Casaril M, Stanzial A M, Tognella P, Pantalena M, Capra F, Colombari R, Corrocher R
Istituto di Patologia Medica, Policlinico Borgo Roma, Universita di Verona, Italy.
Hepatogastroenterology. 2000 Jan-Feb;47(31):220-5.
BACKGROUND/AIMS: In chronic viral hepatitis, an enhanced iron load is related to lower response to interferon. Furthermore, iron, through the production of oxygen radicals, may stimulate hepatocyte necrosis and the activation of cells responsible for synthesis and deposition of extracellular matrix. We investigated the relationship between iron load, evaluated by serum assays, and liver fibrogenesis in chronic active viral hepatitis.
Serum iron, ferritin, transferrin saturation and serum markers of hepatic fibrogenesis (Laminin and the amino-terminal peptide of procollagen III-NPIIIP-) were assayed in 102 patients (47 females, 55 males, mean age 42.48 years) affected by chronic hepatitis C virus and in 81 healthy controls (47 males, 34 females). In hepatitis C virus patients (studied before alpha-interferon treatment) a semiquantitative score for portal inflammation, necrosis and fibrosis was applied to liver biopsy.
Serum indices of iron load were higher in hepatitis C virus patients than in controls, and were higher in cirrhotic than in chronic hepatitis cases. Ferritin and serum iron were positively correlated with NPIIIP and laminin; moreover cases with ferritin levels over the normal limit for sex and age had higher levels of NPIIIP and laminin than cases with normal or poor iron status.
Our data suggest that even a mild increase of iron load stimulates hepatic fibrogenesis, probably adding oxygen free radical injury to the damage of viral infection.
背景/目的：在慢性病毒性肝炎中，铁负荷增加与对干扰素的反应降低有关。此外，铁通过产生氧自由基，可能刺激肝细胞坏死以及负责细胞外基质合成和沉积的细胞的活化。我们研究了通过血清检测评估的铁负荷与慢性活动性病毒性肝炎中肝纤维化之间的关系。
对102例慢性丙型肝炎病毒感染患者（47例女性，55例男性，平均年龄42.48岁）和81例健康对照者（47例男性，34例女性）检测血清铁、铁蛋白、转铁蛋白饱和度以及肝纤维化血清标志物（层粘连蛋白和Ⅲ型前胶原氨基端肽-NPIIIP-）。对丙型肝炎病毒患者（在α干扰素治疗前进行研究）的肝活检应用门静脉炎症、坏死和纤维化的半定量评分。
丙型肝炎病毒患者的血清铁负荷指标高于对照组，肝硬化患者高于慢性肝炎患者。铁蛋白和血清铁与NPIIIP和层粘连蛋白呈正相关；此外，铁蛋白水平超过性别和年龄正常上限的患者，其NPIIIP和层粘连蛋白水平高于铁状态正常或较差的患者。
我们的数据表明，即使铁负荷轻度增加也会刺激肝纤维化，可能在病毒感染损伤的基础上增加氧自由基损伤。
