Department of Neurology, Affiliated Hospital of Qingdao University, No. 1677 Wutaishan Road, Huangdao District, Qingdao, Shandong Province, China.
Department of Urology, Affiliated Hospital of Qingdao University, Qingdao, China.
Neurol Sci. 2018 Dec;39(12):2141-2149. doi: 10.1007/s10072-018-3563-3. Epub 2018 Sep 19.
CD1 and immunoglobulin G Fc receptor (FcγR) genes have been proposed to be involved in the pathogenesis of Guillain-Barré syndrome (GBS). However, results of different studies are conflicting. This meta-analysis aimed to systematically examine the association between CD1 and FcγR gene polymorphisms and GBS. A comprehensive literature search through PubMed, EmBase, ScienceDirect, and Cochrane Library was performed to identify all eligible studies. The strength of association was assessed by pooled odds ratios (ORs) and corresponding 95% confidence intervals (95% CI) in allelic, dominant, recessive, homozygous and heterozygous genetic models. Four case-control studies about polymorphisms of exon 2 in CD1A and CD1E genes and GBS risk and five studies (six cohorts) about FcγR gene polymorphisms and GBS risk were included in this meta-analysis. The association between exon 2 of CD1E gene polymorphism and GBS was marginally significant in Caucasians in allelic model (OR = 1.193, 95% CI = 1.001-1.423, P = 0.049). FcγRIIA gene polymorphism was significantly associated with GBS risk in Caucasians under allelic model (OR = 1.553, 95% CI = 1.018-2.368, P = 0.041) and dominant model (OR = 1.320, 95% CI = 1.027-1.697, P = 0.030). However, no significant association was found between polymorphisms in exon 2 of CD1A, FcγRIIIA and FcγRIIIB genes and GBS susceptibility. This meta-analysis suggested that FcγRIIA gene polymorphism may contribute to GBS risk in Caucasians and revealed a certain trend toward significance in the association of exon 2 of CD1E gene with GBS in Caucasians. Further studies with larger sample size are required to validate these results.
CD1 和免疫球蛋白 G Fc 受体 (FcγR) 基因被认为与吉兰-巴雷综合征 (GBS) 的发病机制有关。然而,不同研究的结果存在冲突。本荟萃分析旨在系统评估 CD1 和 FcγR 基因多态性与 GBS 之间的关联。通过 PubMed、EmBase、ScienceDirect 和 Cochrane Library 进行全面的文献检索,以确定所有符合条件的研究。通过合并优势比 (OR) 及其相应的 95%置信区间 (95%CI),在等位基因、显性、隐性、纯合子和杂合子遗传模型中评估关联强度。纳入了 4 项关于 CD1A 和 CD1E 基因外显子 2 多态性与 GBS 风险的病例对照研究和 5 项关于 FcγR 基因多态性与 GBS 风险的研究(6 个队列)。CD1E 基因外显子 2 多态性与 GBS 的关联在白种人在等位基因模型中具有边缘显著性(OR=1.193,95%CI=1.001-1.423,P=0.049)。FcγRIIA 基因多态性与白种人 GBS 风险在等位基因模型(OR=1.553,95%CI=1.018-2.368,P=0.041)和显性模型(OR=1.320,95%CI=1.027-1.697,P=0.030)下显著相关。然而,CD1A、FcγRIIIA 和 FcγRIIIB 基因外显子 2 多态性与 GBS 易感性之间没有显著关联。本荟萃分析表明,FcγRIIA 基因多态性可能导致白种人 GBS 风险增加,并揭示了 CD1E 基因外显子 2 与 GBS 之间的关联具有一定的显著性趋势。需要更大样本量的进一步研究来验证这些结果。