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Aldosterone is the principal physiological salt-retaining mineralocorticoid, but it is unsuitable for routine medical use since it is rapidly inactivated when given orally. Desoxycorticosterone (DCA, DOCA, desoxycortone) was used for a long time, but it had to be taken sublingually (or implanted or injected) to avoid inactivation during passage through the liver. Overdosage of desoxycorticosterone, leading to hypertensive encephalopathy and permanent brain damage, has been described [ ].
The approximate potency of various mineralocorticoids relative to cortisone is shown in Table 1 .
| Compound | Route of administration | Mineralocorticoid effect | Glucocorticoid effect |
|---|---|---|---|
| Cortisone | Oral | 1 | 1 |
| Desoxycorticosterone | Sublingual | 50 | Negligible |
| Fludrocortisone | Oral | 150 | 10–20 |
| Aldosterone | Injected | 500 | None |
Fludrocortisone is the compound that is most often used at present for long-term mineralocorticoid treatment. The dose of fludrocortisone needed in chronic adrenocortical insufficiency varies very widely, from 0.05 to 1.0 mg/day. In salt-losing forms of the congenital adrenogenital syndrome up to 0.2 mg/day may be needed. In doses appropriate to the individual’s needs, adverse reactions to the glucocorticoid effects of fludrocortisone rarely prove problematic; the main problem is to adjust the dosage (as well as salt intake) to these needs, since the adverse effects that can be experienced mainly reflect relative overdosage; if high doses are to be used, meticulous monitoring is required.
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