A. Tsatsoulis et al., Study of growth hormone secretion and action in growth-retarded children with juvenile chronic arthritis (JCA), GROWTH H I, 9(2), 1999, pp. 143-149
The stimulated and spontaneous growth hormone (GH) secretion and the respon
se to GH action were assessed in growth-retarded children with juvenile chr
onic arthritis (JCA), in order to determine the underlying mechanisms of gr
owth 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 resp
onses to insulin-induced hypoglycaemia and clonidine stimulation; (3) asses
sment of the nocturnal pulsatile GH secretion by measuring GH in blood samp
les obtained every 20 min from 20.00 to 08.00 h; and (4) the IGF-I generati
on test. As a control, the latter test was also performed in eight aged-mat
ched 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 ba
seline 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 n
mol/l, mean+/-SD) and IGFBP-3 (2.1+/-0.2 mg/l) levels were lower in the pat
ients compared with the controls (43.0+/-3.7 nmol/l and 2.8+/-0.2 mg/l, res
pectively, 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 a
nd 73%, respectively), but only a small increase in the patients (31 and 14
%).
It appears that stimulated and spontaneous GH secretion is normal in childr
en with active systemic JCA, but the response to endogenous and exogenous G
H with regard to IGF-I and IGFBP-3 production is impaired, indicating a deg
ree of GH insensitivity in such children. (C) 1999 Churchill Livingstone.