Primary hyperaldosteronism -- a condition in which too much of the hormone aldosterone1 is produced by the adrenal glands and can lead to high blood pressure (hypertension) and lower levels of potassium in the blood -- is not as common as was thought. These are the conclusions of authors of an Article in this week's edition of The Lancet.
In previous decades, the prevalence of primary hyperaldosteronism (PH) in the general hypertensive population was estimated at 1%. However, several studies since 1999 have suggested this prevalence is over 10%. The main characteristic of PH is hypertension due to aldosterone excess, and thus the condition is almost exclusively found in hypertensive patients. Although there is still debate, most researchers agree that resistant hypertension (ie, that is not controlled by blood pressure-lowering drugs) is the condition with the highest probability of PH. This is because the aldosterone system is poorly influenced by hypertensive drugs. In addition, primary care physicians are generally not familiar with PH and thus the condition can remain undiagnosed for many years, leading to resistant hypertension. It follows that the prevalence of PH in patients with resistant hypertension could be much higher than 10%. Dr Stella Douma, Dr Michael Doumas, Hippokration Hospital, Thessaloniki, Greece, and colleagues analysed 20 years of data from their clinic to add to this debate.
Patients with resistant hypertension (blood pressure >140/90 mm Hg despite a three drug regimen, including a diuretic) who attended the hospital outpatient clinic were assessed for PH. Serum aldosterone and plasma renin*activity were determined and their ratio calculated. Patients with a positive test (ratio >65.16 and aldosterone concentrations >416pmol/L) underwent salt suppression tests**. And diagnosis of PH was further confirmed by the response to treatment with sprionolactone.***
Over the 20-year period, 1616 patients with resistant hypertension were analysed. Of these, 338 had a ratio of >65.16 and aldosterone concentrations >416 pmol/L. The salt suppression tests revealed that 182 patients (11.3%) had PH, and their response to treatment with spironolactone further confirmed this. Low potassium levels (hypokalaemia) were only seen in 83 of the patients with PH (45.6%).
The authors conclude: "Although the prevalence of primary hyperaldosteronism in patients with resistant hypertension is high, it is substantially lower than previously reported. On the basis of this finding, we could assume that the prevalence of primary hypoaldosteronism in the general unselected hypertension population is much lower than currently reported. Thus, the notion of an epidemic of primary hyperaldosteronism is not supported."
In an accompanying Comment, Dr Norman M Kaplan, University of Texas Southwestern Medical Center at Dallas, TX, USA discusses the clinical implications of the findings, namely that doctors should only look for primary hyperaldosteronism in patients with truly resistant hypertension and unprovoked hypokalaemia.
Dr Michael Doumas, Hippokration Hospital, Thessaloniki, Greece T) +30 694 7006001 (mobile) /+30 2310 821795 E) michalisdoumas@yahoo.co.uk
Dr Norman M Kaplan, University of Texas Southwestern Medical Center at Dallas, TX, USA T) +1 214 648 2103 E) norman.kaplan@utsouthwestern.edu
Notes to editors
1aldosterone is a steroid hormone in the adrenal glands, and acts on the kidneys to cause the conservation of sodium, secretion of potassium, increased water retention, and increased blood pressure.
*renin activity is important as the body's aldosterone production is normally regulated by renin levels
**salt suppression tests: When large amounts of salt are given to hypertensive patients aldosterone levels drop in patients with ‘regular' hypertension, but not in patients with primary hypoaldosteronism as the adrenal gland continues to produce aldosterone even in the presence of the salt.
***spironolactone is a drug which is an antagonist of aldosterone, ie, it competes with aldosterone molecules for same active sites on the surface of cells. The drug works by increasing the excretion of water and sodium, while decreasing the excretion of potassium.
http://multimedia.thelancet.com/pdf/press/hyperaldosteroinism.pdf
Journal
The Lancet