Glucocorticoids replacement therapy

Lifelong glucocorticoid replacement therapy may be necessary for patients with adrenal insufficiency, and mineralocor-ticoid replacement therapy usually is required for those with Addison s disease. 

Monitor morning cortisol or response to ACTH stimulation every 3 to 6 months to assess for HPA axis recovery. Discontinue glucocorticoid replacement therapy when cortisol concentrations are greater than 19 mcg/dL (524 nmol/L) on either test. 

Peacey SR, Guo CY, Robinson AM, Price A, Giles MA, Eastell R, Weetman AP. Glucocorticoid replacement therapy are patients overtreated and does it matter Clin Endocrinol 1997 46 255-61. 

Zelissen PM, Croughs RJ, van Rijk PP, Raymakers JA. Effect of glucocorticoid replacement therapy on bone mineral density in patients with Addison disease. Ann Intern Med 1994 120(3) 207-10. 

Patients with CAH require lifelong glucocorticoid replacement therapy to correct the deficiency in cortisol secretion. This in turn suppresses ACTH production, excess adrenal 17-hydryoxyprogesterone,and excess androgen production. Hydrocortisone is the cortico-... 

The client usually will need to take mineral and glucocorticoid replacement therapy. This statement does not need more teaching. 

Mazziotti G, Porcelli T, Bianchi A, Cimino V, Patelli I, Mejia C, Fusco A, Giampietro A, Marinis LD, Giustina A. Glucocorticoid replacement therapy and vertebral fractures in hypopituitary adult males with GH deficiency. Eur J Endocrinol 2010 163(1) 15-20. 

An endocrine disorder first described by the British Physician Thomas Addison in the mid 1800 s. The adrenal glands fail to produce sufficient amounts of glucocorticoid hormones (cortisol) and sometime mineralocorticoid (aldosterone). If left untreated it is life-threatening, the patient will show muscle weakness, hyperpigmentation and even depression. Typical treatment is hydrocortisone replacement therapy. 

Fludrocortisone is used for replacement therapy for primary and secondary adrenocortical deficiency. Even though this drug lias both mineralocorticoid and glucocorticoid activity, it is used only for its mineralocorticoid effects. 

Evaluate patients at risk for adrenal insufficiency as a result of treatment(s) of Cushing s syndrome and initiate glucocorticoid and miner-alocorticoid replacement therapy as appropriate. 

The answer is e. (Katzung, p 672. Hardman, pp 1477—1978.) Fludrocortisone is a synthetic steroid compound that exhibits profound mineralo-corticoid activity and some glucocorticoid activity Electrolyte and water metabolisms are affected by the administration of this compound. Fludrocortisone promotes the reabsorption of Na and the urinary excretion of K and hydrogen ions in the collecting duct of the nephron. The drug is indicated for mineralocorticoid replacement therapy in primary" adrenal insufficiency... 

Because most adrenal crises occur because of glucocorticoid dose reductions or lack of stress-related dose adjustments, patients receiving corticosteroid-replacement therapy should add 5 to 10 mg hydrocortisone (or equivalent) to their normal daily regimen shortly before strenuous activities such as exercise. During times of severe physical stress (e.g., febrile illnesses, after accidents), patients should be instructed to double their daily dose until recovery. 

I. Replacement therapy. The adrenal cortex (AC) produces the glucocorticoid cortisol (hydrocortisone) and the mine-ralocorticoid aldosterone. Both steroid hormones are vitally important in adaptation responses to stress situations, such as disease, trauma, or surgery. Cortisol secretion is stimulated by hypophyseal ACTH, aldosterone secretion by angiotensin 11 in particular (p. 124). In AC failure (primary AC insuffiency ... 

Pharmacology The naturally occurring adrenal cortical steroids have both anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. These compounds are used as replacement therapy in adrenocortical deficiency states and may be used for their anti-inflammatory effects. 

The observation that mitotane (Lysodren) could produce adrenocortical necrosis in animals led to its use in the palliation of inoperable adrenocortical adenocarcinomas. A reduction in both tumor size and adrenocortical hormone secretion can be achieved in about half of the patients taking the drug. Because normal adrenocortical cells also are affected, endogenous glucocorticoid production should be monitored and replacement therapy administered when appropriate. 

In the treatment of secondary adrenocortical insufficiency, lower doses of cortisol are generally effective, and fluid and electrolyte disturbances do not have to be considered, since patients with deficient corticotrophin secretion generally do not have abnormal function of the zona glomerulosa. Since cortisol replacement therapy is required for life, adequate assessment of patients is critical to avoid the serious long-term consequences of excessive or insufficient treatment. In many cases, the doses of glucocorticoid used in replacement therapy are probably too high. Patients should ideally be administered three or more doses daily. To limit the risk of osteoporosis, replacement therapy should be carefully assessed on an individual basis and overtreatment avoided. 

D. Dexamethasone is a fluorinated glucocorticoid that is more potent and longer acting than cortisol. While devoid of salt-retaining activity in therapeutic doses, this glucocorticoid does possess most of the adverse effects observed with cortisol. Because it lacks mineralocorticoid activity, dexamethasone is not used in replacement therapy. 

Cortisone acetate and hydrocortisone are usually the corticoids of choice for replacement therapy in patients with primary adrenocortical insufficiency (such as Addison s disease), or after adrenalectomy where both glucocorticoid and mineralo-corticoid replacement is needed. In secondary adrenal insufficiency, associated with inadequate corticotrophin (ACTH) secretion, glucocorticoid replacement alone is usually adequate [62]. 

Glucocorticoids are also used as hormonal replacement therapy in patients in whom the adrenal cortex has been destroyed by some pathological process. The resulting... 

Synthetic glucocorticoids are prednisolone, prednisone, methylprednisolone, dexamethasone, betamethasone and triamcinolone (Table 13.2). Hydrocortisone is available as either succinate or phosphate salts for oral and intravenous administration. It is the drug of choice when a rapid effect is required, e.g. acute adrenal insufficiency, or as peri-operative replacement therapy. Prednisolone can also be given intravenously. It has about 0.8 of the mineralocorticoid activity of hydrocortisone. Prednisone is a prodrug that is converted to prednisolone in the body. For chronic therapy, synthetic steroids without mineralocorticoid activity are preferred, such as dexamethasone, betamethasone or triamcinalone. Beclo-metasone passes membranes poorly and is more active topically than when given orally. It is used as an aerosol for chronic rhinitis and asthma, and topically in severe eczema. Fludrocortisone is a synthetic halogenated derivate of cortisol that is used for its mineralocorticoid effect. 

Glucocorticoids can even cause osteoporosis when they are used for long-term replacement therapy in the Addison s disease, as has been shown by a study of 91 patients who had taken glucocorticoids for a mean of 10.6 years, in whom bone mineral density was reduced by 32% compared with age-matched controls (SEDA-19, 377 198). However, these results contrasted with the results of a Spanish study in patients with Addison s disease, in which no direct relation was found between replacement therapy and either bone density or biochemical markers of bone turnover of calcium metabolism (alkaline phosphatase, osteocalcin, procollagen I type, parathormone, and 1,25-dihydroxycolecalciferol) (SEDA-19, 377 199). 

Lukert BP, Johnson BE, Robinson RG. Estrogen and progesterone replacement therapy reduces glucocorticoid-induced bone loss. J Bone Miner Res 1992 7(9) 1063-9. 

The adrenal glands are sensitive to the toxic effects of suramin both glucocorticoid and mineralocorticoid functions can be impaired at doses normally used, necessitating replacement therapy (1081). 

Drugs with mineralocorticoidlike activity (aldosterone agonists) are frequently administered as replacement therapy whenever the natural production of mineralo-corticoids is impaired. Mineralocorticoid replacement is usually required in patients with chronic adrenocortical insufficiency (Addison disease), following adrenalectomy, and in other forms of adrenal cortex hypofunction. These conditions usually require both mineralocorticoid and glucocorticoid replacement. 

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