Lack of growth hormone response to acute administration of dexamethasone in anorexia nervosa

High plasma growth hormone (GH) levels, associated with abnormal hormone responses to provocative stimuli, point to an altered GH secretion in anorexia nervosa. The GH-releasing effect of acutely administered glucocorticoids, firmly established in normal subjects, has not been reported in these patients, In this study, acute iv administration of 4 mg of dexamethasone, compared with saline, increased plasma GH in nine normal-weight women (AUC 848.2 \ub1 127.95 vs 242.8 \ub1 55.35 \u3bcg\ub7l-1 min-1, p < 0.05, respectively) but was ineffective in 11 anorectic patients (AUC 3271.8 \ub1 1407.11 vs 2780.0 \ub1 1162.04 \u3bcg\ub7l-1 min-1 NS). After dexamethasone, a significant lowering of plasma cortisol was observed in normal women (AUC 25367.0 \ub1 3128.43 vs 47347.1 \ub1 4456.61 nmol\ub7l-1\ub7min-1 after dexamethasone and saline, respectively, p < 0.05), but not in anorectic patients (AUC 77809.3 \ub1 8499.92 vs 78454.9 \ub1 7603.62 nmol\ub7l-1\ub7min-1, NS), In both groups, plasma adrenocorticotrophin (ACTH) displayed a significant decrease after dexamethasone (AUC 523.6 \ub1 92.08 vs 874.2 \ub1 115.03 pmol\ub7l-1 min-1, p < 0.05, after dexamethasone and saline, respectively, in anorectic patients and 377.5 \ub1 38.41 vs 1004.9 \ub1 200.51 pmol\ub7l-1\ub7min-1, p < 0.05, in controls), However, when considering the hormonal decremental areas, a significant dexamethasone-induced ACTH inhibition, compared to saline, was evidenced in normal (\u394AUC -414.4 \ub1 65.75 vs 222.9 \ub1 42.40 pmol\ub7l-1\ub7min-1, p < 0.05) but not in anorectic women (\u394AUC -254.2 \ub1 96.92 vs 2.9 \ub1 132.32 pmol\ub7l-1\ub7min-1 NS). In conclusion, compared to normal subjects, anorectic patients do not display an increase of plasma GH levels and show a lower degree of inhibition of the hypothalamic-pituitary-adrenal axis following acute iv administration of dexamethasone. This observation broadens the array of the abnormal GH responses to provocative stimuli in anorexia nervosa and supports the existence, in these patients, of a decreased hypothalamic somatostatin secretion, although the possibility of a reduced tissue sensitivity to glucocorticoids cannot be excluded