Glucocorticoid therapy

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  

Addison s disease), both cortisol and aldosterone must be replaced when ACTH production is deficient (secondary AC insufficiency), cortisol alone needs to be replaced. Cortisol is effective when given orally (30 mg/d, 2/3 a.m., 1/3 p.m.). In stress situations, the dose is raised by 5- to 10-fold. Aldosterone is poorly effective via the oral route instead, the mineralocorticoid fludrocortisone (0.1 mg/d) is given. 

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Desired effects. As anti-allergies, immunosuppressants, or anti-inflammatory drugs, glucocorticoids display excellent efficacy against undesired inflammatory reactions. 

Measures for Attenuating or Preventing Drug-induced Cushing s Syndrome 

Besides the adverse effects just described, glucocorticoid therapy is contraindicated under the following circumstances diabetes mellitus, digitalis therapy, glaucoma, hypertension, infection, osteoporosis, peptic ulcer, tuberculosis, and viral infection. 

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Vitamin D withdrawal is an obvious treatment for D toxicity (219). However, because of the 5—7 d half-life of plasma vitamin D and 20—30 d half-life of 25-hydroxy vitamin D, it may not be immediately successful. A prompt reduction in dietary calcium is also indicated to reduce hypercalcemia. Sodium phytate can aid in reducing intestinal calcium transport. Calcitonin glucagon and glucocorticoid therapy have also been reported to reduce semm calcium resulting from D intoxication (210). 

Corticotropin is used for diagnostic testing of adrenocortical function. This drug may also be used for the management of acute exacerbations of multiple sclerosis, nonsuppurative thyroiditis, and hypercalcemia associated with cancer. It is also used as an anti-inflammatory and immunosuppressant drug when conventional glucocorticoid therapy lias not been effective (see Display 50-1). 

Administration of a short-acting glucocorticoid on alternate days and before 9 AM, when glucocorticoid plasma levels are still relatively high, does not affect the release of ACTH later in the day, yet it gives the patient the benefit of exogenous glucocorticoid therapy. 

MANAGING INFECTION. The nurse should report any slight rise in temperature, sore throat, or other signs of infection to the primary health care provider as soon as possible because of a possible decreased resistance to infection during glucocorticoid therapy. Nursing personnel and visitors with any type of infection or recent exposure to an infectious disease should avoid patient contact. 

LONG-TERM OR HIGH-DOSE GLUCOCORTICOID THERAPY... 

Monitor for adverse reactions from hydrocortisone administration. Glucocorticoid therapy at physiologic replacement doses should not lead to the development of Cushing s syndrome. However, careful monitoring should still be performed. Use the smallest effective dose. 

All patients starting or receiving long-term systemic glucocorticoid therapy should receive at least 1,500 mg elemental calcium and 800 to 1,200 units of vitamin D daily and practice a bone-healthy lifestyle. 

Glucocorticoid therapy with IV hydrocortisone 100 mg every 8 hours should be given until coexisting adrenal suppression is ruled out. 

The well-appreciated adverse effects of glucocorticoids include hyperglycemia, hypertension, osteoporosis, fluid retention and electrolyte disturbances, myopathies, psychosis, and reduced resistance to infection. In addition, glucocorticoid use may cause adrenocortical suppression. Specific regimens for withdrawal of glucocorticoid therapy have been suggested. 

Immunocompromised host (including patients with acquired immune deficiency syndrome, transplants, or receiving chronic glucocorticoid therapy)... 

The early addition of adjunctive glucocorticoid therapy to anti-PCP regimens has been shown to decrease the risk of respiratory failure and improve survival in patients with AIDS and moderate to severe PCP (Pa02 <70 mm Hg or [alveolar-arterial] gradient >35 mm Hg). 

Orally administered glucocorticoids have substantial adverse effects, including immunosuppression, suppression of the synthesis of endogenous glucocorticoids themselves (that can be a problem when glucocorticoid therapy is stopped), resorption of bone, and retention of water. Nonetheless, they are important drugs for control of inflammation. They also augment resistance to stress. 

Glucocorticoid therapy is indicated in selected patients with inflammatory bowel disease, chronic ulcerative colitis as well as Crohn s disease. Agents include prednisolone, hydrocortisone and budes-onide, the latter having a predominantly local effect... 

During the period of withdrawal from extended glucocorticoid therapy... 

C) The physician should rapidly reduce glucocorticoid therapy to physiological doses. 

A. Glucocorticoid treatment of rheumatoid arthritis does not eradicate all symptoms, nor does it reverse the degenerative process. Suppression of the hypothalamic-pituitary-adrenal axis is an unwanted side effect of glucocorticoid therapy. While development of a sense of well-being may be attributed to the relief of symptoms, it is not the primary basis for employing the potent glucocorticoids. 

Compston JE. Management of bone disease in patients on long term glucocorticoid therapy. Gut 1999 44 770-772. 

DaSilva JA and Bijlsma JW. Optimizing glucocorticoid therapy in rheumatoid arthritis. Rheumatol Dis Chn North Am 2000 26 859-880. 

Drug interactions Excessive glucocorticoid therapy may inhibit the growth-promoting effects of human growth hormone. 

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