M. Scacchi et al., LACK OF GROWTH-HORMONE RESPONSE TO ACUTE ADMINISTRATION OF DEXAMETHASONE IN ANOREXIA-NERVOSA, European journal of endocrinology, 132(2), 1995, pp. 152-158
High plasma growth hormone (GH) levels, associated with abnormal hormo
ne responses to provocative stimuli, point to an altered GH secretion
in anorexia nervosa. The GH-releasing effect of acutely administered g
lucocorticoids, firmly established in normal subjects, has not been re
ported 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 +/- 127.95 vs 242.8 +/- 55.35 mu g.l(-
1).min(-1), p < 0.05, respectively) but was ineffective in 11 anorecti
c patients (AUC 3271.8 +/- 1407.11 vs 2780.0 +/- 1162.04 mu g.l(-1).mi
n(-1), NS). After dexamethasone, a significant lowering of plasma cort
isol was observed in normal women (AUC 25367.0 +/- 3128.43 vs 47347.1
+/- 4456.61 nmol.l(-1).min(-1), after dexamethasone and saline, respec
tively, p < 0.05), but not in anorectic patients (AUC 77809.3 +/- 8499
.92 vs 78454.9 +/- 7603.62 nmol.l(-1).min(-1), NS). In both groups, pl
asma adrenocorticotrophin (ACTH) displayed a significant decrease afte
r dexamethasone (AUC 523.6 +/- 92.08 vs 874.2 +/- 115.03 pmol.l(-1).mi
n(-1) p < 0.05, after dexamethasone and saline, respectively, in anore
ctic patients and 377.5 +/- 38.41 vs 1004.9 +/- 200.51 pmol.l(-1).min(
-1), p < 0.05, in controls). However, when considering the hormonal de
cremental areas, a significant dexamethasone-induced ACTH inhibition,
compared to saline, was evidenced in normal (Delta AUC -414.4 +/- 65.7
5 vs 222.9 +/- 42.40 pmol.l(-1).min(-1), p < 0.05) but not in anorecti
c women (Delta AUC -254.2 +/- 96.92 vs 2.9 +/- 132.32 pmol.l(-1).min(-
1), NS). In conclusion, compared to normal subjects, anorectic patient
s do not display an increase of plasma GH levels and show a lower degr
ee of inhibition of the hypothalamic-pituitary-adrenal axis following
acute iv administration of dexamethasone. This observation broadens th
e array of the abnormal GH responses to provocative stimuli in anorexi
a nervosa and supports the existence, in these patients, of a decrease
d hypothalamic somatostatin secretion, although the possibility of a r
educed tissue sensitivity to glucocorticoids cannot be excluded.