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作 者:倪若愚[1] 王心禾[1] 罗端德[1] 张佩弦[1] 张锦坤[1]
机构地区:[1]同济医科大学附属协和医院,武汉市430022
出 处:《胃肠病学和肝病学杂志》1997年第4期335-337,350,共4页Chinese Journal of Gastroenterology and Hepatology
基 金:国家自然科学基金资助
摘 要:目的:探讨慢性肝病时内毒素及其它肠腔抗原进入门脉系统的途径.方法:本研究共收集HBsAg阳性的慢性肝炎病人13例,纤维内镜下取乙状结肠粘膜,进行病理和超微病理学观察.结果:研究发现,结肠粘膜上皮细胞表面糖衣减少或消失,微绒毛排列紊乱、变形,紧密连接松解、线粒体和内质网变性等.病变与肝损伤严重程度相关.轻度慢性肝炎没有或病变很轻,重度慢性肝炎及肝硬化则病变明显.结论:严重肝损伤可引起肠粘膜病变,成为内毒素及其它抗原进入门脉的路径,是引起内毒素血症和高球蛋白血症的直接原因.To find out the passage throgh which the endotoxin and other antigens get into portal system.Methods: Thirteen patients with chronic hepatitis B were enrolled in this study. Colon mucosa specimens were collected with fibroendo-cope and studied under microscope and electron microscope.Results:In this study we could see that the glycocolyx on the pithelial cells of colon was decreased or even disappeared. The microvilli on the epithellial cells were disarrranged and de-ormed . The loosing of tight junction, the degeneration such as dilation, vesiculation, degranulation and disaggregation of endo-lasmic reticula,the swelling of mitochondria and their cristea in the epithelial cells also could be found in this study.These athological changes had corellationship with the severity of the disease. They were easily found in cirrhosis patients, but ardly found in mild chronic hepatitis patients.Conclusion:Severe liver damage can lead pathologic injury in intestinal mu-osa, which provide a route for endotoxin and other antigens to enter the portal vein.This might be the direct cause of endo-oxiemia and hyperglobuliemia.
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