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Association of the C344T aldosterone synthase gene variant with essential hypertension: a meta-analysis

Sookoian, Silviaa; Gianotti, Tomas Fernándeza; González, Claudio Danielb; Pirola, Carlos Josea

doi: 10.1097/01.hjh.0000254372.88488.a9

Background: The CYP11B2 gene (CYP11B2) encoding aldosterone synthase has been associated with essential hypertension and some, but not all, studies have reported that the C−344T variant may influence the risk of the disease.

Objective: We performed a systematic review of the literature by means of a meta-analysis to evaluate the influence of the C−344T CYP11B2 polymorphism on arterial hypertension and intermediate phenotypes.

Methods: From 485 reports, we included 42 observational studies, case–control and cohort at baseline. Fixed and random effect models were used to pool data from individual studies.

Results: From 19 heterogeneous studies including 5343 essential hypertensive and 5882 control subjects, we found a significant association between hypertension and the C−344T variant in fixed but not in random effect models [for homozygous CC: odds ratio (OR), 0.834; 95% confidence interval (CI), 0.760–0.914; P < 0.0001, n = 11 225]. Besides, homozygous CC subjects had lower plasma renin activity (D, −0.161; 95% CI, −0.279 to −0.043; P < 0.01, n = 1428) but no difference in plasma aldosterone levels (D, −0.006; 95% CI, −0.081 to 0.07; P = 0.88, n = 2872). Limiting the quantitative analysis of blood pressure to 13 studies including only untreated individuals, no significant association was found for systolic arterial blood pressure (D, 0.042; 95% CI, −0.057 to 0.141; P = 0.41, n = 1775) and diastolic arterial blood pressure (D, 0.026; 95% CI, −0.073 to 0.125; P = 0.61, n = 1775).

Conclusion: Homozygous individuals for the −344C CYP11B2 allele are at 17% lower risk of hypertension with respect to homozygous TT subjects.

aCardiología Molecular, Instituto de Investigaciones Medicas, A. Lanari, Argentina

bDepartamento de Farmacologia, Facultad de Medicina, Universidad de Buenos Aires, Ciudad Autónoma de Buenos Aires, Argentina

Received 15 April, 2006

Revised 23 May, 2006

Accepted 7 August, 2006

Correspondence and requests for reprints to Carlos J. Pirola, PhD, FAHA, Instituto de Investigaciones Medicas, A. Lanari. Cardiología Molecular, Combatiente de Malvinas 3150, 1427-Ciudad Autónoma de Buenos Aires. Argentina Tel: +54 11 4514 8701 ext. 167; fax: +54 11 4523 8947; e-mail:; alternative e-mail:

Sponsorship: This study was supported by grants B119 (Universidad de Buenos Aires) and PICT 05-08719 and 25920 (Agencia Nacional de Promoción Científica y Tecnológica) and PIP 5195 (Consejo Nacional de Investigaciones Científicas y Técnicas). S.S. and C.J.P. are members of Consejo Nacional de Investigaciones Científicas y Técnicas. S.S. and T.F.G. are recipients of a Health Ministry Fellowship (Beca Ramón Carrillo-Arturo Oñativia Ministerio de Salud y Ambiente de la Nación, Convocatoria 2006).

© 2007 Lippincott Williams & Wilkins, Inc.