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Journal Article
Meta-Analysis
Lack of Association Between TGF-β1 and MDR1 Genetic Polymorphisms and Cyclosporine-Induced Gingival Overgrowth in Kidney Transplant Recipients: A Meta-analysis.
Transplantation Proceedings 2017 July
BACKGROUND: Gingival 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.
METHODS: The 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.
RESULTS: Three 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).
CONCLUSIONS: No 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.
METHODS: The 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.
RESULTS: Three 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).
CONCLUSIONS: No 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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