Growth hormone deficiency impedes the rise in plasma insulin-like growth factor I levels associated with precocious puberty

• Published in: The Journal of pediatrics Vol. 115; no. 1; pp. 64 - 68
• Main Authors: Cara, José F., Burstein, Stephen, Cuttler, Leona, Moll, George William, Rosenfield, Robert L.
• Format: Journal Article
• Language: English
• Published: New York, NY Mosby, Inc 01.07.1989; Elsevier
• Subjects: Adolescent; Biological and medical sciences; Body Height; Child; Child, Preschool; Endocrinopathies; Female; Growth Hormone - deficiency; Growth Hormone - therapeutic use; Humans; Hypothalamus. Hypophysis. Epiphysis (diseases); Insulin-Like Growth Factor I - blood; Male; Medical sciences; Non tumoral diseases. Target tissue resistance. Benign neoplasms; Puberty, Precocious - complications; Somatomedins - blood; Endocrinopathy; Somatomedin C; Deficiency; STH; Precocious puberty; Proteins; Protein hormone; Concomitant disease; Treatment; Adenohypophyseal hormone; Pituitary diseases; Hormonal investigation; Somatic growth
• ISSN: 0022-3476; 1097-6833
• DOI: 10.1016/S0022-3476(89)80330-0

We tested the hypothesis that growth hormone (GH) mediates the rise in insulin-like growth factor I (IGF-I) concentrations in children with precocious puberty. We studied three groups of patients. Group 1 included six children with GH deficiency and precocious puberty (precocious GH-deficient); group 2 included 10 GH-sufficient patients with idiopathic true precocious puberty (precocious GH-sufficient); and group 3 included 9 prepubertal children with GH deficiency (prepubertal GH-deficient). Growth rates, pubertal status, and plasma IGF-I concentrations were determined at regular intervals. The precocious children with GH deficiency had a mean (±SD) growth rate of 7.2±2.1 cm/yr, significantly below that of the precocious GH-sufficient patients (10.5±2.5 cm/yr, p<0.05) but above that of the prepubertal GH-deficient children (3.9±1.4 cm/yr, p<0.05). The mean IGF-I concentration in the precocious GH-deficient children was 0.77±0.39 U/ml, significantly lower than the mean level of 2.2±0.67 U/ml in the precocious GH-sufficient patients ( p<0.01). However, precocious GH-deficient patients had significantly higher IGF-I values than the prepubertal GH-deficient children (0.24±0.10 U/ml, p<0.05). IGF-I values did not rise with the onset of precocious puberty in four of the precoclous GH-deficient children evaluated before and after the development of precocious puberty. However, three patients who began GH treatment did have a rise in plasma IGF-I concentrations to levels of 1.2, 3.4, and 3.7 U/ml, respectively. These findings are compatible with the concept that sex steroids increase IGF-I levels in precocious puberty primarily by increasing GH production. A small but direct effect of sex steroids on IGF-I production may also exist. The onset of precocious puberty in children with organic GH deficiency may mask the abnormal growth pattern of these children and delay diagnosis; determinations of plasma IGF-I concentrations may be helpful in assessing the GH status of these patients.