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Glucocorticoids are used in adrenal replacement therapy when adrenal insufficiency occurs, or as pharmacologic agents. Following withdrawal of glucocorticoids used for pharmacologic therapy adrenal insufficiency can persist for months, especially during times of stress. The only differences among the various glucocorticoids are their ratio of glucocorticoid to mineralocorticoid activity, their capacity to bind to various binding proteins, their molar potency, and their biologic half life. Dexamethasone is commonly used in reducing increased intracranial pressure and brain edema. Neurosurgical experience indicates that the optimal doses are 10 to 100 times those that would thoroughly saturate all available glucocorticoid receptors, suggesting that this action of dexamethasone may not be mediated through the glucocorticoid receptor.

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Glucocorticoid replacement therapy is complicated by undesirable side effects with even minor overtreatment or undertreatment. Pediatric glucocorticoid replacement therapy is based on the endogenous secretory rate of cortisol, which may be as low as 6 mg/m2 in younger children and 9 mg/m2 in older children and adolescents, but there is considerable variation in the “normal” cortisol secretory rate among different children of the same size. Several additional factors must be considered in tailoring a specific child’s glucocorticoid replacement regimen as discussed below.

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The Cause of Adrenal Insufficiency

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When treating autoimmune adrenalitis or other forms of Addison disease, it is prudent to err slightly on the side of undertreatment. This will eliminate the possibility of glucocorticoid induced iatrogenic growth retardation and will permit the pituitary to continue to produce normal to slightly elevated concentrations of corticotropin (ACTH). This ACTH will continue to stimulate the remaining functional adrenal steroidogenic machinery and also provide a convenient means of monitoring therapy. By contrast, when treating severe, virilizing congenital adrenal hyperplasia, the adrenal should be suppressed more completely, as essentially all adrenal steroidogenesis will result in the production of unwanted androgens, with their consequent virilization and rate of advancement of bony maturation that is more rapid than the rate of advancement of height. However, overtreatment will also compromise growth.

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Presence or Absence of Associated Mineralocorticoid Deficiency

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Children with mild degrees of mineralocorticoid insufficiency (eg, simple virilizing congenital adrenal hyperplasia [CAH]) may continue to have mildly elevated ACTH values, suggesting insufficient glucocorticoid replacement in association with elevated plasma renin activity (PRA). In some children, the ACTH is elevated in response to chronic, compromised hypovolemia, attempting to stimulate the adrenal to produce more mineralocorticoid. In such children without overt signs of mineralocorticoid insufficiency, treatment with mineralocorticoid replacement may permit one to decrease the amount of glucocorticoid replacement needed to suppress plasma ACTH. This reduction in glucocorticoid therapy reduces the likelihood that adult height will be compromised.

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Formulation of Glucocorticoid Used for Treatment

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Very potent, long acting glucocorticoids, such as dexamethasone or prednisone, are preferred in the treatment of adults but are rarely appropriate for replacement therapy in children. As children are continually growing and changing their ...

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