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Impaired GH secretion to provocative stimuli in two families with hypocalciuric hypercalcaemia.

Authors :
Cecconi, Elisabetta
Bogazzi, Fausto
Cetani, Filomena
Grasso, Lucia
Marcocci, Claudio
Genovesi, Maura
Procopio, Massimo
Gasperi, Maurizio
Pinchera, Aldo
Ghigo, Ezio
Martino, Enio
Source :
Clinical Endocrinology. Nov2003, Vol. 59 Issue 5, p604. 3p.
Publication Year :
2003

Abstract

To determine whether hypercalcemia per se might be responsible for an impairment in GH secretion. Prospective study. Six subjects of two unrelated families with familial hypocalciuric hypercalcaemia (FHH), an autosomal dominant disorder due to inactivating mutations in the calcium receptor gene, leading to an increase in serum calcium levels and inappropriately normal serum PTH concentrations. Forty normal subjects, matched for sex and age served as controls. Serum GH concentrations were measured after GHRH-Arginine (GHRH-Arg) stimulation test; serum IGF-I, ACTH, cortisol, FT4, FT3, TSH, PRL, LH, FSH levels were measured under basal conditions. All subjects (two male, four female, age range 24–74 years) had increased serum ionized calcium levels (range 1·36–1·56 mmol/l) and five of six patients had normal PTH levels (range for all patients was 14–68 ng/l). Basal serum GH concentrations ranged from 0·1 to 7·0 µg/l. Mean serum GH secretory peak after GHRH-Arg stimulation test was reduced in five subjects (mean 9·3 ± 3·6 µg/l, P < 0·006 vs. Controls, mean 67·0 ± 44·0 µg/l, cut-off, 16·0 µg/l) and normal in one subject (38·7 µg/l). However, serum IGF-I levels were reduced only in two patients (29 and 57 µg/l) and normal in four subjects (range 127–208 µg/l). The basal secretion of the other anterior pituitary hormones was within their normal ranges. The results of the present study support the concept that elevated serum calcium levels impair GH secretion. However, the clinical relevance of GH deficiency in FHH remains to be elucidated. [ABSTRACT FROM AUTHOR]

Subjects

Subjects :
*HYPERCALCEMIA
*SOMATOTROPIN

Details

Language :
English
ISSN :
03000664
Volume :
59
Issue :
5
Database :
Academic Search Index
Journal :
Clinical Endocrinology
Publication Type :
Academic Journal
Accession number :
11168261
Full Text :
https://doi.org/10.1046/j.1365-2265.2003.01891.x