Growth Hormone Release In Children Research Articles

Puberty, statural growth, and growth hormone release in children with cerebral palsy.

Children with cerebral palsy (CP) are smaller than normally growing children.. The association between the growth hormone (GH) axis and growth in children with CP during puberty is unknown. We compared growth and markers of the GH axis in pre-pubertal and pubertal children with moderate to severe CP and without CP over a three-year period. Twenty children with CP, ages 6-18, Gross Motor Function Classification System levels III-V, were compared to a group of sixty-three normally growing children of similar age. Anthropometry, Tanner stage, bone age, and laboratory analyses were performed every six months for three years. Laboratory values included spontaneous overnight GH release, fasting IGF-1 and IGFBP-3. Repeated measures models were used to evaluate interactions among Tanner stage and group (children with CP vs. reference children), taking into account gender, age, and nutritional status. Children with CP grew more slowly than those without CP at all Tanner stages (p<0.01). Patterns of IGF-1 and GH secretion in children with CP were similar to those of the reference group; however, the concentrations of IGF-1 (p<0.01) and GH (p<0.01) were lower in girls with CP, with a similar trend for boys (p=0.10 and 0.14, respectively). Diminished circulating IGF-1 and GH concentrations may explain the differences in growth between the two groups.

Neuroregulation of growth hormone during exercise in children.

Physical exercise is an important physiological stimulus to growth hormone (GH) release in man. Many neurotransmitters are involved in GH regulation. We studied the effect of the cholinergic pathway on GH secretion induced by physical exercise. Particularly, we studied the effect of a cholinergic muscarinic agonist on GH-induced physical exercise, both in children and adults. Moreover, we investigated the refractoriness of GH secretion after a second physical exercise stimulus. Three different protocols were performed: 1) GH response to physical exercise in children and adults; 2) effect of pyridostigmine on exercise-induced GH secretion in children and adults; 3) GH response to two consecutive exercises in children and adults. Our data show that in children GH peak after physical exercise is higher than in adults. Pyridostigmine enhances GH release in children and in adults. Exercise stimulus was able to release GH in the second test only in children, while the refractory phase did not permit a new GH release in adults. The shift to a modality of neural control of GH secretion peculiar of adults is likely due to neuroregulatory mechanisms which may be partly dependent on long-term variation in hormonal milieu.

Age-related growth hormone-releasing activity of growth hormone secretagogues in humans.

Growth hormone-releasing peptides (GHRPs) are synthetic molecules with strong, dose-related and reproducible growth hormone (GH)-releasing activity in humans. GHRPs act at both the pituitary and the hypothalamic level, where specific receptors have been located. In adults, GHRPs release more GH than does GH-releasing hormone (GHRP), whilst their co-administration has a synergistic effect, indicating that they have, at least partially, different mechanisms of action. However, normal activity of GHRH-secreting neurones is needed to achieve the full GH-releasing effect of GHRPs. In contrast to GHRH, the GH-releasing activity of GHRPs is not further increased by substances acting via inhibition of hypothalamic somatostatin, and is only blunted by substances that stimulate hypothalamic somatostatin release. Even free fatty acids and exogenous somatostatin, which act directly on somatotrophs, do no more than blunt the effect of GHRPs. Thus, the GH-releasing activity of GHRPs is partially refractory to inhibitory influences, GHRPs act, at least in part, by antagonism of somatostatin activity, both at the pituitary and the hypothalamic level. The GH-releasing effect of GHRPs is not dependent on gender, but undergoes age-related variations. Gonadal steroids seem to influence the activity of GHRPs only in childhood. The reduced GH response to GHRPs in the elderly is probably due mainly to concomitant GHRH hypoactivity and somatostatinergic hyperactivity. A preserved GH-releasing effect of GHRPs has been reported in acromegaly, anorexia nervosa, hyperthyroidism and in critically ill patients. GHRPs have also been found to increase GH release in children with idiopathic short stature, in GH deficiency and in obese patients, in whom there is a well-known reduction of somatotroph function. The GH response to GHRPs is markedly reduced in hypothyroidism and Cushing's syndrome.

Growth hormone (GH)-releasing effects of synthetic peptide GH-releasing peptide-2 and GH-releasing hormone (1-29NH 2) in children with GH insufficiency and idiopathic short stature

To investigate how growth hormone (GH)-releasing peptide (GHRP) and GH-releasing hormone (GHRH) interact in patients with short stature, we examined the acute effects of GHRH1-29NH 2, GHRP-2, and the combination of GHRH1-29NH 2 and GHRP-2 on GH release in children with GH insufficiency ([GHI] group A) and idiopathic short stature ([ISS] group B). Ten children with GHI (aged 11.8 ± 1.1 years; height, −4.2 ± 0.5 SDS) and five children with ISS (aged 11.1 ± 1.2 years; height, −3.2 ± 0.1 SDS) were studied. Intravenous bolus infusions of GHRH1-29NH 2 (1 μg/kg), GHRP-2 (1 μg/kg), and GHRH plus GHRP-2 (each 1 μg/kg), were administered in a randomized order. Because of the variability of GH responses, results were analyzed by a nonparametric statistical method. Patients in group A showed low GH responses to both GHRH1-29NH 2 and GHRP-2 stimulation: in only three of 10 and one of nine cases, respectively, were the peak GH levels above 5.0 μg/L. GH area under the curve (AUC) 90 minutes after GHRP-2 administration was slightly less than for GHRH1-29NH 2 (179 ± 150 v 214 ± 68 μg/L · min, P = .06). In group B, GH responses to GHRH1-29NH 2 and GHRP-2 were approximately of the same magnitude (1,943 ± 819 v 1,981 ± 887 μg/L · min, P = .9). After a combined challenge with GHRH1-29NH 2 and GHRP-2, five of eight children in group A had peak GH concentrations greater than 5 μg/L. GH AUC of the GHRH1-29NH 2 plus GHRP-2 test in group A (1,136 ± 764 μg/L · min) was significantly greater than GH AUC of the GHRP-2 bolus ( P = .02) but was not different from GH AUC of GHRH1-29NH 2 ( P = .09). A dramatic response to combined GHRH1-29NH 2 and GHRP-2 administration was observed in group B, with peak GH levels above 100 μg/L in four of five children. GH AUC of the GHRH1-29NH 2 and GHRP-2 combined study (7,035 ± 1,513 μg/L · min) was significantly greater than the AUC obtained after administration of GHRH1-29NH 2 (1,943 ± 819 μg/ L · min, P = .015) or GHRP-2 (1,982 ± 887, P = .014) alone. Thus, although intravenous bolus GHRP-2 was shown to release GH in children with various forms of short stature, the response is likely to be dependent on the presence of endogenous or exogenous GHRH.

Effects of oral glucose administration on spontaneous and growth hormone (GH)-releasing hormone-stimulated GH release in children and adults

Effects of oral glucose administration on spontaneous and growth hormone (GH)-releasing hormone-stimulated GH release in children and adults

Corticoid-induced growth hormone (GH) secretion in GH-deficient and normal children.

Acute administration of corticoids is a potent stimulus of GH secretion in man. To ascertain their mechanism and point of action as well as the suitability of this novel test in the diagnosis of GH-deficient states, normal controls and GH-deficient children were studied. They were selected based on auxological criteria and the GH response to provocative stimuli. The GH-deficient children presented a blunted GH (mean +/- SEM; microgram/L) discharge after insulin-induced hypoglycemia (2.9 +/- 0.4), propranolol-exercise (7.4 +/- 1.5), and clonidine (6.5 +/- 0.8) compared with values in the normal children (7.2 +/- 2.2, 15.8 +/- 2.4, and 15.6 +/- 1.8, respectively). As expected, GH-releasing hormone (GHRH)-induced GH discharge in GH-deficient children (33.2 +/- 4.9) was similar to that in the control children (35.1 +/- 6.0). Administration of 2 mg/m2 body surface dexamethasone, iv, to normal children induced, 3 h later, a mean GH peak of 14.1 +/- 1.2 micrograms/L. This was significantly higher that the corticoid-induced GH peak in GH-deficient children (6.7 +/- 1.1 micrograms/L). The corticoid-induced areas under the secretory curve were 1130 +/- 55 and 616 +/- 54 for the control and GH-deficient children, respectively. GH release in children after dexamethasone administration followed the pattern previously described for adults, i.e. there were no modifications of basal GH levels in the first 2 h, the GH peak appeared around the third hour, and the GH levels remained increased until the fourth hour after dexamethasone administration. Individually considered, practically all control children, but only 2 of 12 GH-deficient children, presented a dexamethasone-induced GH peak over the 10 micrograms/L level. In both normal and GH-deficient patients, corticoids appeared just as potent a stimulus as propranolol-exercise and clonidine, and more potent than hypoglycemia. This new stimulus showed a pattern similar to that of the hypothalamic stimuli, but clearly different with respect to the pituitary one (GHRH), suggesting that corticoids activate GH secretion by acting at hypothalamic level. In conclusion, acute administration of corticoids could be a suitable test in the diagnostic armamentaria of GH-deficient states.

Nocturnal growth hormone release in children with short stature and atopic dermatitis.

This study was designed to test the hypothesis that children with atopic dermatitis and short stature fail to release growth hormone after falling asleep. Peak serum growth hormone response to arginine was compared with peak growth hormone concentration during sleep in 6 children with atopic dermatitis and short stature (greater than 3 SD below the mean) aged 7 to 12 years, and 5 control children aged 9 to 12 years without atopic dermatitis or asthma but with unexplained short stature (greater than 3 SD below the mean). All 5 control children achieved normal levels of growth hormone after falling asleep, whereas 3 of the 6 children with dermatitis did not. All patients with dermatitis were capable of releasing growth hormone after arginine stimulation. The results suggest that in some prepubertal children with atopic dermatitis and short stature there may be an impairment of growth hormone release during stage 4 sleep.

Clinical Utility of Cycle Exercise for the Physiologic Assessment of Growth Hormone Release in Children

The clinical utility of exercise as a stimulus for the physiologic assessment of growth hormone (GH) deficiency was examined in healthy children. In response to exercise tests performed on different days, serum GH concentrations exceeded 7 micrograms/L on both days in 9 of 10 children. Although there is variation in this method of physiologic testing in the response of serum GH concentration (significant mean differences in GH peak values, 27.1 vs 19.8 micrograms/L for the two tests), the exercise test proved clinically valid in that diagnostic levels of GH were exceeded on both days 90% of the time. We conclude that this exercise evaluation protocol has clinical utility for the assessment of GH deficiency in children.

Change in the Growth Hormone(GH) Response to GH-Releasing Factor(GRF) Caused by Exogenous GH in Short Children.

To determine whether exogenous GH induces feedback of GH release in children, growth hormone-releasing factor (GRP) tests were performed before and after 10-day GH administration. Sixteen non-obese short boys, aged 5-14 yr, with normal GH response to pharmacological tests were studied. Mean basal and peak serum GH levels in GRF tests before and after exogenous GH were not significantly different. The subjects were divided into two groups, A and B, according to the percent change in integrated areas under the GH curves in GRF tests (GH AUC) before and after 10-day GH administration. Group A consisted of 6 boys with decreased GH AUC and group B consisted of 10 boys with increased GH AUC. Mean peak GH in GRF tests and mean GH AUC were significantly higher before exogenous GH in group A than in group B. The boys in group A were all prepubertal, while 4 boys in group B had begun their early pubertal change. The mean age in group A (7.8 +/- 1.8 yr) was significantly lower than that of group B (11.9 +/- 2.4 yr). GH AUC before exogenous GH showed a significant correlation with the percent change in AUC (= -0.742, p less than 0.01). These data demonstrated that the exogenous GH suppressed the GH response to GRF in prepubertal children with good response to GRF before exogenous GH, while it exaggerated the GH response to GRF in older children with relatively poor response before GH.

Growth hormone release in children after cranial irradiation.

Growth retardation due to growth hormone (GH) deficiency is common in children after radiotherapy to the brain. Different methods for assessment of GH secretion were compared in 19 children who had received radiotherapy to the brain as part of treatment for a tumor of the brain, eye or epipharynx. GH was measured over a 24-hour period (72 sampling periods of 20 min each), as well as after administration of growth hormone-releasing hormone (GHRH) and arginine-insulin (AITT) tests. We found the 24-hour GH profile to be disturbed in all children; there was a low overall secretion with few peaks of low amplitude but a diurnal rhythm still discernable. In 16 children a prompt rise in GHRH after GHRH1-40 was seen indicating hypothalamic damage. The GH response after GHRH was not found to be correlated to the spontaneous secretion over 24 h. The results of the AITT showed discrepancies to the 24-hour GH profile in individual cases making this test unreliable in spite of a good overall correlation between the tests. Therefore, we suggest measurement of spontaneous secretion when GH-secretory capability is to be evaluated after cranial irradiation for a brain tumor.

Stimulatory effect of levodopa and propranolol upon plasma growth hormone release in children and adolescents.

Stimulatory effect of levodopa and propranolol upon plasma growth hormone release in children and adolescents.

Reassessment of Glucagon-propranol Test for Growth Hormone Release in Children

Pediatrics InternationalVolume 20, Issue 2 p. 57-57 Reassessment of Glucagon-propranol Test for Growth Hormone Release in Children Seizo Suwa, Seizo Suwa Department of Pediatrics, Kanagawa Children's Medical Center (Director: Seizo Suwa)Search for more papers by this authorEtsuro Tokuhiro, Etsuro Tokuhiro Department of Pediatrics, Kanagawa Children's Medical Center (Director: Seizo Suwa)Search for more papers by this authorHatae Maesaka, Hatae Maesaka Department of Pediatrics, Kanagawa Children's Medical Center (Director: Seizo Suwa)Search for more papers by this authorToshiaki Tanaka, Toshiaki Tanaka Department of Pediatrics, Kanagawa Children's Medical Center (Director: Seizo Suwa)Search for more papers by this author Seizo Suwa, Seizo Suwa Department of Pediatrics, Kanagawa Children's Medical Center (Director: Seizo Suwa)Search for more papers by this authorEtsuro Tokuhiro, Etsuro Tokuhiro Department of Pediatrics, Kanagawa Children's Medical Center (Director: Seizo Suwa)Search for more papers by this authorHatae Maesaka, Hatae Maesaka Department of Pediatrics, Kanagawa Children's Medical Center (Director: Seizo Suwa)Search for more papers by this authorToshiaki Tanaka, Toshiaki Tanaka Department of Pediatrics, Kanagawa Children's Medical Center (Director: Seizo Suwa)Search for more papers by this author First published: December 1978 https://doi.org/10.1111/j.1442-200X.1978.tb00171.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume20, Issue2December 1978Pages 57-57 RelatedInformation

Effect of single small dose Somatostatin/GRIF/ on growth hormone release in children

Twenty healthy children without any endocrine or metabolic disorders received 5 ug/kg bv:. cyclic GRIF in single dose i.v. Saline infusion was given to five children using control. The serum GH content was measured in the first three hours after the injection. The lowest values were obtaiaed in the fifth and the ninetieth minutes, the highest ones in the thirtieth, hundredfiftieth and hundred eightieth minutes. Eigtheen of twenty GH reserve was demonstrable./ 5 ng/ml/The difference between the effect of GRIF end saline was significant. Rebound of GH is described after a single /bolus/ small dose GRIF in healthy children with a standardized radioimmunoassay method. The suppression of GH secretion with exogenous GRIF can start a contraregulation in the way of CRF and the struggle between endojenous GRF and GRIF resultes in a second GH peak.

Evaluation of growth hormone release in children using arginine and L-dopa in combination.

L-Dopa in a dose ranging from 125-500 mg and arginine monochloride in a dose of 0.5 gm/kg were given simultaneously to 56 children with short stature (height less than third percentile). Sixteen of these children were subsequently diagnosed as having growth hormone deficiency. The diagnosis of hyposomatotropism was based on clinical findings and on responses to the combination test and to arginine and L-dopa administered as separate tests. All of the remaining 40 children had a normal GH response of greater than 6 ng/ml to the combination test. However, in this group, nine children were identified who responded to the combination test but who failed to respond to arginine and L-dopa in individual tests. The data suggest that a positive response to arginine and L-dopa in combination in children, who do not respond to the usual provocative tests when administered individually, may fail to identify children with partial GH deficiency who would benefit from treatment. The integrated stimulated GH response in the 31 children in whom a normal GH response to all three tests occurred suggests that the effects of L-dopa and arginine are additive.

Effect of L-dopa on the secretion of plasma growth hormone in children and adolescents.

SUMMARYThe stimulation of growth hormone release in children by L‐dopa has been studied. An oral dose of 0.5 g L‐dopa was administered to fourteen children with, and to fifteen children without, hypothalamic‐pituitary insufficiency. In the control group, L‐dopa induced a release of pituitary growth hormone, the peak of which occurred from 30 to 60 min after ingestion. Nine out of fifteen control subjects showed peak levels of plasma growth hormone greater than 8 ng/ml. None of the patients with hypothalamic‐pituitary insufficiency showed levels greater than 5 ng/ml. In five out of six children with measurable amounts of plasma HGH, and in fourteen children with a lack of HGH, there was a good correlation between the HGH response after L‐dopa, insulin hypoglycaemia and arginine infusion. It is concluded that the administration of one oral dose of L‐dopa can be used as a provocative test of growth hormone secretion.

Effect of synthetic beta 1–24 corticotropin on growth hormone release in children

Effect of synthetic beta 1–24 corticotropin on growth hormone release in children

Growth and growth hormone. 3. Growth hormone release in children with primary hypothyroidism and thyrotoxicosis.

ABSTRACT Growth hormone release was assessed utilizing insulin-induced hypoglycemia and arginine infusion in 13 children with primary hypothyroidism and in 10 patients with thyrotoxicosis. In the hypothyroid group there were 6 blunted and 7 normal responses, with a mean peak concentration of serum growth hormone (SGH) of 7.9 ng/ml which differed significantly from the controls (p<.02). The hypothyroid patients also exhibited a delayed peak in SGH compared to normal subjects. There was no correlation between the severity or duration of the hypothyroidism and growth hormone response. It was shown that thyroid deficiency is inconstantly associated with an abnormal growth hormone response to insulin-induced hypoglycemia and arginine infusion which was reversible after treatment with thyroid hormone. The impaired growth hormone release found in some patients with primary hypothyroidism may be indistinguishable from that observed in hypo pituitary subjects. The growth hormone response in the group of children w...