铁与慢性肝损伤

• 作 者: 谭力学
• 机 构: 重庆医科大学附属第二医院消化内科 重庆400010
• 出 处: 国外医学(医学地理分册)
• 发表日期: 2003年04期
• 关键词: 遗传性血色病 酒精性脂肪肝 慢性肝损伤 肝炎病毒 门脉循环 枯否细胞 铁负荷 酒精性肝损伤 肝细胞损害 干扰素治疗

铁代谢异常对慢性肝损伤的影响日益为人们所关注 ,铁负荷过度通过活性氧中间体导致脂质过氧化损伤 ,及影响 T细胞和枯否细胞的功能从而导致肝细胞损伤。铁与肝炎病毒具有协同毒性作用。铁会影响慢性肝炎患者对干扰素的应答。铁负荷可促发酒精性肝损伤。铁和高胰岛素血症在非酒精性脂肪肝的发病机制中具有协同作用。遗传性血色病系 HFE基因突变导致铁过量从肠粘膜细胞转移入门脉循环 ,以致过量的铁质在肝内沉积从而导致肝纤维化、肝硬化发生。

The impact of abnormal iron metabolism on chronic liver injury is attracting more and more attention. Iron overload leads to lipid peroxidation injury through reactive oxygen intermediates and affects the function of T cells and Kupffer cells, leading to hepatocellular injury. Iron and hepatitis virus have synergistic toxic effects. Iron can affect the response to interferon in patients with chronic hepatitis. Iron load can trigger alcoholic liver injury. Iron and hyperinsulinemia have synergistic effects in the pathogenesis of nonalcoholic fatty liver disease. Hereditary hemochromatosis Department of HFE gene mutations lead to excessive iron transfer from the intestinal mucosal cells into the portal circulation, resulting in excessive deposition of iron in the liver leading to liver fibrosis, cirrhosis of the liver.