Intracellular adhesion molecule-1 K469E gene polymorphism and risk of diabetic microvascular complications: a meta-analysis

PLoS One. 2013 Jul 26;8(7):e69940. doi: 10.1371/journal.pone.0069940. Print 2013.

Abstract

Background: A number of studies evaluated the association of intracellular adhesion molecule-1 (ICAM-1) K469E (rs5498, A/G) gene polymorphism with diabetic microvascular complications (DMI) including diabetic nephropathy (DN) and diabetic retinopathy (DR) in different populations. However, the results of individual studies remain conflicting.

Methods: A comprehensive search was conducted to identify all eligible studies of the above-mentioned associations. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were assessed using the fixed or random effect model.

Results: Seven studies involving 3411 subjects were included. Overall, the meta-analysis showed a significant association of the A allele with increased risk of DMI susceptibility in a recessive model (OR = 1.37, 95% CI 1.04-1.80, P = 0.02). In the subgroup analysis stratified by ethnicity, significant association was found in Asians but not in Caucasians (OR = 1.78, 95% CI 1.13-2.81, P = 0.01; OR = 1.10, 95% CI 0.79-1.54, P = 0.58, respectively). Moreover, it showed a significant association between the A allele and risk of DN in a recessive model (OR = 1.25, 95% CI 1.02-1.55, P = 0.04).

Conclusions: This meta-analysis suggested that the K469E polymorphism in ICAM-1 gene might affect individual susceptibility to DMI and showed a discrepancy in different ethnicities. Further investigations are needed to validate the association.

Publication types

  • Meta-Analysis

MeSH terms

  • Diabetic Angiopathies / complications*
  • Diabetic Angiopathies / genetics*
  • Diabetic Nephropathies / complications
  • Diabetic Nephropathies / genetics
  • Diabetic Retinopathy / complications
  • Diabetic Retinopathy / genetics
  • Genetic Predisposition to Disease*
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics*
  • Microvessels / pathology*
  • Polymorphism, Single Nucleotide / genetics*
  • Publication Bias
  • Risk Factors

Substances

  • ICAM1 protein, human
  • Intercellular Adhesion Molecule-1

Grants and funding

The authors have no support or funding to report.