Article ID Journal Published Year Pages File Type
5728691 Transplantation Proceedings 2017 8 Pages PDF
Abstract

•This is the first meta-analysis assessing TGF-β1 and MDR1 genes and CsA-induced GO after KT.•There are potential associations between TGF-β11 and MDR1 variants and the severity of CsA-induced GO.•The role of codons 10 and 25 in TGF-β1 secretion is controversial.•No significance was found in TGF-β1 and MDR1 variants and CsA-induced GO after KT.

BackgroundGingival overgrowth (GO) induced by cyclosporine (CsA), one of the common complications after kidney transplantation, is associated with a genetic component. However, the effect of TGF-β1 and MDR1 gene polymorphisms on the pathogenesis of CsA-induced GO remains to be determined. This study aimed to determine the association between TGF-β1 and MDR1 gene polymorphisms and CsA-induced GO in kidney transplant recipients.MethodsThe Pubmed, Embase, Cochrane Library, and Chinese CNKI (China National Knowledge Infrastructure) and Wanfang databases were comprehensively searched. Data were extracted and pooled results estimated from odds ratios (ORs) and 95% confidence intervals (CIs). In addition, quality assessment and publication bias of each eligible study were examined.ResultsThree trials focusing on the relationship between TGF-β1 +869T>C and +915G>C and 3 studies on MDR1 C3435T gene polymorphisms and the onset of CsA-induced GO were included. No association between the +869T>C polymorphism and CsA-induced GO was found in the dominant model (TT+TC vs CC: OR, 0.77; 95% CI, 0.29-2.10; P = .614). In the recessive model, no association was found between the +915G>C polymorphism and CsA-induced GO (CC vs GG+GC: OR, 1.40; 95% CI, 0.81-2.43; P = .225). And in the dominant model, no significance was calculated between MDR1 C3435T gene polymorphisms and CsA-induced GO in kidney transplant recipients (TT vs CC+CT: OR, 1.14; 95% CI, 0.62-2.09; P = .68).ConclusionsNo significant association exists between TGF-β1 +869T>C, and +915G>C and MDR1 C3435T gene polymorphisms and the pathogenesis of CsA-induced GO in kidney transplant recipients.

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