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(Hypertension. 2008;51:e7.)
© 2008 American Heart Association, Inc.

Letters to the Editor

Response to About an Epidemic of Primary Aldosteronism

Vascular Biology and Hypertension Program, University of Alabama at Birmingham, Birmingham, Alabama

An extract of the first 100% of the full text is provided, because this article has no abstract.

I appreciate Plouin’s¹ thoughtful comments. In discussing idiopathic hyperaldosteronism, I was referring back to Padfield’s work² indicating that the underlying pathophysiologies of idiopathic versus primary aldosteronism secondary to an aldosterone-producing adenoma are different, with the former seeming to manifest a heightened response to angiotensin II and the latter a blunted response. This is not to suggest that idiopathic hyperaldosteronism is distinct from primary aldosteronism, as I agree that it is a subtype of the disorder.

I further agree with Plouin¹ that suppression testing cannot distinguish between the 2 subtypes of primary aldosteronism. As discussed in my review, lateralization of aldosterone secretion by adrenal vein sampling is required to confirm a probable aldosterone-producing adenoma and a likely favorable response to surgery.

Disclosures

None.

1. Plouin PF. About an epidemic of primary aldosteronism. Hypertension. 2008: 51: e6.[Free Full Text]

2. Padfield PL. Primary aldosteronism, a common entity? The myth persists. J Human Hypertens. 2002; 16: 159–162.[CrossRef][Medline] [Order article via Infotrieve]