Preservation of Dopaminergic and x003B1;-Adrenergic Function in Children with Growth Hormone Neurosecretory Dysfunction∗

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Abstract
The integrity of dopaminergic and a-adrenergic neurotransmitter regulation of GH secretion was examined in children with decreased GH secretion. Children with GH neurosecretory dysfunction (GHND; n= 16) those with classical GH deficiency (n = 9), and short but otherwise normalchildren (n = 12) underwent 24 h GH studies (blood sampling every 20 min for 24h) and provocative tests using arginine, insulin hypoglycemia, L-dopa (dopaminergic) and clonidine (α-adrenergic), and GH-releasing hormone (GHRH). GHND was defined as children with height in the first percentile or below, growth velocity of 4 cm⁄yr or less, low plasma somatomedin-C for age, delayed skeletal age by 2 or more yr, peak serum GH responses to any one (or more) provocative test of 10 ng⁄ml or more, and mean 24-h GH concentration below 3 ng⁄ml. GHND and GHdeficient children had reduced endogenous GH secretion, expressed as mean serum 24-h GH concentration [1.6 ± 0.1 (± SEM) and 2.1 ± 0.1 vs. 6.1 ± 0.5 ng⁄ml (GH-deficient and GHND vs. normal, respectively); P < 0.01]. The mean peak serum GH levels after arginine [8.2 ± 2.0 vs. 20.8 ± 6.6 ng⁄ml (GHND vs. normal); P < 0.05] and insulin [9.3 ± 1.0vs. 16.2 ± 1.7 ng⁄ml (GHND us. normal); P vs. 14.6 ± 4.7 ng⁄ml (GHND us. normal); P = NS] and clonidine [19.0 ± 2.2 vs. 23.3 ± 3.8 ng⁄ml (GHND vs. normal); P = NS] were preserved in GHND children. In GH-deficient children, mean peak serum GH concentrations after all four provocative tests were low (arginine, 2.7 ± 0.8; insulin, 2.6 ± 0.8; L-dopa, 3.0 ± 0.9; clonidine, 3.4 ± 1.0 ng⁄ ml; all P < 0.01 vs. normal). The mean peak serum GH concentration after GHRH was blunted in GH-deficient children (9.1 ± 1.7 ng⁄ml) compared to those in GHND (32.9 ± 8.5 ng⁄ml) and normal (43.2 ± 6.4 ng⁄ml) children (P < 0.01). The area under the GH curve after GHRH stimulation was greater for normal than GHND children (P < 0.05). These data demonstrate preservation of dopaminergic and α-adrenergic neurotransmitter pathways in GHND children. They further suggest a defect in the release of pituitary GH secondary to an abnormality in alternative neurotransmitter pathways resulting in decreased GHRH and⁄or increased somatostatin secretion.