Insertion/deletion polymorphism of the ACE gene increased risk of Behcet disease: evidence from a meta-analysis
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 relat...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
King Faisal Specialist Hospital and Research Centre
2013-09-01
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| Series: | Annals of Saudi Medicine |
| Online Access: | https://www.annsaudimed.net/doi/full/10.5144/0256-4947.2013.437 |
| Summary: | 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 between 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. |
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| ISSN: | 0256-4947 0975-4466 |