目的了解燃煤型砷中毒人体肝脏损害后的病理改变情况,为进一步阐明中毒机制提供客观的形态学依据。方法经常规病史询问、生化检查等排除长期酗酒、血吸虫及传染性肝炎等疾病后的自愿者中随机抽选出的39名患者进行常规肝脏穿刺,组织标拳用1%中性甲醛固定,切片做HE及Nasson三色染色。对照组为病区12km外非燃用高砷煤20~45岁健康人10例。结果Ⅰ级砷中毒病人主要表现为肝细胞多呈轻至中度肿胀变性,肝窦和汇管区炎细胞浸润,汇管区的纤维组织增生袁现轻微,无一例发生肝硬化。Ⅱ级砷中毒病人肝细胞肿胀变性明显加重,汇管区炎细胞及纤维组织较Ⅰ级加重,中度以上纤维组织增生有6例。所有Ⅲ级砷中毒病例均发现有不同程度的纤维组织增生。Ⅲ级砷中毒病人中肝细胞肿胀变性、汇管区的纤维组织增生更为明显,淋巴细胞浸润增加,肝硬化发生数增多。结论燃煤性砷中毒人群的肝组织肝细胞因中毒情况的加重而组织学改变不断加深,砷中毒级别越高纤维组织增生程度越明显(P〈0.001)。同时,燃煤型砷中毒对人体的损害是多方面的,这与其它地区由砷引起的中毒反应有相似之处。
Objective To observing the pathological changes of liver in arsenism patients caused by coal burning, and to provide objective evidences for clarifying of poisoning mechanism. Methods 39 patients with liver damage were subjects who were from the arsenism patients in the endemic area. According to the skin keratosis condition, the subjects were divided into 3 groups, mild (grade Ⅰ ), inter mediate (grade Ⅱ ) and severe (grade Ⅲ ). HE and Masson methods were taken to detect liver biopsy sample. Results The main changes of grade Ⅰ patients were mild or medium swelling and degeneration, infiltrating of inflammatory, cell in hepatic sinusoid and portal area, mild hyperplasia of fibrous tissue in portal area. In grade Ⅱ patients swelling and degeneration of liver cell, infiltrating of inflammatory cell and hyperplasia of fibrous tissue in portal area were more severe than those in grade Ⅰ patients. There was hepatocirrhosis in some patients. For grade Ⅲ patients, the changes above were more serious and more hepatocirrhosis patients were found. Positive correlation-ship was found between the degree of fibrous tissue hyperplasia and arsenic poisoning condition. Conclusion In arsenism patients caused by coal burning, with the aggravation of disease condition, the changes of liver pathology become more serious and obvious. The characteristic of liver pathology in the patients is a gradual advancing process of hepatocirrhosis.