Withdrawal of a somatostatin infusion (SSIW) is followed by a rebound rise of GH in both animals and normal adult men, a phenomenon Likely mediated by endogenous GHRH function. In the present study, we have evaluated the GH response to SSIW a group of 28 prepubertal children (18 boys and 10 girls; aged 3.7-11.1 yr). Six children had GH deficiency [GHD; GH responses to pyridostigmine (PD)+GHRH and to clonidine <20 and <7 mu g/L, respectively], 4 children had GH neurosecretory dysfunction (GHND; GH responses to PD+GHRH and to clonidine greater than or equal to 20 and >7 mu g/L, respectively; mean integrated nighttime GH concentrations <3 mu g/L), and 18 children were short normal children [normal controls (NC)]. All children received a constant infusion of SS at the dose of 3 mu g/Kg . h for 90 min. SSIW elicited a clear-cut GH rise in NC children (13.7 +/- 1.0 mu g/L), but not in GH-deficient children, regardless of the underlying etiology (GHD, 1.6 +/- 0.4 mu g/L; GHND, 2.4 +/- 0.3 mu g/L). The GH response to SSIW was similar between GHD and GHND children. There was no overlapping of the maximum SSIW-stimulated GH peaks between NC and GHD or GHND children. In conclusion, we have demonstrated that SSIW elicits a significant GH rise in NC children, but not in GH-deficient children, regardless of the underlying etiology (GHD or GHND). This resulted in complete discrimination of NC from GHD or GHND children. Were these present findings confirmed on a larger number of children, SSIW, because of its testing efficaciousness and safety, procedural simplicity, and economy holds promise of being a useful diagnostic tool for GH-dependent growth disorders.
