Endocrine Abstracts (2011) 26 S2.3

Non-surgical therapy of primary aldosteronism

M Stowasser

Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Greenslopes and Princess Alexandra Hospitals, Brisbane, Queensland, Australia.

Unilateral laparoscopic adrenalectomy for unilateral primary aldosteronism (PA) results in cure of hypertension in 50–60% and improvement in all remaining patients. For those with bilateral PA or with unilateral PA but unsuitable for surgery, treatment with mineralocorticoid receptor (MR) blockers (spironolactone 12.5–50 mg/day or eplerenone 25–100 mg/day) or with sodium channel antagonists (amiloride 2.5–20 mg/day) is effective, but regular biochemical monitoring is required to avoid potentially dangerous hyperkalemia and azotemia. The extent to which renin becomes ‘unsuppressed’ can help indicate the degree of aldosterone blockade induced by any given treatment dose. Spironolactone is most effective but associated with side effects due to actions on sex steroid receptors, a problem addressed with introduction of the more specific but weaker eplerenone. One study reported the two drugs to be of similar efficacy in lowering BP in PA. Patients with glucocorticoid-remediable PA show excellent BP responses to low dose glucocorticoids (e.g. dexamethasone 0.25–0.5 mg/day), but can also be treated effectively by aldosterone blockade.

In addition to beneficial BP effects, both adrenalectomy and (possibly to a less rapid or pronounced degree) spironolactone result in improved cardiovascular function. Most importantly, the excess cardiovascular morbidity associated with PA (over ‘essential hypertension’) is reversed with surgical or spironolactone treatment. In addition, both surgery and (again to a possibly lesser degree) spironolactone and/or amiloride treatment are associated with improved quality of life. These data provide compelling support for detecting individuals with PA who may then benefit from the improved clinical outcomes afforded by specific therapy. Given that non-BP-dependent adverse effects of aldosterone excess appear salt-dependent, it is conceivable that amiloride, by promoting salt excretion, confers similar cardiovascular protection to that seen with spironolactone through mechanisms not requiring direct MR antagonism. Further study is required to address this question.

The emergence of aldosterone synthase inhibitors represents another promising new treatment option.

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