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Division of Internal Medicine, Department of Experimental and Clinical Pathology and Medicine, University of Udine, 33100 Udine, Italy
Address all correspondence and requests for reprints to: Leonardo A. Sechi, M.D., Clinica Medica, University of Udine, Piazzale S. Maria della Misericordia, 1, 33100 Udine, Italy. E-mail: sechi{at}uniud it.
Context: The relationship between aldosterone and glucose metabolism is poorly understood, and there is substantial disparity among findings of studies that have examined glucose tolerance and insulin sensitivity in patients with primary aldosteronism.
Objective: The objective of the study was to determine the outcome of glucose tolerance and insulin sensitivity in patients with primary aldosteronism after treatment.
Design: This was a prospective study of patients who received a diagnosis of primary aldosteronism and were followed up for an average period of 5.7 yr (range, 3–9 yr).
Setting: The study was conducted at a university referral center.
Patients: A consecutive sample of 47 patients with tumoral or idiopathic aldosteronism was followed up after either surgical or medical treatment. Patients with primary aldosteronism were compared with 247 patients with essential hypertension with the same severity and duration of disease and 102 normotensive subjects.
Main Outcome Measures: Short- and long-term changes in glucose tolerance and insulin sensitivity were measured.
Results: After adjustment for age, gender, and body mass index, patients with primary aldosteronism had greater homeostasis model assessment index (P < 0.05) and plasma insulin response to an oral glucose load (P < 0.05) and lower quantitative insulin sensitivity check index (P < 0.01) than normotensive controls. Changes in insulin sensitivity were significantly greater in essential hypertension than primary aldosteronism, and this difference was confirmed by assessment with the hyperinsulinemic-euglycemic clamp (P < 0.01). Treatment of primary aldosteronism decreased blood pressure significantly, and during the initial 6 months of follow-up, parameters of insulin sensitivity were restored to normal. Analysis of subsequent follow-up showed nonsignificant changes in glucose metabolism parameters in both adrenalectomized and spironolactone-treated patients.
Conclusions: Insulin resistance is present in patients with tumoral and idiopathic aldosteronism, but the defect appears less severe than in patients with essential hypertension. Treatment with surgery or aldosterone antagonists restores rapidly and persistently normal sensitivity to insulin.
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