Annals of Saudi medicine · 2013
Insertion/deletion polymorphism of the ACE gene increased risk of Behcet disease: evidence from a meta-analysis.
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Mandal Raju Kumar, Yaday Suraj Singh, Panda Aditya K, Khattri Sanjay
Аннотация
BACKGROUND AND OBJECTIVES: Endothelial dysfunction has a role in the development of the Behcet disease (BD). Local renin-angiotensin system (RAS) plays a crucial role in the endothelial control, and angiotensin-converting enzyme (ACE) is the monitoring component of the RAS. We investigated the relationship between the ACE Ins/Del (I/D) variants and the risk of BD.
DESIGN AND SETTINGS: A meta-analysis was conducted from all published studies on the associations be.tween the ACE I/D polymorphism and BD.
METHODS: We systemically searched all published studies from PubMed and EMBASE, and data were quantitatively synthesized. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated for allele, homozygous, heterozygous, and combined genetic models.
RESULTS: Out of 5 eligible studies, 676 healthy controls and 534 BD cases were included in the present meta.analysis. D allele carrier was significantly associated with increased BD risk (D vs I: P=.002; OR=1.321, 95% CI=1.111-1.570). Homozygous mutant DD genotype also revealed 1.5-fold increased risk (DD vs II; P=.004; OR=1.573, 95% CI=1.156-2.141). In addition, the dominant genetic model demonstrated an increased risk of developing BD (DD vs II+ID: P=.001; OR=1.610, 95% CI=1.242-2.087).
CONCLUSION: The current study suggests that ACE gene polymorphism (Ins/Del) contributes an increased susceptibility to BD. However, larger studies with stratified case control population and biological characterization are needed to validate this finding.
DESIGN AND SETTINGS: A meta-analysis was conducted from all published studies on the associations be.tween the ACE I/D polymorphism and BD.
METHODS: We systemically searched all published studies from PubMed and EMBASE, and data were quantitatively synthesized. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated for allele, homozygous, heterozygous, and combined genetic models.
RESULTS: Out of 5 eligible studies, 676 healthy controls and 534 BD cases were included in the present meta.analysis. D allele carrier was significantly associated with increased BD risk (D vs I: P=.002; OR=1.321, 95% CI=1.111-1.570). Homozygous mutant DD genotype also revealed 1.5-fold increased risk (DD vs II; P=.004; OR=1.573, 95% CI=1.156-2.141). In addition, the dominant genetic model demonstrated an increased risk of developing BD (DD vs II+ID: P=.001; OR=1.610, 95% CI=1.242-2.087).
CONCLUSION: The current study suggests that ACE gene polymorphism (Ins/Del) contributes an increased susceptibility to BD. However, larger studies with stratified case control population and biological characterization are needed to validate this finding.