Measurement Of Aldosterone Concentrations Research Articles

The relation between aldosterone concentrations in plasma and saliva during pregnancy.

The concentrations of aldosterone and glucocorticoids (cortisol + cortisone) were measured in saliva and plasma samples obtained from healthy women during early (11-19 weeks), mid (24-29 weeks) and late (32-37 weeks) pregnancy. There was a progressive increase in mean aldosterone levels in both saliva and plasma throughout pregnancy, though at each stage of pregnancy the range was very wide. Glucocorticoid levels increased up to mid-pregnancy and then remained constant. At no stage were aldosterone and glucocorticoid levels significantly correlated. The proportion of free (non-protein bound) aldosterone in plasma, and the saliva:plasma ratio of aldosterone did not differ from the non-pregnant range at any stage of pregnancy. We conclude that measurement of aldosterone concentration in saliva is a convenient and valid method for the estimation of plasma free aldosterone in pregnancy and so provide a non-invasive technique for assessing aldosterone status throughout pregnancy.

2 Primary hyperaldosteronism

Summary Primary hyperaldosteronism is an uncommon condition, probably occurring in less than one per cent of all hypertensive patients. Most often it is associated with an aldosterone-producing adenoma (Conn's syndrome). In perhaps one-third of patients an adrenocortical tumour is not identified, when the glands usually show nodular hyperplasia of the zona glomerulosa (idiopathic hyperaldosteronism). Much rarer forms include a glucocorticoidremediable abnormality and hyperaldosteronism associated with an adrenal carcinoma. Primary hyperaldosteronism can occur in all age groups. Adenomas are commoner in females, but idiopathic hyperaldosteronism occurs with equal frequency in both sexes. Symptoms of hypokalaemia are sometimes present, but often the patient is asymptomatic. Hypertension is almost invariable and may be severe. The biochemical hallmarks are aldosterone excess associated with low plasma levels of renin and angiotensin II. Hypokalaemia is usual, although sometimes intermittent, while plasma sodium is often high—normal or even raised. The biochemical changes are usually more marked in patients with adenoma than in those with the idiopathic form, although there is considerable over-lap among individuals. It is recommended that all hypertensive patients be screened for primary hyperaldosteronism by repeated measurements of plasma potassium. The more complex aldosterone and renin assays should be reserved for those with unexplained hypokalaemia. While primary hyperaldosteronism associated with an adrenocortical adenoma (Conn's syndrome) is a distinct clinical entity, considerable evidence suggests that idiopathic hyperaldosteronism is a variant of essential hypertension. Differentiating these two forms is of clinical importance, as treatment is different. Analysis of clinical and biochemical data by statistical techniques such as quadric analysis and measurement of postural plasma aldosterone changes may distinguish the two groups, but will not localize an adenoma. Larger tumours may be identified by adrenal venography, scintillation scanning, ultrasonography or computed tomography. Measurement of aldosterone concentrations in each adrenal vein is probably the most accurate method for localizing small tumours. For convenience and safety, however, computed tomography is probably the initial investigation of choice. Removal of an aldosterone-producing adenoma results in a fall in blood pressure to normal or near-normal in most patients and is usually the treatment of choice. Should surgery be contraindicated, long-term treatment with spironolactone (or amiloride) is an effective alternative. Patients with idiopathic hyperaldosteronism should be treated with spironolactone or amiloride.