Chemical Name : Fludrocortisone
Florinef Information : Florinef (Fludrocortisone Acetate) 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.
In Addison's disease, the combination of Florinef tablets with a glucocorticoid such as hydrocortisone or cortisone provides substitution therapy approximating normal adrenal activity with minimal risks of unwanted effects.
The usual dose is 0.1 mg of Florinef (Fludrocortisone Acetate) daily, although dosage ranging from 0.1 mg three times a week to 0.2 mg. daily has been employed. In the event transient hypertension develops as a consequence of therapy, the dose of Florinef (Fludrocortisone Acetate) should be reduced to 0.05 mg. daily. Florinef (Fludrocortisone Acetate) is preferably administered in conjunction with cortisone (10 mg. to 37.5 mg. daily in divided doses) or Cortef (hydrocortisone) (10 mg. to 30 mg. daily in divided doses).
Florinef Side Effects : The drug's mineralocorticoid activity (retention of sodium and water) causes Florinef side effects like hypertension, edema, cardiac enlargement, congestive heart failure, potassium loss, and hypokalemic alkalosis.
When Florinef is used in the small dosages recommended, the glucocorticoid side effects often seen with cortisone and its derivatives are not usually a problem; however the following Florinef side effects should be kept in mind, particularly when Florinef is used over a prolonged period of time or in conjunction with cortisone or a similar glucocorticoid.
Musculoskeletal : Florinef side effects like muscle weakness, steroid myopathy, loss of muscle mass, osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humeral heads, pathologic fracture of long bones, and spontaneous fractures.
Gastrointestinal:Florinef side effects like peptic ulcer with possible perforation and hemorrhage, pancreatitis, abdominal distention, and ulcerative esophagitis.
Corticosteroids are thought to act, at least in part, by controlling the rate of synthesis of proteins. Although there are a number of instances in which the synthesis of specific proteins is known to be induced by corticosteroids, the links between the initial actions of the hormones and final metabolic effects have not been completely elucidated.
The physiologic action of Florinef is similar to that of hydrocortisone. However, the effects of Florinef, 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. The consequence of these three primary effects together with similar actions on cation transport in other tissues appear to account for the entire spectrum of physiological activities that are characteristic of mineralocorticoids. In small oral doses, fludrocortisone acetate produces marked sodium retention and increased urinary potassium excretion. It also causes a rise in blood pressure, apparently because of these effects on electrolyte levels.
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