Nantong University, Qixiu Road 19#, Nantong city, Jiangsu, People's Republic of China.
Dig Dis Sci. 2012 Dec;57(12):3065-75. doi: 10.1007/s10620-012-2293-2. Epub 2012 Jul 3.
Studies investigating the associations between glucocorticoid receptor gene polymorphisms and glucocorticoid resistance in inflammatory bowel disease report conflicting results.
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.
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.
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.
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.
研究糖皮质激素受体基因多态性与炎症性肠病中糖皮质激素抵抗之间的关系的研究结果相互矛盾。
我们进行了一项荟萃分析，以评估三种最常研究的糖皮质激素受体基因（ER22/23EK、N363S 和 BclI）多态性与炎症性肠病中糖皮质激素抵抗之间的可能关联。
从 1950 年至 2012 年 2 月，检索评估 ER22/23EK、N363S 和 BclI 基因多态性对炎症性肠病中糖皮质激素抵抗影响的文章。提取相关数据后，进行荟萃分析以评估糖皮质激素受体基因多态性与炎症性肠病中糖皮质激素抵抗之间的关系。
共纳入 5 项符合条件的研究，共 942 例。我们的分析表明，ER22/23EK 多态性与炎症性肠病中糖皮质激素抵抗无关[GG 与 GA+AA：比值比（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 等位基因对炎症性肠病中糖皮质激素抵抗没有显著影响（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没有关联（CC 与 CG+GG：OR=1.22，95%CI 0.70-2.13）。对于克罗恩病（CD）和溃疡性结肠炎（UC），这三种单核苷酸多态性（SNP）与糖皮质激素抵抗之间也没有统计学显著关联。漏斗图的形状未检测到发表偏倚。
目前的荟萃分析没有发现证据表明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。然而，对于某些 SNP，这种荟萃分析的效力相对较小。应进行更多设计良好的队列研究，以充分描述这种关联。
