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(Hypertension. 2009;53:585.)
© 2009 American Heart Association, Inc.

Editorial Commentaries

Aldosterone and Metabolic Dysfunction

An Unresolved Issue

Eduardo Pimenta; David A. Calhoun

From the Endocrine Hypertension Research Center and Clinical Center of Research Excellence in Cardiovascular Disease and Metabolic Disorders (E.P.), University of Queensland School of Medicine, Princess Alexandra Hospital, Brisbane, Australia; and the Vascular Biology and Hypertension Program (D.A.C.), University of Alabama at Birmingham.

Correspondence to Eduardo Pimenta, Hypertension Unit, Princess Alexandra Hospital, Ipswich Rd, Woolloongabba, Brisbane, Queensland, Australia, 4102. E-mail e.pimenta@uq.edu.au

An extract of the first 250 words of the full text is provided, because this article has no abstract.

A large body of evidence suggests that aldosterone excess is a common cause of hypertension with a prevalence of primary aldosteronism (PA) of 10% in patients with mild-to-moderate hypertension and 20% in patients with resistant hypertension.¹ Experimental and clinical data also demonstrate that aldosterone excess contributes importantly to the development and progression of cardiorenal disease. This effect is attributed in part to aldosterone-induced target organ inflammation and fibrosis. Separately, a growing number of studies link aldosterone with the metabolic syndrome in general and with separate components of the syndrome, specifically, hypertension, insulin resistance, and dyslipidemia. If cause and effect is proven, that is, if aldosterone is confirmed to independently contribute to the development of the metabolic syndrome, it would further explain the increased cardiovascular risk of patients with PA.

In this issue of Hypertension, Matrozova et al² compared glucose and lipid profiles in a large cohort of patients with PA to matched controls with primary hypertension. The prevalence of hyperglycemia (impaired fasting glucose or diabetes mellitus) and blood levels of glucose and lipids did not differ between PA and control subjects, whereas the prevalence of impaired fasting glucose was actually lower in PA patients. The authors further report that fasting plasma glucose and serum lipid levels did not differ within the subtypes of PA, ie, those with an aldosterone-producing adenoma versus idiopathic hyperaldosteronism. In addition, neither fasting plasma glucose or serum lipids levels improved after adrenalectomy. The authors conclude that PA is not associated with carbohydrate and lipid abnormalities . . . [Full Text of this Article]

Related Article:

Fasting Plasma Glucose and Serum Lipids in Patients With Primary Aldosteronism: A Controlled Cross-Sectional Study

Joanna Matrozova, Olivier Steichen, Laurence Amar, Sabina Zacharieva, Xavier Jeunemaitre, and Pierre-François Plouin
Hypertension 2009 53: 605-610. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				J. Matrozova, O. Steichen, F. de Medecine, and P.-F. Plouin Response to Metabolic Dysfunction in Primary Aldosteronism Hypertension, June 1, 2009; 53(6): e38 - e38. [Full Text] [PDF]