Increased susceptibility of sepsis associated with CD143 deletion/insertion polymorphism in Caucasians: a meta analysis

Int J Clin Exp Pathol. 2014 Sep 15;7(10):6551-8. eCollection 2014.

Abstract

Background: Several lines of evidence have reported that serum angiotensin-converting enzyme (CD143) levels are genetically regulated by insertion/deletion (ins/del) polymorphism in intron 16 of the CD143 gene. In addition, published data on the association of ins/del polymorphism and sepsis risk yielded contradictory conclusions. Therefore, we determined to perform a meta-analysis to validate the association of much debate. Methods and major findings: Relevant literature was identified through weekly searches in databases and references of systematic reviews and the single studies incorporated in this meta-analysis. We combined ORs and its 95% CIs for several genetic models to evaluate the risk of sepsis associated with ins/del polymorphism. A total of seven studies were considered eligible for this analysis. We found significantly increased risk of sepsis in relation to the homozygote ins/ins (OR: 1.32, 95% CI: 1.04-1.68, P: 0.4201, for ins/ins vs. del/del), heterozygote del/ins (OR: 1.33, 95% CI: 1.11-1.61, P: 0.7937, for del/ins vs. del/del) and the two genotypes combined (OR: 1.33, 95% CI: 1.11-1.59, P: 0.7018, for ins/ins + del/ins vs. del/del). Subgroup analysis by age group showed a significant association in pediatric sepsis, but not in adult sepsis.

Conclusions: The statistical data suggest that the CD143 gene ins/del polymorphism may influence the risk of sepsis, especially pediatric sepsis.

Keywords: CD143-ins/del polymorphism-sepsis.

Publication types

  • Meta-Analysis
  • Review

MeSH terms

  • Adult
  • Age Factors
  • Chi-Square Distribution
  • Child
  • Genetic Predisposition to Disease
  • Homozygote
  • Humans
  • Odds Ratio
  • Peptidyl-Dipeptidase A / genetics*
  • Phenotype
  • Polymorphism, Genetic*
  • Risk Factors
  • Sepsis / enzymology
  • Sepsis / ethnology
  • Sepsis / genetics*
  • White People / genetics*

Substances

  • ACE protein, human
  • Peptidyl-Dipeptidase A