Capocaccia L, Merli M, Piat C, Servi R, Zullo A, Riggio O
2. Gastroenterologia, Università La Sapienza, Roma, Italy.
Ital J Gastroenterol. 1991 Jul-Aug;23(6):386-91.
Alterations in trace element concentrations may be observed in patients with chronic liver disease. Notably, selenium and zinc levels are reduced both in serum and in liver tissue of cirrhotic patients. Low selenium levels have been involved in the pathogenesis of liver damage as this element is important in controlling the levels of toxic oxygen radicals in the cells. Zinc deficiency has been involved in the pathogenesis of a number of clinical findings in chronic liver disease. These include the possible role of zinc deficiency in the pathogenesis of hepatic encephalopathy, by inducing alterations in urea metabolism. In CC14 cirrhotic rats oral zinc supplementation reduces ammonia levels and increases OCT activity in the liver. Oral zinc supplementation has been also proposed in the treatment of cirrhotic patients with chronic hepatic encephalopathy, the results however are not yet conclusive.
在慢性肝病患者中可观察到微量元素浓度的改变。值得注意的是,肝硬化患者的血清和肝组织中硒和锌水平均降低。低硒水平参与了肝损伤的发病机制,因为该元素在控制细胞内有毒氧自由基水平方面很重要。锌缺乏参与了慢性肝病许多临床症状的发病机制。这些包括锌缺乏在肝性脑病发病机制中可能发挥的作用,即通过诱导尿素代谢改变。在四氯化碳诱导的肝硬化大鼠中,口服补充锌可降低氨水平并增加肝脏中的鸟氨酸氨基甲酰转移酶(OCT)活性。口服补充锌也被提议用于治疗患有慢性肝性脑病的肝硬化患者,然而结果尚无定论。