Journal of neuroimmunology · 2012
The effect of TNF-alpha, FcγR and CD1 polymorphisms on Guillain-Barré syndrome risk: evidences from a meta-analysis.
СтатьяМетаанализПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Wu Li-Ya, Zhou You, Qin Chao, Hu Bang-Li
Аннотация
BACKGROUND AND OBJECTIVES: The findings on the associations between potential genetic variants and risk of Guillain-Barré syndrome (GBS) are controversial. We conducted a meta-analysis for candidate genes to provide the evidences for the current understanding of the genetic association with GBS.
METHODS: We searched relevant studies without language restriction in PubMed, Embase and Cochrane library through May 2011. The strengths of the associations between genetic variants and GBS risk were estimated by odds ratios (ORs) with 95% confidence intervals (CIs). Random-effects models or fixed effects model was applied based on the heterogeneity test.
RESULTS: We identified 12 case-control studies involving 1,590 GBS cases and 2,154 controls for the analysis. Because of limited eligible data, our meta-analysis specifically focused on 6 genetic variants of 3 candidate genes, TNF-α, FcγR and CD1. We found that TNF-α 308 G/A polymorphism was significantly associated with the risk of GBS in the overall population (GG+GA vs. AA: OR=0.32, 95%CI=0.16-0.62; GG vs. AA: OR=0.36, 95%CI=0.19-0.68). Subgroup analysis further provided evidence of significant association between TNF-α 308 G/A and risk of the GBS in Asian population (GG+GA vs. AA: OR=32, 95%CI=0.11-0.93; GG vs. AA: OR=0.32, 95%CI=0.15-0.68). In addition, we did not observe significant associations between FcγRIIA R/H, FcγRIIIA F/V, FcγRIIIB NA1/NA2, CD1A 1/2 and CD1E 1/2 polymorphisms and susceptibility for developing GBS.
CONCLUSIONS: Our findings showed that TNF-α 308A allele might be a moderate risk factor for GBS. However, the results should be interpreted with caution due to the limited number of studies available.
METHODS: We searched relevant studies without language restriction in PubMed, Embase and Cochrane library through May 2011. The strengths of the associations between genetic variants and GBS risk were estimated by odds ratios (ORs) with 95% confidence intervals (CIs). Random-effects models or fixed effects model was applied based on the heterogeneity test.
RESULTS: We identified 12 case-control studies involving 1,590 GBS cases and 2,154 controls for the analysis. Because of limited eligible data, our meta-analysis specifically focused on 6 genetic variants of 3 candidate genes, TNF-α, FcγR and CD1. We found that TNF-α 308 G/A polymorphism was significantly associated with the risk of GBS in the overall population (GG+GA vs. AA: OR=0.32, 95%CI=0.16-0.62; GG vs. AA: OR=0.36, 95%CI=0.19-0.68). Subgroup analysis further provided evidence of significant association between TNF-α 308 G/A and risk of the GBS in Asian population (GG+GA vs. AA: OR=32, 95%CI=0.11-0.93; GG vs. AA: OR=0.32, 95%CI=0.15-0.68). In addition, we did not observe significant associations between FcγRIIA R/H, FcγRIIIA F/V, FcγRIIIB NA1/NA2, CD1A 1/2 and CD1E 1/2 polymorphisms and susceptibility for developing GBS.
CONCLUSIONS: Our findings showed that TNF-α 308A allele might be a moderate risk factor for GBS. However, the results should be interpreted with caution due to the limited number of studies available.