SOMATOSTATIN PRETREATMENT ENHANCES GROWTH-HORMONE (GH) RESPONSIVENESSTO GH-RELEASING HORMONE - A POTENTIAL NEW DIAGNOSTIC-APPROACH TO GH DEFICIENCY

Despite the availability of numerous testing procedures to evaluate GH secretion in short children, there is still controversy about the mos t reliable test in the diagnosis of GH deficiency. We have recently de monstrated that in normal short children, priming with the long-acting somatostatin analog, SMS 201-995 (SMS), significantly potentiates the ir GH response to subsequent GHRH challenge. In the present study, we used the combined SMS + GHRH test in patients with GH deficiency to va lidate the hypothesis that this test would better discriminate between normal short children and those with truly diminished GH secretion. W e studied 24 children classified into three groups according to their GH peak response to up to four conventional tests: 1) children with no rmal short stature and normal GH response (NSSA: GH peak greater than or equal to 10 mu g/L, n = 6); 2) children with normal short stature w ith borderline GH response (NSSB: GH peak greater than or equal to 7 m u g/L but <10 mu g/L, n = 4); and 3) GH-deficient children (GHD: GH pe ak <7 mu g/L, n = 14). Two study protocols were performed in all subje cts: SMS (1 mu g/kg, sc) was randomly administered or omitted (control test) at 0800 h and GHRH (1 mu g/kg, iv) was given 5 h later. Plasma GH levels were measured every 30 min from 0800 h until 2 h after the G HRH injection. Pretreatment with SMS significantly augmented the GH pe ak response and the GH area under the GH concentration curve over 2 h after GHRH injection in the NSSA group, compared with control tests, b ut had no effect in the other two groups. While there was wide overlap of individual peak GH values to both the conventional tests and to th e GHRH injection in the control test among the three groups of childre n, pretreatment with SMS resulted in complete discrimination between G HD and normal short children; the mean GH peak response to GHRH after SMS pretreatment was 8- to B-fold lower in the GHD subjects (5.2 +/- 0 .8 mu g/L) compared with both the NSSA (44.0 +/- 14.3 mu g/L; P < 0.01 ) and NSSB (42.9 +/- 5.0 mu g/L; P < 0.01) groups and, more importantl y, there was no overlap in the individual GH responses between GHD and normal short children. These results demonstrate that the combined SM S + GHRH test clearly discriminates normal short children from those w ith GHD. In view of its testing economy, safety, and accuracy, this co mbined test could become the test of choice to establish a diagnosis o f GK deficiency in the slowly growing child.