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Glucocorticoid receptor gene polymorphisms and glucocorticoid resistance in inflammatory bowel disease: A meta-analysis

机译:炎症性肠病中糖皮质激素受体基因多态性与糖皮质激素抵抗的荟萃分析

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Background: Studies investigating the associations between glucocorticoid receptor gene polymorphisms and glucocorticoid resistance in inflammatory bowel disease report conflicting results. Aims: We conducted a meta-analysis to assess the possible association between the three most commonly investigated glucocorticoid receptor gene (ER22/23EK, N363S, and BclI) polymorphisms and glucocorticoid resistance in inflammatory bowel disease. Methods: Articles evaluating the effect of ER22/23EK, N363S, and BclI gene polymorphism on glucocorticoid resistance in inflammatory bowel disease were identified from 1950 to February 2012. After extraction of relevant data, meta-analyses were performed to assess the association between glucocorticoid receptor gene polymorphisms and glucocorticoid resistance in inflammatory bowel disease. Results: A total of five eligible studies with 942 cases were included. Our analysis showed that ER22/23EK polymorphisms were not associated with glucocorticoid resistance in inflammatory bowel disease [GG versus GA + AA: odds ratio (OR) = 0.58, 95 % confidence interval (CI) 0.16-2.08]. In N363S polymorphisms, AG + GG allele showed no significant effect on glucocorticoid resistance in inflammatory bowel disease compared with AA allele (OR = 1.19, 95 % CI 0.33-4.30). In BclI polymorphisms, there was also no association of CG + GG allele with glucocorticoid resistance (CC versus CG + GG: OR = 1.22, 95 % CI 0.70-2.13). For Crohn's disease (CD) and ulcerative colitis (UC), no statistically significant associations between these three single-nucleotide polymorphisms (SNPs) and glucocorticoid resistance were found. The shape of the funnel plot did not detect publication bias. Conclusions: The current meta-analysis found no evidence that glucocorticoid receptor gene polymorphisms (ER22/23EK, N363S, and BclI) are associated with glucocorticoid resistance in inflammatory bowel disease treatment. However, this meta-analysis is underpowered for relatively large effect sizes in some SNPs. More well-designed cohort studies should be conducted to fully characterize such an association.
机译:背景:炎症性肠病中糖皮质激素受体基因多态性与糖皮质激素耐药性之间关系的研究报道了相互矛盾的结果。目的:我们进行了一项荟萃分析,以评估炎性肠病中三种最常研究的糖皮质激素受体基因(ER22 / 23EK,N363S和BclI)多态性与糖皮质激素抵抗之间的可能关联。方法:从1950年至2012年2月,鉴定评价ER22 / 23EK,N363S和BclI基因多态性对炎性肠病中糖皮质激素抵抗的影响的文章。提取相关数据后,进行荟萃分析以评估糖皮质激素受体之间的关联。基因多态性与炎症性肠病的糖皮质激素抵抗。结果:共纳入五项合格研究,共942例。我们的分析表明,ER22 / 23EK基因多态性与炎症性肠病的糖皮质激素耐药性无关[GG vs GA + AA:优势比(OR)= 0.58,95%置信区间(CI)0.16-2.08]。在N363S多态性中,与AA等位基因相比,AG + GG等位基因对炎性肠病的糖皮质激素抵抗没有显着影响(OR = 1.19,95%CI 0.33-4.30)。在BclI多态性中,CG + GG等位基因与糖皮质激素抵抗也无关联(CC与CG + GG:OR = 1.22,95%CI 0.70-2.13)。对于克罗恩氏病(CD)和溃疡性结肠炎(UC),在这三个单核苷酸多态性(SNP)与糖皮质激素抵抗之间未发现统计学上显着的关联。漏斗图的形状未检测到发布偏差。结论:目前的荟萃分析没有发现糖皮质激素受体基因多态性(ER22 / 23EK,N363S和BclI)与炎症性肠病治疗中糖皮质激素抵抗有关。但是,对于某些SNP中相对较大的效应量,此荟萃分析功能不足。应该进行更精心设计的队列研究以充分表征这种关联。

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