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(Hypertension. 2008;51:e6.)
© 2008 American Heart Association, Inc.
Letters to the Editor |
Assistance Publique-Hôpitaux de Paris, Hypertension Unit, Hôpital Européen Georges Pompidou, and, Faculté de Médecine, Université Paris Descartes, Paris, France
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To The Editor:
I agree with Calhouns1 conclusion that there is currently an epidemic of elevated aldosterone:renin ratio rather than an epidemic of primary aldosteronism (PA). I disagree, however, with the assertion that it is "inappropriate to consider idiopathic hyperaldosteronism (presumed secondary to adrenal hyperplasia) to be a type of PA" and that PA should be confirmed by a suppression test.
According to World Health Organizations International Classification of Disease (10th Revision, version for 2007), the E26.0 category (primary hyperaldosteronism) has 2 subheadings: Conns syndrome and PA because of adrenal hyperplasia (bilateral). Conns syndrome (or aldosterone-producing adenoma [APA]) and PA because of bilateral adrenal hyperplasia (or idiopathic PA) differ in renin and aldosterone plasma levels, renin usually being lower and aldosterone usually higher in APA than in idiopathic PA, and, theoretically, in the response to dynamic tests. Stimulation and suppression tests have been designed under the assumption that the surgically remediable form of PA, APA, is associated with angiotensin-unresponsive aldosterone hypersecretion. The predicted response to stimulation tests is a fall or no change in aldosterone concentration in cases of APA and an angiotensin-dependent rise in cases of essential hypertension or idiopathic PA. However, several studies reported that 30% to 70% of patients with APA display an increase in aldosterone levels with ambulation. Stimulation tests do not help identify subjects with PA and an APA,2 a lateralized aldosterone hypersecretion on adrenal venous sampling,2 or a favorable BP outcome after surgery.2 Many suppression tests have been proposed for the confirmation of PA
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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] |
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D. A. Calhoun Response to About an Epidemic of Primary Aldosteronism Hypertension, February 1, 2008; 51(2): e7 - e7. [Full Text] [PDF] |
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