title: Study of growth hormone secretion and action in growth-retarded children with juvenile chronic arthritis (JCA).
abstract: The stimulated and spontaneous growth hormone (GH) secretion and the response to GH action were assessed in growth-retarded children with juvenile chronic arthritis (JCA), in order to determine the underlying mechanisms of growth retardation in such children. Six children (4 boys and 2 girls aged 10.7-13.8 years) with active JCA of systemic onset were included in the study which involved: (1) anthropometric measurements; (2) assessment of GH responses to insulin-induced hypoglycaemia and clonidine stimulation; (3) assessment of the nocturnal pulsatile GH secretion by measuring GH in blood samples obtained every 20 min from 20.00 to 08.00 h; and (4) the IGF-I generation test. As a control, the latter test was also performed in eight aged-matched children with physiological delay in puberty. Biosynthetic hGH (0.1 IU/kg BW) was administered s. c. for 4 days and blood samples were taken at baseline and the morning after the last GH injection for measurement of IGF-I and IGFBP-3. All six children with JCA were prepubertal and their growth velocity was <3 cm/year. The GH responses to both stimulation tests were normal (peak GH >20 mU/l). Analysis of the pulsatile GH secretion during the night revealed three-to-four GH pulses of normal amplitude (>20 mU/l). IGF-I (26.7+/-4.6 nmol/l, mean+/-SD) and IGFBP-3 (2.1+/-0.2 mg/l) levels were lower in the patients compared with the controls (43.0+/-3.7 nmol/l and 2.8+/-0.2 mg/l, respectively, P<0.01). Following stimulation with exogenous hGH, there was a significant increase in IGF-I and IGFBP-3 levels in the control group (85 and 73%, respectively), but only a small increase in the patients (31 and 14%). It appears that stimulated and spontaneous GH secretion is normal in children with active systemic JCA, but the response to endogenous and exogenous GH with regard to IGF-I and IGFBP-3 production is impaired, indicating a degree of GH insensitivity in such children.
authors.affiliation: Endocrine Unit, Department of Medicine, Department of Paediatrics, University of Ioannina, Ioannina, Greece. atsatsou@cc.uoi.gr
authors.forename: A
authors.initials: A
authors.lastname: Tsatsoulis
authors.forename: A
authors.initials: A
authors.lastname: Siamopoulou
authors.forename: C
authors.initials: C
authors.lastname: Petsoukis
authors.forename: A
authors.initials: A
authors.lastname: Challa
authors.forename: E
authors.initials: E
authors.lastname: Bairaktari
authors.forename: K
authors.initials: K
authors.lastname: Seferiadis
mesh_terms: D000293:Adolescent; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D001171:Arthritis, Juvenile / Q000378:metabolism*; D002648:Child; D003000:Clonidine / Q000494:pharmacology; D005260:Female; D005951:Glucose Tolerance Test; D006130:Growth Disorders / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000096:biosynthesis; D008297:Male; D013997:Time Factors
chemical_list: D000316:Adrenergic alpha-Agonists; D018972:Insulin-Like Growth Factor Binding Protein 3; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D003000:Clonidine