The methylenetetrahydrofolate reductase 1298 A>C polymorphism is associated with an increased risk of inflammatory bowel disease: evidence from a meta-analysis

ABSTRACT

Objective

The association between genetic variants in methylenetetrahydrofolate reductase (MTHFR) and risk for inflammatory bowel disease (IBD) has been widely studied. However, the results are equivocal. In this meta-analysis, we aimed to determine the association between MTHFR polymorphisms and susceptibility to IBD.

Methods

We retrieved studies from the PubMed, Web of Science, Ovid, and China National Knowledge Infrastructure databases. Data were analyzed using STATA software; odds ratios (OR) and confidence intervals (CI) were calculated using fixed or random effects models.

Results

A marginally significant association of the MTHFR 677 C > T polymorphism and patients’ IBD risk was observed in the overall analysis (OR = 1.11, 95% CI, 1.01–1.23), but not in the analysis of high-quality studies. However, for the MTHFR 1298 A > C polymorphism, a significant association was found between the MTHFR 1298 AC/CC genotypes and IBD risk in the overall analysis (OR = 1.26, 95% CI, 1.10–1.44), in the high-quality studies (OR = 1.20, 95% CI, 1.02–1.41), and in patients with ulcerative colitis (OR = 1.28, 95% CI, 1.10–1.48).

Conclusions

Evidence from this meta-analysis indicates that the MTHFR 1298 A > C polymorphism may be responsible for susceptibility to IBD and ulcerative colitis.

KEYWORDS:

• Crohn’s disease
• Inflammatory bowel disease
• Meta-analysis
• Methylenetetrahydrofolate reductase
• Polymorphism
• Ulcerative colitis

Author contributions

LY designed and wrote the manuscript. YP and WL collected the data and performed the statistical analyses. TX assisted in the performance of the statistical analyses. All authors gave final approval of the version to be published and agree to be accountable for all aspects of the work.

Disclosure Statement

The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer Disclosures

Peer reviewers on this manuscript have no relevant financial relationships or otherwise to disclose.

Supplementary material

Supplemental data for this article can be accessed here.

Additional information

Funding

This work was supported by the National Natural Science Foundation of China (No. 81901379), Major Projects of the Education Department of Sichuan Province (No. 18ZA0158), the Chendu Medical College (Nos. CYZ17-17 and CYTD17-05) and the First Affiliated Hospital of Chengdu Medical College (No. CYFYGQ-001).