重型血友病A患儿关节出血后IL-1β、IL-6、TNF-α释放与关节病变形成的相关性研究

摘要

目的 探讨重型血友病A患儿关节出血后IL-1β、IL-6、TNF-α 释放与关节病变形成的相关性.方法 方便选取该院(2015年1月-2017年1月)收治的重型血友病A患儿60例,无关节出血组(n=20),关节出血组(n=36),急性关节出血组(n=20),慢性关节出血组(n=15),应用酶联免疫吸附实验测定血清TNF-α、IL-6、IL-1β 水平.结果 急性关节出血组关节病变患者细胞内TNF-α 信使核糖核酸表达水平(6.695±2.523)ng/L,明显高于无关节病变患者(1.791±1.479)ng/L,差异有统计学意义(t=4.934 6,P＜0.05);急性关节出血组关节病变细胞内IL-6、IL-1β 信使核糖核酸表达水平分别为(0.912±0.525)ng/L、(1.879±1.542)ng/L;无关节病变者分别为(1.263±0.647)ng/L、(0.971 8±0.517)ng/L,急性关节出血组关节病变与无关节病变细胞内IL-6、IL-1β 信使核糖核酸表达水平对比差异无统计学意义(t=1.336 2、1.592 9,P＞0.05).结论 重型血友病A患儿急性关节出血TNF-α、IL-6、IL-1β 水平明显升高,以TNF-α 表达水平最高,且伴关节病变患儿TNF-α 水平也明显升高,因此关节病变形成的关键因子为TNF-α.%Objective To investigate the relationship between the release of IL-1β, IL-6 and TNF-α and the formation of joint lesions in children with severe hemophilia A. Methods 60 patients with severe hemophilia A admitted to our hospital (January 2015 to January 2017), no joint bleeding group (n=20), joint bleeding group (n=36), acute joint bleeding group were selected (n=20), chronic joint bleeding group (n=15), serum TNF-α, IL-6, IL-1β levels were determined by enzymelinked immunosorbent assay. Results The expression level of TNF-α messenger ribonucleic acid in patients with acute joint hemorrhage was (6.695±2.523)ng/L, which was significantly higher than that of patients without joint disease (1.791±1.479) ng/L. The difference was statistically significant (t=4.934 6, P＜0.05); acute joint expression levels of IL-6 and IL-1β messenger RNA in the joints of the hemorrhagic group were (0.912±0.525)ng/L and (1.879±1.542)ng/L, respectively. The patients without joint lesions were (1.263±0.647)ng/L and (0.971 8±0.517)ng/L, respectively. There was no significant difference in the expression levels of IL-6 and IL-1β messenger RNA in articular lesions (t=1.336 2, 1.592 9, P＞0.05). Conclusion The levels of TNF-α, IL-6 and IL-1β in patients with severe hemophilia A are significantly increased, and the expression level of TNF-α is the highest, and the level of TNF-α is also significantly increased in children with joint disease. Therefore, the key factor for the formation of joint lesions is TNF-α.