Abstract
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.
Highlights
Many clinical and epidemiological studies have reported that higher serum uric acid (UA) is related to increased risk of gout, obesity, hypertension hyperlipidemia, renal insufficiency, insulin resistance, cardiovascular and cerebrovascular diseases in general population [1,2,3]
According to our search strategy and inclusion criteria, five studies with full-text articles were remained the relationship of Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism with hyperuricemia [19,20,21,22,23]
The present meta-analysis examining MTHFR C677T in 558 patient and 912 control subjects indicated that carriers of the T allele and the mutation (TT) genotype are at a statistically significant increased risk of hyperuricemia
Summary
Many clinical and epidemiological studies have reported that higher serum uric acid (UA) is related to increased risk of gout, obesity, hypertension hyperlipidemia, renal insufficiency, insulin resistance, cardiovascular and cerebrovascular diseases in general population [1,2,3]. Serum UA increases with age [1,4] and is higher in men than in women possibly because of estrogens [5,6] and is considered as a marker of renal dysfunction, as well as a risk factor of renal disease progression. The uric acid is the end product of purines catabolism and hyperuricemia is the result of imbalance among production (liver) and excretion (renal and fecal) of 70% and 30%, respectively. Methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) is reported as one of these genetic factors in several studied [9,10,11]
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