Rai V
Both genetic and environmental factors play roles in hyperuricemia and susceptibility may be modified by functional polymorphisms in folate metabolic genes, such as methylenetetrahydrofolate reductase (MTHFR). Several case control studies investigated association between C677T polymorphism with hyperuricemia but the sample size was small in these studies and the association power was weak. The aim of the present meta-analysis was to evaluate association between MTHFR C677T polymorphism and hyperuricemia. This meta-analysis recruited 6 published studies which were selected by search of electronic databases up to August 2013, including 558 hyperuricemic cases and 912 healthy controls. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the association between MTHFR C677T polymorphism and hypeuricemia susceptibility using fixed effect models. Statistically significant relationship was found between C677T polymorphism and hyperuricemia with all genetic models (Additive model T vs. C: OR=1.8401, 95% CI=1.55-2.18, p<0.0001; Homozygote model TT vs. CC: OR=2.9873, 95% CI=2.06-4.33, p<0.0001; Co-dominant CT vs. CC: OR=2.3785, 95 % CI=1.85-3.04, p<0.0001; Dominant model TT+CT vs. CC: OR=2.5233, 95% CI=1.99-3.19, p<0.0001; Recessive model TT vs. CT+CC: OR=2.2628, 95% CI=1.61-3.17, p<0.0001). In conclusion, the MTHFR C677T polymorphism was associated with an increased risk of hyperuricemia.
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