Growth Hormone (GH) Provocative Testing Frequently Does Not Reflect Endogenous GH Secretion*

Bercu, Barry B.; Shulman, Dorothy I.; Root, Allen W.; Spiliotis, Bessie E.

doi:10.1210/jcem-63-3-709

Cited by 242 publications

(100 citation statements)

References 26 publications

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“…It has been suggested that some children with idiopathic short stature (ISS), including familial short stature and/or constitutional delay, may have a low spontaneous GH secretion in contrast to normal serum GH responses to provocative testing, a condition called 'GH neurosecretory dysfunction' (Bercu et al, 1986;Spiliotis et al, 1984). Although this term cannot be clearly defined, even less adequately than the term G H deficiency (GHD), GH secretion certainly varies among the children with ISS and it is suggested that some of these children may produce less G H than they need for adequate growth (AlbertssonWikland & Rosberg, 1988;Zadik et al, 1992a).…”

Section: Discussionmentioning

confidence: 99%

Long‐term results of growth hormone therapy in children with short stature, subnormal growth rate and normal growth hormone response to secretagogues

Wit

Boersma

Keizer-Schrama³

et al. 1995

Clinical Endocrinology

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Summary BACKGROUND AND OBJECTIVE Growth hormone treatment In children with Idiopathic short stature (ISS) leads to growth acceleration in the first years, but the effect on final height is still poorly documented. We therefore studied the long‐term effect of GH therapy in children with Idiopathic short stature. DESIGN We have treated 27 prepubertal children with ISS with recombinant human GH (rhGH) in an initial dosage of 2 IU/m2 body surface/day subcutaneously, which was doubled either after the first year if the height velocity increment was less than 2 cm/year, or thereafter if height velocity fell below the P50 for bone age. Growth and bone maturation of the treatment group (ISS group, n= 21) were compared to those of an untreated control group with ISS (ISS controls, n= 27) and of a group of rhGH treated children with isolated GH deficiency (GHD group, n= 7). RESULTS In 9 patients of the ISS group still on treatment, height standard deviation score (HSDS) for chronological age increased from −3.8±0.7 to −2.3±0.9 (mean±standard deviation) over 6 years, while in matched ISS controls HSDS for age did not change. HSDS for age in the GHD group increased from −3.9±0.6 to −1.8±0.7 after 4 years, significantly more than the ISS group. Bone maturation was accelerated In the ISS and GHD groups. HSDS for bone age and predicted adult height did not change in either group. Final height in 12 children of the ISS group was −2.6±1.0 SDS. In the untreated controls final height was similar. A low integrated GH concentration over 24 hours, a low GH peak to provocative stimuli, and minimal initial BA delay predicted a favourable outcome. CONCLUSION rhGH treatment In this group of children with Idiopathic short stature did not increase average final height. Part of the heterogeneity of the response can be attributed to the variation in endogenous GH secretion and initial bone age delay.

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Section: Discussionmentioning

confidence: 99%

Long‐term results of growth hormone therapy in children with short stature, subnormal growth rate and normal growth hormone response to secretagogues

Wit

Boersma

Keizer-Schrama³

et al. 1995

Clinical Endocrinology

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“…However, this should be partly compensated for by the design of this study with age-and sex-matched healthy controls. The evaluation of 12 or 24 h GH profiles has been suggested to be superior to stimulation tests (37,38), but this is still controversial (39).…”

Section: Cf-ngt Cf-dm Cf-ngt and Cf-dmmentioning

confidence: 99%

Normal spontaneous and stimulated GH levels despite decreased IGF-I concentrations in cystic fibrosis patients

Laursen¹,

Lanng

Rasmussen

et al. 1999

European Journal of Endocrinology

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Objective: The aim of the present study was to investigate whether patients with cystic fibrosis (CF) are GH resistant with increased GH release and decreased concentrations of IGF-I as a result of malabsorption, increased catabolism and impaired glucose tolerance. Design: Twenty CF patients were included, ten with normal glucose tolerance (five male, five female, median age 25.5 years (range 20-31)) and ten with diabetes mellitus (five male, five female, median age 25.3 years (range 17-45). Twenty healthy individuals served as controls (ten male, ten female, median age 28.4 years (range 18-36)). Methods: GH status was evaluated by 12 h spontaneous GH release during the night time, argininestimulated GH release and the basal concentrations of IGF-I and insulin-like growth factor-binding protein-3 (IGFBP-3). Twelve hour spontaneous GH profiles were estimated using a constant blood withdrawal technique with sampling every 30 min and the Pulsar method was used for the analysis of profiles. Results: No significant differences were found in spontaneous and stimulated GH release in CF patients compared with healthy controls, whereas IGF-I and IGFBP-3 were significantly decreased in CF patients compared with healthy controls. The combination of reduced IGF-I and IGFBP-3 with normal GH release points to a relative GH resistance or a disturbance in the pituitary axis in patients with CF. The spontaneous GH release, the stimulated GH release and the basal concentrations of IGF-I and IGFBP-3 were not significantly different in diabetic CF patients compared with CF patients with normal glucose tolerance and the presence of diabetes mellitus was not consistent with increased GH resistance in CF patients. Conclusion: CF patients with normal glucose tolerance and diabetic CF patients had normal GH release and decreased concentrations of IGF-I indicating a relative GH resistance.

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“…Because blood IGF-1 reveals overall GH secretion during the period of prior 24 hrs and minimally fluctuates over this period [5][6][7], its concentration has been a reliable indicator of GH secretion [1,3,8]. Thus, the recent criteria for surgical cure of acromegaly mandate normalization of IGF-1.…”

mentioning

confidence: 99%

Gradual declination of IGF-1 over a year after transsphenoidal adenomectomy of GH producing pituitary adenomas

et al. 2011

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InsulIn-lIke growth factor-1 (IGF-1), primarily produced in the liver under the control of growth hormone (GH) [1][2][3][4], mediates most of the major activities of GH [1,2]. Because blood IGF-1 reveals overall GH secretion during the period of prior 24 hrs and minimally fluctuates over this period [5][6][7], its concentration has been a reliable indicator of GH secretion [1,3,8]. Thus, the recent criteria for surgical cure of acromegaly mandate normalization of IGF-1. In the previous report, we showed that the decrease in IGF-1 was slower in operated acromegalic patients than would be expected from the half-life of the carrier protein-bound peptide [9]. And we suggested that this slow decline allows us to postpone decisions regarding the patients' postoperative status and the administration abstract. To know the longitudinal shift of blood IGF-1 of cured acromegaly, we conducted retrospective survey of changes in blood IGF-1 over two years, which has not been previously investigated. Blood IGF-1 levels were measured for longer than 2 years after TSS in 37 patients whose nadir GH during postoperative oral glucose tolerance test (OGTt) was under 1 ng/mL. Blood IGF-1 very gradually declined after three months; 230.6 (mean) ng/mL at 3-12 months, 202.3 ng/mL at 12-24 months, and 198.6 ng/mL at 24-36 months. Their SD values, calculated based on standard IGF-1 values of age-and sex-matched Japanese population, also slowly decreased after three months; 1.69 (mean) at 3-12 months, 1.23 at 12-24 months, and 1.12 at 24-36 months. Very slow decrease of the IGF-1 levels continued beyond the first several months and even the first year after TSS. The declination of values is greater than that associated with aging. This declination may be at least partially a reflection of the slow decrease and late normalization of GH secretion.Key words: Acromegaly, Insulin-like growth factor-1 (IGF-1), Growth hormone, Declination, Transsphenoidal surgery of additional therapy for at least one month after surgery. Since then, we have been monitoring the IGF-1 fluctuations in postoperative acromegalic patients and have observed that IGF-1 very gradually decreased over a year in some patients. In order to know the longitudinal shift of the IGF-1, if any, we retrospectively assessed the blood IGF-1 levels serially for more than two years in postoperative acromegalics. Materials and Methods Subjects and methodPatients were 37, 12 males and 25 females, acromegalics who underwent transsphenoidal surgery since 2001 to 2008, whose nadir GH during postoperative OGTt was under 1 ng/mL, and in whom IGF-1 levels were serially measured over two years. The patients' ages ranged from 20 to 76 years (53.5±11.7, mean±SD). The mean preoperative IGF-1 level was 895.0 ± 360.1 (SD) ng/mL. The IGF-1 levels were measured during 1-4 weeks, 1-3 months, 3-12 months, 12-24 months,

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Growth Hormone (GH) Provocative Testing Frequently Does Not Reflect Endogenous GH Secretion*

Cited by 242 publications

References 26 publications

Long‐term results of growth hormone therapy in children with short stature, subnormal growth rate and normal growth hormone response to secretagogues

Long‐term results of growth hormone therapy in children with short stature, subnormal growth rate and normal growth hormone response to secretagogues

Normal spontaneous and stimulated GH levels despite decreased IGF-I concentrations in cystic fibrosis patients

Gradual declination of IGF-1 over a year after transsphenoidal adenomectomy of GH producing pituitary adenomas

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