Jin Xiaochun, Yin Shuzhou, Zhang Youtao, Chen Xu
1Department of Anesthesiology,Suzhou Kowloon Hospital,Shanghai Jiao Tong University School of Medicine,Suzhou,People's Republic of China.
2Department of Clinical Laboratory,First Affiliated Hospital of Soochow University,Suzhou,People's Republic of China.
Cardiol Young. 2018 Jun;28(6):811-815. doi: 10.1017/S1047951118000380. Epub 2018 Apr 16.
IL-10, as a proinflammatory and anti-inflammatory cytokine, has been thought to have an important role in the development of Kawasaki disease. Variation in the IL-10 gene might lead to altered protein production, which may result in Kawasaki disease. Several studies have been performed to investigate the IL-10 -592 A/C polymorphism and Kawasaki disease risk. Unfortunately, the results of previous studies were inconsistent. Therefore, we performed a meta-analysis to derive a more precise estimation of the association between the IL-10 -592 A/C polymorphism and Kawasaki disease risk.
The association between the IL-10 -592 A/C polymorphism and Kawasaki disease risk was assessed by odds ratios (ORs) together with their 95% confidence intervals (CIs). Six studies were enrolled in the present meta-analysis.
Overall, no significant association between IL-10 -592 A/C polymorphism and Kawasaki disease risk was found under allele contrast (A versus C: OR=0.95, 95% CI=0.77-1.18, p=0.668), homozygote comparison (AA versus CC: OR=0.86, 95% CI=0.56-1.31, p=0.475), heterozygote comparison (CA versus CC: OR=0.88, 95% CI=0.65-1.19, p=0.479), recessive genetic model (AA versus CA/CC: OR=0.96, 95% CI=0.73-1.28, p=0.801), or dominant genetic model (AA/CA versus CC: OR=0.85, 95% CI=0.64-1.13, p=0.275).
We conclude that IL-10 -592 A/C polymorphism was not associated with Kawasaki disease risk in the Chinese population. However, more primary large-scale and well-designed studies are still required to further evaluate the interaction of IL-10 -592 A/C polymorphism with Kawasaki disease risk.
白细胞介素-10(IL-10)作为一种促炎和抗炎细胞因子,被认为在川崎病的发展中起重要作用。IL-10基因的变异可能导致蛋白质产生改变,这可能引发川崎病。已经进行了多项研究来调查IL-10 -592 A/C多态性与川崎病风险的关系。不幸的是,先前研究的结果并不一致。因此,我们进行了一项荟萃分析,以更精确地估计IL-10 -592 A/C多态性与川崎病风险之间的关联。
通过比值比(OR)及其95%置信区间(CI)评估IL-10 -592 A/C多态性与川崎病风险之间的关联。本荟萃分析纳入了六项研究。
总体而言,在等位基因对比(A与C:OR = 0.95,95% CI = 0.77 - 1.18,p = 0.668)、纯合子比较(AA与CC:OR = 0.86,95% CI = 0.56 - 1.31,p = 0.475)、杂合子比较(CA与CC:OR = 0.88,95% CI = 0.65 - 1.19,p = 0.479)、隐性遗传模型(AA与CA/CC:OR = 0.96,95% CI = 0.73 - 1.28,p = 0.80)或显性遗传模型(AA/CA与CC:OR = 0.85,95% CI = 0.64 - 1.13,p = 0.275)下,均未发现IL-10 -592 A/C多态性与川崎病风险之间存在显著关联。
我们得出结论,在中国人群中,IL-10 -592 A/C多态性与川崎病风险无关。然而,仍需要更多的原发性大规模且设计良好的研究来进一步评估IL-10 -592 A/C多态性与川崎病风险之间的相互作用。