Vitamin D receptor ApaI gene polymorphism and tuberculosis susceptibility: a meta-analysis

Genet Test Mol Biomarkers. 2014 May;18(5):323-9. doi: 10.1089/gtmb.2013.0451. Epub 2014 Feb 26.

Abstract

Aim: Vitamin D performs its actions through the vitamin D receptor (VDR), which acts as a transcriptional factor. Many case-control studies have been performed in the past to elucidate the association of the ApaI polymorphism of VDR gene and the risk of tuberculosis (TB). However, these studies have shown inconsistent and conflicting results. In the present study, a meta-analysis was performed to investigate the potential relationship between the VDR ApaI gene polymorphism and the risk of TB.

Methodology: A quantitative synthesis was performed for the published studies based on the association between the VDR ApaI gene polymorphism and the risk of TB retrieved from PubMed (Medline) and EMBASE web databases. A meta-analysis was performed, and pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated for all the genetic models.

Results: We observed a decreased risk of TB in allelic contrast (a vs. A: p=0.009; OR=0.869, 95% CI=0.782 to 0.965), homozygous (aa vs. AA: p=0.006; OR=0.724, 95% CI=0.575 to 0.910), and heterozygous (aA vs. AA: p=0.698; OR=0.948, 95% CI=0.722 to 1.243) comparisons. Similarly, dominant (aa+Aa vs. AA: p=0.032; OR=0.842, 95% CI=0.720 to 0.985) and recessive (aa vs. AA+Aa: p=0.027; OR=0.796, 95% CI=0.650 to 0.975) models also demonstrated a decreased risk of TB, whereas a heterozygous genotype (Aa vs. AA: p=0.109; OR=0.873, 95% CI=0.740 to 1.030) did not indicate any association with the risk of TB. There was no evidence of publication bias and heterogeneity test.

Conclusions: This meta-analysis suggests that ApaI polymorphism of the VDR gene is significantly associated with a decreased risk of TB. However, future larger studies with groups of populations are warranted to analyze this association.

Publication types

  • Meta-Analysis

MeSH terms

  • Deoxyribonucleases, Type II Site-Specific / genetics*
  • Genetic Predisposition to Disease*
  • Humans
  • Polymorphism, Genetic*
  • Receptors, Calcitriol / genetics*
  • Tuberculosis / genetics*

Substances

  • Receptors, Calcitriol
  • Deoxyribonucleases, Type II Site-Specific
  • GGGCCC-specific type II deoxyribonucleases