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为了解年龄1月～6月HEV-IgM和CMV-IgM阳性的婴儿肝炎综合征(婴肝)患儿血清IFN-α、IL-6、IL-8和TNF-α水平的变化及其临床意义,应用ELISA法检测了52例HEV-IgM和54例CMV-IgM阳性的婴肝患儿血清中上述4种细胞因子(CK)的含量。结果:①HEV阳性婴肝组IFN-α、IL-6、IL-8和TNF-α的含量分别为575.24ng/L±136.82ng/L、49.68ng/L±24.52ng/L、59.58ng/L±28.52ng/L和368.24ng/L±146.42ng/L,其含量均高于正常对照组。②CMV阳性婴肝组以上4项CK,含量分别为614.82ng/L±142.48ng/L、57.84ng/L±28.82ng/L、64.76ng/L±32.72ng/L和442.36ng/L±162.48ng/L,亦明显高于正常对照组。③两疾病组中IL-6和INF-α(r_1=0.46、r_2=0.52,P<0.01)、IL-8和TNF-α(r_1=0.58、r_2=0.62,P<0.01)分别呈正相关。结果表明,血清CK的明显增高与婴肝的病损程度有密切联系,CK可作为本病的分期、活动情况及预后判定指标之一;在本疾病过程中,血清IL-6和TNF-α、IL-8和TNF-α可能是两对辅助因子,在增强机体免疫力的同时,也参与整个炎症反应,诱导活性氧产生,引起中性粒细胞介导的毒性损伤,加重肝细胞炎症和免疫自损。
In order to understand the changes of serum levels of IFN-α, IL-6, IL-8 and TNF-α in children with HEV-IgM and CMV-IgM positive infant hepatitis from January to June, and their clinical significance Serum levels of the four cytokines (CK) in 52 cases of HEV-IgM and 54 cases of CMV-IgM-positive infants were detected by ELISA. Results: ①The levels of IFN-α, IL-6, IL-8 and TNF-α in HEV positive infant group were 575.24ng / L ± 136.82ng / L, 49.68ng / L ± 24.52ng / L, 59.58ng / L ± 28.52ng / L and 368.24ng / L ± 146.42ng / L, respectively, which were higher than those in normal control group. ② The above four items of CK in CKV positive infants group were 614.82ng / L ± 142.48ng / L, 57.84ng / L ± 28.82ng / L, 64.76ng / L ± 32.72ng / L and 442.36ng / L ± 162.48ng / L, also significantly higher than the normal control group. ③ IL-6 and INF-α (r_1 = 0.46, r_2 = 0.52, P <0.01), IL-8 and TNF-α (r_1 = 0.58, r_2 = 0.62, P <0.01) were positively correlated in the two disease groups. The results showed that the serum CK increased significantly with the degree of infant liver damage are closely related, CK can be used as the disease stage, activity and prognosis of indicators; in the course of the disease, serum IL-6 and TNF-α , IL-8 and TNF-α may be two pairs of cofactors, while enhancing the body immunity, but also participate in the whole inflammatory response, induce reactive oxygen species production, cause neutrophil-mediated toxic injury, aggravate hepatocellular inflammation and Immune self-injury.