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(Hypertension. 2008;51:e7.)
© 2008 American Heart Association, Inc.
Letters to the Editor |
Vascular Biology and Hypertension Program, University of Alabama at Birmingham, Birmingham, Alabama
I appreciate Plouins1 thoughtful comments. In discussing idiopathic hyperaldosteronism, I was referring back to Padfields 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.
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2. Padfield PL. Primary aldosteronism, a common entity? The myth persists. J Human Hypertens. 2002; 16: 159–162.[CrossRef][Medline] [Order article via Infotrieve]
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