀。摄入15小时后入院时，他的血清氨基转移酶浓度升高，且存在凝血病。高氨基转移酶血症和凝血病在第二天恶化，但之后通过支持治疗得以缓解。第14天获取的活检标本的组织学检查显示肝细胞局灶性缺失（被网状纤维和胶原纤维取代）、肝细胞气球样变或水样变性，以及门周区和小叶中心区有小肝细胞的快速再生。疾病快速起病伴门周肝细胞损伤，这与细胞色素P450产生的对甲酚肝毒性代谢产物所致损伤不一致，体外研究曾提出过这种损伤机制。甲酚摄入后肝脏损伤可能涉及经由门静脉或动脉循环介导的直接短暂毒性作用。
