Hepatitis C, iron status, and disease severity:: Relationship with HFE mutations
Hepatitis C, iron status, and disease severity:: Relationship with HFE mutations
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DOI：
10.1053/gast.2003.50046
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发表时间：
2003-02-01
期刊：
影响因子：
29.4
通讯作者：
Kowdley, KV
中科院分区：
文献类型：
--
作者：
Tung, BY;Emond, MJ;Kowdley, KV
背景与目的：轻度至中度肝铁负荷在慢性丙型肝炎患者中很常见。我们试图确定血色素沉着症基因HFE的突变是否与丙型肝炎患者的铁超载和疾病进展加速有关。研究方法：共研究了316例慢性丙型肝炎患者：198例连续患者因代偿性肝病接受肝活检，118例因终末期肝病接受肝移植。血清铁研究，定量肝铁浓度，组织学活动指数，和HFE基因型进行了测定。结果如下：在代偿性肝病患者中，HFE突变的存在与血清铁水平、血清转铁蛋白-铁饱和度、血清铁蛋白水平和肝铁指数的升高独立相关（P <0.05）。在调整丙型肝炎病毒感染持续时间后，HFE突变也与桥接纤维化或肝硬化的存在独立相关（比值比，18; 95%置信区间，1.7 - 193）。HFE突变与终末期肝病患者的铁负荷无关。代偿期和终末期肝病患者的HFE突变患病率无显著差异（分别为42%和33%; P = 0.67）。结论：HFE突变的存在与慢性丙型肝炎代偿性肝病患者的铁负荷和晚期纤维化独立相关，特别是在控制疾病持续时间后。这些结果表明，HFE突变加速丙型肝炎的肝纤维化，但可能不是导致进展为终末期肝病的原因。
Background & Aims: Mild to moderate hepatic iron loading is common in patients with chronic hepatitis C. We sought to determine whether mutations in the hemochromatosis gene, HFE, are associated with iron overload and acceleration of disease progression in hepatitis C patients. Methods: A total of 316 patients with chronic hepatitis C were studied: 198 consecutive patients undergoing liver biopsy for compensated liver disease and 118 who underwent liver transplantation for end-stage liver disease. Serum iron studies, quantitative hepatic iron concentration, histologic activity index, and HFE genotype were determined. Results: Among patients with compensated liver disease, the presence of HFE mutations was independently associated with elevations in serum iron level, serum transferrin-iron saturation, serum ferritin level, and hepatic iron index (P < 0.05). After adjustment for duration of infection with hepatitis C virus, HFE mutations were also independently associated with the presence of bridging fibrosis or cirrhosis (odds ratio, 18; 95% confidence interval, 1.7-193). HFE mutations were not independently associated with iron loading in patients with end-stage liver disease. There was no significant difference in the prevalence of HFE mutations between patients with compensated and endstage liver disease (42% vs. 33%, respectively; P = 0.67). Conclusions: The presence of HFE mutations is independently associated with iron loading and advanced fibrosis in patients with compensated liver disease from chronic hepatitis C, especially after controlling for duration of disease. These results suggest that HFE mutations accelerate hepatic fibrosis in hepatitis C but may not be responsible for progression to end-stage liver disease.