E. Rossi et al., ACUTE AND CHRONIC EFFECTS OF HUMAN RECOMBINANT GH (HRGH) ON ADRENAL STEROIDOGENESIS IN CHILDREN AFFECTED WITH ISOLATED GH DEFICIENCY (IGHD), The Journal of clinical endocrinology and metabolism, 80(7), 1995, pp. 2251-2254
In a previous study we demonstrated that, in children affected with is
olated GH deficiency, an acute high-dose human recombinant GH (hrGH) t
reatment increases the 11-deoxycortisol and induces an IGF-I responsiv
eness to ACTH. The aim of the present study was to reevaluate, in the
same children, the adrenal and IGF-I responsiveness to ACTH after a ch
ronic replacement-dose GH therapy. Ten children (seven males and three
females, mean age 7 years) affected with isolated GH deficiency under
went a synthetic ACTH 1-17 test before and after sc administration of
human recombinant GH at a dose of 0.6 UI/kg/week for 3 months. After t
herapy, the 11-deoxycortisol responsiveness to ACTH significantly decr
eased compared with that observed after acute treatment (P < 0.001), a
nd so it returned to baseline. No differences were detected in the res
ponsiveness to ACTH of cortisol, dehydroepiandrosterone-sulphate, D4-a
ndrostenedione, and 17-hydroxyprogesterone. On the other hand, the chr
onic treatment induced an IGF-I responsiveness to ACTH (P < 0.001). In
conclusion, our study demonstrates that, in isolated GH deficiency, r
eplacement doses of hrGH do not modify the adrenal steroid basal level
s or its responsiveness to ACTH, whereas both replacement and high dos
es of hrGH induce an IGF-I responsiveness to ACTH.