In:
Journal of the Renin-Angiotensin-Aldosterone System, Hindawi Limited, Vol. 12, No. 4 ( 2011-12), p. 617-623
Abstract:
Background and objective: High-altitude pulmonary oedema (HAPE) is a non-cardiogenic hydrostatic oedema involving a genetic component. Considering the low incidence of HAPE, sample sizes in current reports are relatively limited. We aimed to assess the association between the angiotensin-converting enzyme (ACE) I/D polymorphism and HAPE via a meta-analysis of published and unpublished data. Materials and methods: We searched PubMed, CBM, CNKI, and Cochrane Library Database before 20 November 2010. A random-effects model was applied (STATA) and study quality was assessed in duplicate. Results: A total of five studies including 305 cases and 662 controls were meta-analysed. The summary odds ratio (OR) indicated that no significant differences in risk of developing HAPE were found between carriers of ACE D and I alleles (OR = 1.20; 95% confidence interval (CI), 0.98–1.48; p = 0.084). Lack of association persisted for genotypes under the recessive mode. However, genotype association under the dominant mode showed D allele carriers significantly conferred a 1.55-fold increased HAPE risk compared with II genotype carriers (95% CI, 1.15–2.08; p = 0.004). Funnel plot and Egger’s test suggested no evidence of publication bias. Conclusions: Our results supported the notion that ACE D allele carriers were at significant increased risk of developing HAPE.
Type of Medium:
Online Resource
ISSN:
1470-3203
,
1752-8976
DOI:
10.1177/1470320311406572
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2011
detail.hit.zdb_id:
2261873-9
Permalink
