LETTER
Diagnosis and Treatment of Primary Aldosteronism
GianPaolo Rossi, MD;
Michele Gregianin, MD; and
Mattco Chisura-Corona, MD
1 July 1995 | Volume 123 Issue 1 | Pages 73-74
TO THE EDITOR:
In their review of primary aldosteronism, Blumenfeld and colleagues [1] reported that a high proportion (almost 10%) of their 82 patients had adrenalectomy despite the presence of idiopathic hyperaldosteronism. However, medical treatment with aldosterone antagonists (not surgery) is deemed to be the treatment of choice for such conditions [2]. Blumenfeld and colleagues reported that three such patients (37.5%) were cured and one had improved after adrenalectomy but failed to provide any histologic data to corroborate the diagnosis of idiopathic hyperaldosteronism. Therefore, it remains possible that those patients, two of whom had lateralized aldosterone secretion, had a small aldosterone-producing adenoma that was undetectable by computed tomographic (CT) scanning.
We have recently reported the results of a prospective comparison of contrast-enhanced CT scanning and magnetic resonance imaging (MRI) in patients with suspected primary aldosteronism [3]. We found that MRI, because of its better tissue characterization, provided better sensitivity than did CT scanning for identifying small aldosterone-producing adenomas.
To differentiate small aldosterone-producing adenomas from idiopathic hyperaldosteronism, Blumenfeld and colleagues proposed the postural test or the measurement of 18-hydroxycorticosterone or of 18-hydroxycortisol and 18-oxocortisol. However, the fact that 16% of their patients with adenomas and 22% with idiopathic hyperaldosteronism had a negative and a positive postural test result, respectively, raises doubts about the usefulness of such testing. In fact, the identification of angiotensin-responsive aldosterone-producing adenomas, which mimic idiopathic hyperaldosteronism, and of functionally autonomous forms of bilateral hyperplasia, may provide a rational explanation for an overlap of responses to the postural test between the two conditions [4, 5]. In addition, 18-hydroxycortisol and 18-oxocortisol cannot currently be measured in most endocrine laboratories in Europe.
During the past decade, we have been using dexamethasone-suppressed Selemium-75-Nor-cholesterol adrenal scintigraphy at our institution, either to corroborate equivocal adrenal vein sampling results or as an alternative to adrenal sampling in patients who refused to have the procedure. When applied to selected series, adrenal scintigraphy was highly specific (close to 100%) in ruling out aldosterone-producing adenomas. Accordingly, it allowed us to avoid unnecessary adrenalectomy in patients with idiopathic hyperaldosteronism.
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Author and Article Information
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University of Padua; 35126 Padua; Italy
1. Blumenfeld JD, Sealey JE, Schlussel Y, Vaughan ED Jr, Sos TA, Atlas SA, et al. Diagnosis and treatment of primary hyperaldosteronism. Ann Intern Med. 1994; 121:877-85.
2. Young WF Jr, Hogan MJ, Klee GG, Grant CS, van Heerden JA. Primary aldosteronism: diagnosis and treatment. Mayo Clin Proc. 1990; 65:96-110.[Medline]
3. Rossi GP, Ghiesura-Corona M, Soattin S, Tregnaghi A, Zanin L, Perale R, et al. Imaging of aldosterone secreting adenomas: a prospective comparison of computed tomography and magnetic resonance imaging in 27 patients with suspected primary aldosteronism. J Hum Hypertens. 1993; 7:357-63.
4. Gordon RD, Gomez-Sanchez CE, Hamlet SM, Tunny TJ, Klemm SA. Angiotensin-responsive aldosterone-producing adenoma masquerades as idiopathic hyperaldosteronim (IHA: adrenal hyperplasia) or low-renin essential hypertension. J Hypertens. 1987; 5(Suppl 5):S103-6.
5. Banks WA, Kastin AJ, Ruiz AE, Biglieri EG. Primary adrenal hyperplasia: a new subset of primary aldosteronism. J Clin Endocrinol Metab. 1984; 58:783-5.
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