Hughes C A, Talbot I C, Ducker D A, Harran M J
Gut. 1983 Mar;24(3):241-8. doi: 10.1136/gut.24.3.241.
Biochemical, histological, and electron-microscopic investigation of seven preterm infants who became jaundiced after prolonged total parenteral nutrition showed conjugated hyperbilirubinaemia apparently due to cholestasis without significant primary liver cell injury. In the absence of evidence indicating a direct toxic effect on the liver of this form of nutrition the necropsy findings in one child and analogy with the effects of total parenteral nutrition in animals suggest that the cholestasis is the result of suppression of trophic and/or secretion-stimulating hormone(s) normally produced by the gut, due to absent enteral nutrition. Biochemical and electron-microscopic findings suggest that liver cell damage occurs after resumption of enteral nutrition.
对7名长期接受全胃肠外营养后出现黄疸的早产儿进行的生化、组织学和电子显微镜检查显示,结合胆红素血症明显是由于胆汁淤积所致,而没有明显的原发性肝细胞损伤。在没有证据表明这种营养形式对肝脏有直接毒性作用的情况下,一名儿童的尸检结果以及与动物全胃肠外营养作用的类比表明,胆汁淤积是由于缺乏肠内营养导致肠道正常产生的营养和/或分泌刺激激素受到抑制的结果。生化和电子显微镜检查结果表明,恢复肠内营养后会发生肝细胞损伤。