Aldosteronism Clinical features Causes and Treatment

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Aldosteronism is a syndrome with hypersecretion of mineralocorticoid aldosterone.
Primary aldosteronism is excessive aldosterone production due to disease of adrenal glands. It is also called nodular hyperplasia or idiopathic hyperaldosteronism.
Nonsuppressible (primary) hypersecretion of aldosterone is a underdiagnosed cause of hypertension.
There is hypokalemia, diastolic hypertension, extra cellular volume expansion, muscle weakness, fatigue, headache, polyuria, polydipsia.
Secondary aldosteronism is excessive aldosterone production due to extra-adrenal causes. There is aldosterone secretion in response to activation of renin angiotensin system.
Aldosterone-producing adenomas Bilateral idiopathic hyperaldosteronism (bilateral adrenal hyperplasia)
It occurs in accelerated phase of hypertension. Secondary aldosteronism is present in many forms of edema e.g. cirrhosis, nephrotic syndrome, CHF. Arterial hypovolaemia stimulates aldosterone secretions resulting in edema.
Familial hyperaldosteronism type I (glucocorticoid-remediable aldosteronism) and type II (the familial occurrence of aldosterone-producing adenoma or bilateral idiopathic hyperplasia or both).

It is due to the progressive destruction of adrenals. It may be due to tuberculosis, histoplasmosis, idiopathic atrophy due to autoimmune causes, HIV, bilateral haemorrhage etc.

If potassium losses are severe, muscular weakness, cramps, tetany, or cardiac arrhythmias may occur
Specific hormone replacement to correct both glucocorticoid and mineralocorticoid deficiencies.
Hydrocortisone is given 20 – 30 mg / day. 2/3^r^d of dose is taken in morning and 1/3^rd in afternoon.
0.1 mg Fludrocortisone (Mineralocorticoid) is given orally.
3-4 g / day of sodium.
Measurement of blood pressure and serum electrolytes is done.
Female patients may require 50 mg of DHEA orally daily.