DIFFERENTIAL DIAGNOSIS BETWEEN HYPOTHALAMIC AND PITUITARY hGH DEFICIENCY WITH THE AID OF SYNTHETIC GH‐RH 1–44

Laron, Zvi; Keret, R; Bauman, B; Pertzelan, A; Ben-Zeev, Z.; Olsen, D. B.; Comaru-Schally, A. M.; Schally, Andrew V.

doi:10.1111/j.1365-2265.1984.tb00130.x

Cited by 31 publications

(8 citation statements)

References 5 publications

(6 reference statements)

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“…Both our findings and those reported in the literature (Laron et al 1984;Pintor et al 1983;Takano et al 1984) show that the GH response to GRH in CAPD (Perfumo et al 1985) and in CT is more marked than in normal children. The same has been found for adults ).…”

Section: Discussionsupporting

confidence: 83%

Growth hormone response to growth hormone-releasing hormone in normal and uraemic children. Comparison with hypoglycaemia following insulin administration

Bessarione¹,

Perfumo²,

Giusti³

et al. 1987

Acta Endocrinologica

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The uraemic syndrome is characterized by several endocrinological disturbances. This study was undertaken in order to evaluate the GH response to growth hormone-releasing hormone (GRH) in children with chronic renal failure (CRF) and to compare the results with those observed after insulin hypoglycaemia. Twenty-two children with CRF, 10 undergoing continuous ambulatory peritoneal dialysis (CAPD) and 12 on conservative treatment (CT), age ranges 2\p=n-\15 years, were studied and the data were compared with those from 14 children with normal renal function and normal hormonal behaviour, affected by short stature (NC), and those form 13 healthy adult volunteers (NA). The GRH test (1 \g=m\g/kgbody weight, iv) was carried out in 8 CAPD, 8 CT, 9 NC and 10 NA subjects. The blood samples were taken every 30 min for 3 h in CAPD and CT and for 2 h in NC and NA starting at 09.00 h. The following hormones were measured: GH, LH, FSH, Prl, TSH and cortisol (F). The insulin test (0.1 U/kg body weight, iv) was carried out in 5 CAPD, 5 CT, 10 NC and 9 NA on blood samples taken every 30 min for 2 h, measuring GH and glycaemia. No adverse effects were observed after the infusion of GRH. GRH administration induced a prompt response in all subjects, but GH plasma levels were significantly higher in uraemic children than in adults (peak value of 43.5 \ m=+-\ 8.2, 45.0 \ m=+-\ 8.4, 27.8 \ m=+-\ 6.0; 13.5 \ m=+-\ 2.6 \g=m\g/ml in CAPD, CT, NC and NA, respectively). The secretory areas were significantly narrower in NC (P < 0.05) and NA (P < 0.01) than in CAPD, and in NA than in CT (P < 0.01). The GH response to insulin did not differ in the 4 groups. The secretory area in CAPD and CT was wider after GRH than after insulin. The GH peak value of CAPD and NC was significantly higher after GRH than following insulin. No significant variation in TSH, LH and FSH was observed after the infusion of the neuropeptide, whereas Prl and F showed a reduction.The behaviour of Prl and F in NA and NC was similar after placebo and GRH.Our data show: a) There is a greater response of GH to GRH in children than in adults; b) compared with the insulin test, GRH stimulation seems to be a reliable means of evaluating GH secretion both in normal and uraemic children owing to the absence of qualitatively different responses and to the freedom from the adverse effects or risks which follow insulin infusion; c) GRH administration does not induce any significant variation on other hypophyseal hormones and the reduction of Prl and F seems to follow the normal sl eep\ x=req-\ wake and circadian behaviour.

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Section: Discussionsupporting

confidence: 83%

Growth hormone response to growth hormone-releasing hormone in normal and uraemic children. Comparison with hypoglycaemia following insulin administration

Bessarione¹,

Perfumo²,

Giusti³

et al. 1987

Acta Endocrinologica

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show abstract

“…In both our patients, a GH response was seen after GRF-44 but not during ITT or gluca¬ gon stimulation, suggesting a hypothalamic defect in GH release (Laron et al 1984). A positive but subnormal response to GRF has been previously reported in 2 other patients with septo-optic dys¬ plasia and growth hormone deficiency (Schriock et al 1984).…”

Section: Discussionmentioning

confidence: 81%

Hypothalamic defects in two adult patients with septo-optic dysplasia

Lam

Wang

et al. 1986

Acta Endocrinologica

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Two adult patients with unilateral hypoplastic optic nerves, absent septa pellucida and hypopituitarism are described. Patient 1, aged 20, presented with diabetes insipidus due to partial vasopressin deficiency. Patients 2, aged 29, presented with focal epilepsy. Both had short stature. They showed absent growth hormone (GH) response to insulin-hypoglycaemia or glucagon, but responded to 100 \g=m\ggrowth hormone releasing factor (GRF-44) with a rise in circulating GH, suggesting a hypothalamic defect in GH release though a co-existing pituitary defect cannot be excluded. Other hypothalamic-pituitary functions were normal. These two patients probably represent the milder form of the clinical spectrum of septo-optic dysplasia which, with the extensive use of CT brain scans, will be increasingly encountered by physicians attending adult patients.

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“…The isolation of GHRH has led to the widespread use of the synthetic peptide and analogs in the evaluation of the somatotroph axis (27)(28)(29). Although such compounds provide important information as to pituitary responsiveness and can indirectly discriminate between hypothalamic and pituitary causes of GH deficiency (30), further assessment could be made if indirectly acting secretagogues that activate hypothalamic pathways regulating GH release displayed greater reproducibility and were better tolerated.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Growth Hormone Release in Man by the Potent D2-Dopamine Agonist CV 205-502: Comparison of Responses to Intravenous and Oral Administration*

Miell

Pralong²,

Corder³

et al. 1990

The Journal of Clinical Endocrinology & Metabolism

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It is well known that dopaminergic agents are stimulators of GH release in man, and although responses are sometimes unreliable, oral L-dopa and iv dopamine have frequently been employed in the evaluation of GH-deficient states. To assess the effects on GH secretion of a new potent D2-dopamine agonist, the octahydrobenzo(g)quinoline CV 205-502 (CV) we have investigated the GH responses in healthy male volunteers to four different iv doses. For this purpose 3 separate groups of 9 subjects were studied. The respective groups were administered on separate occasions 10 micrograms CV and placebo (group 1), 5 micrograms, 2.5 micrograms, and placebo (group 2), and 1 microgram and placebo (group 3). Each subject received drug and placebo in a double blind randomly assigned order, with at least 5 days between their administration. Active compound or placebo was infused over 30 min, and blood sampling was carried out for 72 h after cessation of infusion. Peak GH levels occurred between 45-60 min after the end of the infusion; the observed maximum GH concentrations were 19.2 +/- 2.9 micrograms/L (10 micrograms, iv; P less than 0.001 vs. placebo), 9.61 +/- 2.1 (5 micrograms, iv; P less than 0.001 vs. placebo), 4.7 +/- 1.7 (2.5 micrograms, iv; P less than 0.05 vs. placebo), and 1.9 +/- 0.8 micrograms/L (1 micrograms, iv; P = NS vs. placebo). The mean integrated GH secretion expressed in arbitrary units [area under the response curve (AUC)] up to 3 h postinfusion showed a typical dose-response relationship. Mean values were 1715 +/- 269.4 (10 micrograms, iv; P less than 0.001 vs. placebo), 956.1 +/- 189.9 (5 micrograms, iv; P less than 0.001 vs. placebo), 312.8 +/- 105.8 (2.5 micrograms, iv), and 162.8 +/- 47.5 (1 microgram, iv). In a second study with a separate group of 18 volunteers, we compared the GH response to an oral dose of 100 micrograms CV with those to 5 micrograms CV given iv and placebo treatment. Peak GH values in this study were 20.3 +/- 5.5 micrograms/L (100 micrograms, orally; P less than 0.01 vs. placebo) and 14.6 +/- 2.8 (5 micrograms, iv; P less than 0.001 vs. placebo). Maximum levels occurred 45 min after the infusion and 90 min after ingestion (60 min relative to the end of the infusion).(ABSTRACT TRUNCATED AT 400 WORDS)

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DIFFERENTIAL DIAGNOSIS BETWEEN HYPOTHALAMIC AND PITUITARY hGH DEFICIENCY WITH THE AID OF SYNTHETIC GH‐RH 1–44

Cited by 31 publications

References 5 publications

Growth hormone response to growth hormone-releasing hormone in normal and uraemic children. Comparison with hypoglycaemia following insulin administration

Growth hormone response to growth hormone-releasing hormone in normal and uraemic children. Comparison with hypoglycaemia following insulin administration

Hypothalamic defects in two adult patients with septo-optic dysplasia

Stimulation of Growth Hormone Release in Man by the Potent D2-Dopamine Agonist CV 205-502: Comparison of Responses to Intravenous and Oral Administration*

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