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Primary Aldosteronism May Occur In As Many As 10% Of Hypertensives: Presented at ENDO

By Maggie Schwarz

PHILADELPHIA, PA -- June 23, 2003 -- Researchers detected primary aldosteronism among a high number of patients with hypertension when they used the aldosterone/renin ratio (ARR) followed by fludrocortisone suppression testing (FST), they reported here June 19^th at the Endocrine Society's 85^th Annual Meeting.

To detect primary aldosteronism among patients attending a hypertension clinic, Michael Stowasser, MD, and colleagues from Princess Alexandra Hospital, in Brisbane, Queensland, Australia, and colleagues withdrew antihypertensive medications -- such as beta blockers, diuretics, dihydropyridine calcium channel blockers, and angiotensin receptor blockers. They then measured the ARR after correcting hypokalaemia and standardising patients' diets, posture and time of day of measurement.

The test identified 54 patients with primary aldosteronism. Of 49 patients in whom adrenal venous sampling confirmed primary aldosteronism, 15 had aldosterone production lateralised to one adrenal gland (31%, six of whom were hypokalaemic) and 34 had bilateral production (69%), all of whom were normokalaemic. Fourteen of the unilateral patients underwent unilateral adrenalectomy, and seven were cured of their hypertension. The remainder experienced improvement in their hypertension.

Ten years ago, researchers in Greenslopes Hospital in Brisbane found that by looking for primary aldosteronism in all hypertensive patients -- not just those with low plasma potassium level or very severe hypertension -- their rate of detection of primary aldosteronism increased 10 times, accounting for as many as 10% of their hypertensive patients. Dr. Stowasser's group confirmed these findings.

This high rate of detection depends on a careful, methodical diagnostic workup, which must take into account factors that can affect hormone test results and includes blood tests rather than relying on adrenal computed tomography scanning to distinguish unilateral from bilateral primary aldosteronism, Dr. Stowasser pointed out.

He conceded that adrenal venous sampling is not widely available and asserted that eliminating drugs that affect FST is possible in most cases.

Primary aldosteronism has been thought to account for no more than 1% of cases of hypertension. The news of increased prevalence is positive because if diagnosed, primary aldosteronism can be cured by removal of the overactive adrenal gland, which usually contains a benign aldosterone-producing adenoma.

Dr. Stowasser said that there were no distinguishing features about these patients that raised suspicion of primary aldosteronism. They masqueraded as essential hypertensives.

The study was supported by the University of Queensland, National Heart Foundation of Australia and the Sylvia and Charles Viertel Charitable Foundation.


[Study title: High Rate of Detection of Primary Aldosteronism, Including Surgically Treatable Forms, Associated with the Non-Selective Screening of Hypertensives Attending a Recently Established Hypertension Unit. Abstract OR6-6]

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