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We studied the effect of a single intravenous bolus of 0.5 microgram/kg of growth hormone-releasing factor (GRF) on plasma GH, prolactin (PRL) and somatomedin C (SMC) in 12 short normal children and 24 patients with severe GH deficiency (GHD), i.e. GH less than 5 ng/ml after insulin and glucagon tolerance tests. GRF elicited an increase in plasma GH in both short normal and GHD children. The mean GH peak was lower in the GHD than in the short normal children (8.2 +/- 2.5 vs. 39.2 +/- 5.1 ng/ml, p less than 0.001). In the GHD patients (but not in the short normals) there was a negative correlation between bone age and peak GH after GRF (r = -0.58, p less than 0.005); GH peaks within the normal range were seen in 5 out of 8 GHD children with a bone age less than 5 years. In the short normal children, GRF had no effect on plasma PRL, which decreased continuously between 8.30 and 11 a.m. (from 206 +/- 22 to 86 +/- 10 microU/ml, p less than 0.005), a reflection of its circadian rhythm. In the majority of the GHD patients, PRL levels were higher than in the short normal children but had the same circadian rhythm, except that a slight increase in PRL was observed 15 min after GRF; this increase in PRL was seen both in children with isolated GHD and in those with multiple hormone deficiencies; it did occur in some GHD patients who had no GH response to GRF. Serum SMC did not change 24 h after GRF in the short normal children. We conclude that: (1) in short normal children: (a) the mean GH response to a single intravenous bolus of 0.5 microgram/kg of GRF is similar to that reported in young adults and (b) GRF has no effect on PRL secretion; (2) in GHD patients: (a) normal GH responses to GRF are seen in patients with a bone age less than 5 years and establish the integrity of the somatotrophs in those cases; (b) the GH responsiveness to GRF decreases with age, which probably reflects the duration of endogenous GRF deficiency, and (c) although the PRL response to GRF is heterogeneous, it does in some patients provide additional evidence of responsive pituitary tissue.
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
December 1986,
Journal of endocrinological investigation,
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
January 1985,
Hormone research,
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
April 1985,
Endocrinologia japonica,
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
January 1987,
European journal of pediatrics,
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
October 1987,
Endocrinologia japonica,
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
November 1983,
Lancet (London, England),
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
November 1984,
The Journal of clinical endocrinology and metabolism,
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
August 1977,
The Journal of endocrinology,
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
May 1984,
Clinical endocrinology,
G Van Vliet, and
D Bosson, and
C Robyn, and
M Craen, and
P Malvaux, and
M Vanderschueren-Lodeweyckx, and
R Wolter
September 1985,
Acta endocrinologica,
