| Indication | For partial replacement therapy for primary and secondary adrenocortical insufficiency in Addison's disease and for the treatment of salt-losing adrenogenital syndrome. |
| Pharmacodynamics | Fludrocortisone is a synthetic adrenocortical steroid possessing very potent mineralocorticoid properties and high glucocorticoid activity. It is indicated as partial replacement therapy for primary and secondary adrenocortical insufficiency in Addison’s disease and for the treatment of salt-losing adrenogenital syndrome. The physiologic action of fludrocortisone acetate is similar to that of hydrocortisone. However, the effects of fludrocortisone acetate, particularly on electrolyte balance, but also on carbohydrate metabolism, are considerably heightened and prolonged. Mineralocorticoids act on the distal tubules of the kidney to enhance the reabsorption of sodium ions from the tubular fluid into the plasma; they increase the urinary excretion of both potassium and hydrogen ions. |
| Mechanism of action | Fludrocortisone binds the mineralocorticoid receptor (aldosterone receptor). This binding (or activation of the mineralocorticoid receptor by fludrocortisone) in turn causes an increase in ion and water transport and thus raises extracellular fluid volume and blood pressure and lowers potassium levels. |
| Absorption | Not Available |
| Volume of distribution | Not Available |
| Protein binding | High |
| Metabolism | Hepatic, some renal. |
| Route of elimination | Not Available |
| Half life | 3.5 hours |
| Clearance | Not Available |
| Toxicity | Effects of overexposure include irritation, cardiac edema, increased blood volume, hypertension, cardiac arrhythmias, enlargement of the heart, headaches, and weakness of the extremities. |