The duration of glucocorticoid-induced inhibition that occurs in the hypothalamic-pituitary-adrenal (HPA) axis after discontinuation of treatment is controversial. The main objective of this prospective study was to evaluate the inhibition of the HPA axis by dexamethasone in children and adolescents with acute lymphoid leukemia. Thirty-five patients (median age of 6.9 yr) were evaluated. A stimulus test with ovine CRH (1 microg/kg) was performed before the introduction of dexamethasone (6 mg/m2.d for 28 d), in the 8th and 28th days of glucocorticoid therapy, and 48 h and 1 month after discontinuation of glucocorticoid therapy. Suppression of the basal secretion as well as the maximum concentration of ACTH occurred during glucocorticoid therapy (P < 0.01). The pituitary function before the introduction of dexamethasone was similar to the one seen 48 h and 1 month after withdrawing it. Suppression of the adrenal function was detected during glucocorticoid therapy, which persisted for 48 h after the steroid was removed from treatment (P < 0.01). One month after ceasing the administration of the glucocorticoid, the adrenal function was similar to that before glucocorticoid therapy. According to these results, a clinical and laboratory follow-up of the HPA axis in the month after the cessation of dexamethasone therapy is suggested to determine glucocorticoid replacement.
The glucocorticoid-induced inhibition that occurs after discontinuation of treatment is the most frequent cause of adrenal insufficiency. There are yet some doubts about the best way of evaluating the hypothalamic-pituitary-adrenal (HPA) axis in those patients. The main objective of this study was to evaluate the utility of basal cortisol in diagnosing adrenal insufficiency. Thirty-five children with acute lymphoid leukemia (ALL) receiving glucocorticoid therapy (median age of 6.9 years) were evaluated. A stimulus test with corticotropin releasing hormone (CRH-1 mcg/kg) was performed before the introduction of dexamethasone (6 mg/m2/day, for 28 days), in the 8th and the 28th days of glucocorticoid therapy, and 48 hours and one month after discontinuation of therapy. Suppression of the basal secretion as well as the maximum concentration of cortisol (post-CRH) occurred during glucocorticoid therapy, which persisted for 48 hours after the steroid was removed from treatment (p< 0.01 and p< 0.0001, respectively, for the three tests). One month after ceasing the administration of the glucocorticoid, the basal secretion, as well as the maximum concentration of cortisol, were similar to that before glucocorticoid therapy. There was a positive and statistically significant correlation between basal secretion and maximum concentration of cortisol in all tests. We observed 95% of specificity for the diagnosis of adrenal insufficiency when the inferior limit of basal cortisol was 8.5 mcg/dl. According to these results we concluded that basal secretion of cortisol is a good marker of supra-renal function in evaluating children after discontinuation of glucocorticoid therapy.
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