aldosterone and depresion

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Increased plasma aldosterone in patients with clinical depression

Auteur(s) / Author(s)EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN Enrico ; POLITI Pierluigi ; Résumé / AbstractBackground. Clinical depression has been increasingly recognized as an independent risk factor for adverse cardiovascular events, but the biological mechanisms of this association remain unclear. Recent evidence for reninsystem dysregulation in patients with depression led us to hypothesize that aldosterone-a well-recognized contributor to vascular injury-could be increased in depressed patients. The present study was designed, therefore, to be a cross-sectional investigation of plasma renin and aldosterone levels in depressed patients as compared with healthy controls with no history of psychiatric illness. Methods. A total of 65 depressed patients and 65 age- and gender-matched control subjects were enrolled. Following a fixed sodium and potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the influence of circadian rhythms. Results. Although there were no significant differences in plasma level of renin among subjects with depression and controls (7.9 ′ 5.8 vs. 6.4 ′ 4.3 pg/mL, respectively; p = 0.10), depressed subjects exhibited greater mean aldosterone levels as compared with control subjects (157.2 ′ 67.5 vs. 125.7 ′ 38.1 pg/mL, respectively; p = 0.0014). After adjusting for potential confounders, multivariate logistic regression analysis showed that subjects with depression had 2.77 times higher odds of elevated aldosterone levels compared with healthy control subjects (95% confidence interval, 1.30-5.92, p = 0.008). Conclusions. Our present findings support the hypothesis that hyperaldosteronism could be a common feature among depressed patients, thereby suggesting that increased aldosterone levels may act as a mediator in the pathway linking depression to unfavorable vascular events. Revue / Journal TitleArchives of medical research ISSN 0188-4409 Source / Source2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)] Langue / LanguageAnglais

Editeur / PublisherElsevier, New York, NY, ETATS-UNIS (1992) (Revue)

Localisation / LocationINIST-CNRS, Cote INIST : 18673, 35400013278933.0200

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