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Diagnosis and Treatment of Primary Hyperaldosteronism

Jon D. Blumenfeld, MD; Jean E. Sealey, ScD; Yvette Schlussel, PhD; E. Darracott Vaughan, MD; Thomas A. Sos, MD; Steven A. Atlas, MD; Franco B. Muller, MD; Rhina Acevedo, MD; Stanley Ulick, MD; and John H. Laragh, MD
[+] Article and Author Information

From The New York Hospital-Cornell Medical Center, New York, New York and the Veterans Affairs Medical Center, Bronx, New York. Requests for Reprints: Jon D. Blumenfeld, MD, The Cardiovascular Center, The New York Hospital-Cornell University Medical Center, 520 East 70th Street, Starr 4, New York, NY 10021. Grant Support: In part by Public Health Research Grant RR00047 from the General Clinical Research Centers Program of the Division of Research Resources; by Hypertension SCOR HL 18323, National Institutes of Health; by the Frederick J and Theresa Dow Wallace Fund of the New York Community Trust; and by a grant from the Wolk Heart Foundation. Dr. Blumenfeld is the recipient of a Clinical Associate Physician Grant from the General Clinical Research Centers Program.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1994;121(11):877-885. doi:10.7326/0003-4819-121-11-199412010-00010
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Objective: To characterize the clinical and laboratory features of primary aldosteronism and to evaluate which diagnostic tests can discriminate surgically curable forms of this syndrome.

Design: Retrospective analysis of the following data from 82 patients with primary aldosteronism: blood pressure, serum electrolytes, urinary aldosterone and electrolytes, computed tomographic scans, plasma renin and aldosterone before and during upright posture, atrial natriuretic peptide, and adrenal vein aldosterone and cortisol. Clinical outcomes assessed after treatment included blood pressure, serum electrolytes, and plasma renin activity.

Results: Drug therapy was discontinued before diagnostic tests were done in 56 of 82 patients (34 with adenomas and 22 with hyperplasia). Compared with patients with hyperplasia, those with adenomas had higher systolic (184 mm Hg and 161 mm Hg, respectively; P < 0.001) and diastolic blood pressures (112 mm Hg and 105 mm Hg; P = 0.03), lower serum potassium levels (3.0 mmol/L and 3.5 mmol/L; P < 0.001), and higher serum CO2 (P = 0.001), atrial natriuretic peptide (P = 0.008), and urinary 18-methyl oxygenated cortisol metabolite levels (P = 0.02). In patients with adenomas, aldosterone secretion lateralized to one adrenal gland and did not increase during the postural stimulation test; preoperative urinary aldosterone levels were correlated with diastolic pressures (r = 0.58; P = 0.001). Hypertension was “cured” postoperatively in approximately 35% of patients with adenomas and those with hyperplasia (P > 0.2) but was “improved” more frequently in those with adenomas (P = 0.002). Cured patients from both groups were younger than those not cured (mean ages, 43 years and 54 years, respectively; P = 0.002) and had lower preoperative mean plasma renin activity (0.17 ng/mL per hour and 0.50 ng/mL per hour; P < 0.001). All patients with adenomas in whom aldosterone secretion lateralized were either cured or improved.

Conclusion: Of the 51 patients with primary aldosteronism who had adrenalectomy (43 patients with adenomas and 8 with hyperplasia), those most likely to be cured were younger and had lower plasma renin activity. In patients with adenomas who were cured or improved, aldosterone secretion was more likely to lateralize. Tests that distinguished adenomas from adrenal hyperplasia included the postural stimulation test, urinary excretion rates of 18-oxocortisol and 18-hydroxycortisol, and adrenal vein sampling.

Figures

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Figure 1.
Relation of 24-hour aldosterone excretion to diastolic blood pressure. Top.rPBottom.rP

In patients with an aldosterone-producing adenoma ( = 0.58; = 0.001). In patients with hyperplasia ( = 0.12; > 0.2). closed circle = serum potassium level greater than 3.0 mmol/L; open circle = serum potassium level of 3.0 mmol/L or less.

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Figure 2.
Comparison of the ratio of plasma aldosterone to plasma renin activity for primary aldosteronism (aldosterone-producing adenoma and nonadenomatous adrenal hyperplasia) and renovascular and essential hypertension.

A ratio of greater than 50 helped identify patients with primary aldosteronism.

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Figure 3.
Therapeutic outcomes for primary aldosteronism caused by adenoma (top) and nonadenomatous hyperplasia (bottom).

Values in parentheses represent the percentage of the treatment group.

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Figure 4.
Algorithim for evaluating and treating patients with primary aldosteronism.

18-OHB = 18-hydroxycorticosterone; 18-OH-F = 18-hydroxycortisol; 18-oxo-F = 18-oxocortisol; CT = computed tomography; DOC = deoxycorticosterone; PRA = plasma renin activity.

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