Martín-González Candelaria, Pelazas-González Ricardo, Fernández-Rodríguez Camino, Alemán-Valls Remedios, Martínez-Riera Antonio, Ortega-Toledo Paula, García-Rodríguez Alen, Rodríguez-Gaspar Melchor, González-Reimers Emilio
Servicio de Medicina Interna. Hospital Universitario de Canarias. Universidad de La Laguna. Tenerife, Canary Islands, Spain.
Servicio de Medicina Interna. Hospital Universitario de Canarias. Universidad de La Laguna. Tenerife, Canary Islands, Spain.
J Trace Elem Med Biol. 2020 Sep;61:126542. doi: 10.1016/j.jtemb.2020.126542. Epub 2020 May 4.
In chronic hepatitis C virus (HCV) infection there is increased iron absorption leading to iron overload, a fact that may promote ferritin synthesis. Theoretically, increased ferritin should promote ongoing liver fibrosis but disparate results have been described.
We analyze the behavior of iron metabolism- related variables, comparing them with fibrosis and inflammatory activity in liver biopsy in HCV infected patients.
We analyzed among 90 HCV patients subjected to liver biopsy prior to antiviral treatment the relationships of serum levels of iron, ferritin, transferrin, transferrin saturation index (TSI) and total iron binding capacity (TIBC) with liver fibrosis and histological severity, assessed by Metavir-f, Metavir-a and Knodell indices, as well as with liver function, and also compared the aforementioned iron metabolism- related variables with 34 controls.
Patients showed higher values of sideremia (T = 2.04; p = 0.044) and transferrin (T = 2.29; p = 0.004) compared with controls; but not ferritin, that was significantly higher among the 33 patients who also consumed alcohol (Z = 2.05; p = 0.041). Most patients showed a well preserved liver function (86 cases, Child A). Patients with Child B or C showed higher ferritin levels (Z = 2.68; p = 0.007) and TSI (Z = 2.41; p = 0.016), but lower transferrin and TIBC (Z = 3.25; p = 0.001) than Child A patients. Transferrin and TIBC were directly related to albumin (ρ = 0.24; p = 0.026), whereas bilirubin showed direct relationships with iron (ρ = 0.25; p = 0.016), TSI (ρ = 0.39; p < 0.001) and ferritin (ρ = 0.36; p < 0.001). Both ferritin (ρ = -0.22; p = 0.04) and TSI (ρ = -0.25; p = 0.016) were related to platelet count. No relationships were observed between iron variables and Knodell index, but serum iron, serum transferrin, and TSI were directly related to Metavir-f score (ρ = 0.28; p = 0.009, ρ = 0.22; p = 0.044, and ρ = 0.22; p = 0.044, in this order).
Alterations of iron related variables are relatively subtle in our series of 90 well compensated HCV patients. Serum ferritin was not related to liver fibrosis and increases only when alcoholism co-exists with HCV infection.
在慢性丙型肝炎病毒（HCV）感染中，铁吸收增加导致铁过载，这一事实可能会促进铁蛋白合成。从理论上讲，铁蛋白增加应会促进肝纤维化进展，但已有不同的研究结果报道。
我们分析了与铁代谢相关变量的变化情况，并将其与HCV感染患者肝活检中的纤维化和炎症活动进行比较。
我们对90例接受抗病毒治疗前进行肝活检的HCV患者进行分析，评估血清铁、铁蛋白、转铁蛋白、转铁蛋白饱和度指数（TSI）和总铁结合力（TIBC）水平与肝纤维化及组织学严重程度（通过Metavir - f、Metavir - a和Knodell指数评估）以及肝功能之间的关系，并将上述与铁代谢相关的变量与34名对照者进行比较。
与对照组相比，患者的血清铁（T = 2.04；p = 0.044）和转铁蛋白（T = 2.29；p = 0.004）水平更高；但铁蛋白水平在对照组与患者组间无差异，不过在33例同时饮酒的患者中，铁蛋白水平显著更高（Z = 2.05；p = 0.041）。大多数患者肝功能良好（86例，Child A级）。与Child A级患者相比，Child B级或C级患者的铁蛋白水平（Z = 2.68；p = 0.007）和TSI（Z = 2.41；p = 0.016）更高，但转铁蛋白和TIBC更低（Z = 3.25；p = 0.001）。转铁蛋白和TIBC与白蛋白呈直接相关（ρ = 0.24；p = 0.026），而胆红素与铁（ρ = 0.25；p = 0.016）、TSI（ρ = 0.39；p < 0.001）和铁蛋白（ρ = 0.36；p < 0.001）呈直接相关。铁蛋白（ρ = -0.22；p = 0.04）和TSI（ρ = -0.25；p = 0.016）均与血小板计数相关。未观察到铁变量与Knodell指数之间存在关联，但血清铁、血清转铁蛋白和TSI与Metavir - f评分呈直接相关（依次为ρ = 0.28；p = 0.009，ρ = 0.22；p = 0.044，ρ = 0.22；p = 0.044）。
在我们这组90例病情得到良好控制的HCV患者中，与铁相关变量的改变相对不明显。血清铁蛋白与肝纤维化无关，仅在酒精性肝病与HCV感染并存时升高。
