Delayed diagnosis of primary hyperaldosteronismBMJ 2010; 340 doi: http://dx.doi.org/10.1136/bmj.c2461 (Published 25 May 2010) Cite this as: BMJ 2010;340:c2461
- Jonathan M Grasko, registrar1,
- Hieu H Nguyen, consultant endocrine surgeon2,
- Paul Glendenning, clinical associate professor, consultant endocrinologist and chemical pathologist 13
- 1Department of Core Clinical Pathology and Biochemistry, PathWest Laboratory Medicine WA, Royal Perth Hospital, Perth, WA, 6847, Australia
- 2Department of General Surgery, Sir Charles Gairdner Hospital, Perth, WA, Australia
- 3School of Medicine and Pharmacology, University of Western Australia, Royal Perth Hospital, Perth, WA, Australia
- Correspondence to: P Glendenning
- Accepted 20 April 2010
About 5-13% of patients with hypertension have primary hyperaldosteronism,1 2 3 4 defined as autonomous production of aldosterone, which leads to excessive retention of sodium plus water and resistant hypertension. It is important to identify such patients because they have a higher morbidity and mortality from cardiovascular disease than age and sex matched patients with essential hypertension.2 In addition, surgery can significantly improve long term outcomes in such patients.5
With improved management of hypertension and greater awareness of primary hyperaldosteronism, more investigations are being performed in patients taking antihypertensive agents. Dihydropyridine calcium antagonists increase renin production and reduce aldosterone, thereby reducing the aldosterone:renin ratio—the initial test for primary hyperaldosteronism.6 However, these effects are underappreciated,7 with recent publications reporting insignificant effects on the aldosterone:renin ratio.8 9 10 11 12 We describe three patients who were initially misclassified as having essential hypertension because of repeatedly unremarkable aldosterone:renin ratios while taking dihydropyridine calcium antagonists.
Between 2003 and 2008, three patients were diagnosed with biochemically confirmed primary hyperaldosteronism caused by autonomous aldosterone producing adenomata. All three had initially been misclassified because of repeatedly unremarkable aldosterone:renin ratios while taking dihydropyridine calcium antagonists. They had otherwise been appropriately investigated—other interfering antihypertensive drugs had been withdrawn and plasma potassium had been carefully corrected. Diagnosis was finally confirmed by repeatedly raised ambulatory aldosterone:renin ratios after calcium antagonist withdrawal. All three patients underwent adrenal vein sampling, which confirmed lateralisation of aldosterone secretion, and two patients proceeded to …
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