title: Impaired GH secretion to provocative stimuli in two families with hypocalciuric hypercalcaemia.
abstract: OBJECTIVE
  To determine whether hypercalcemia per se might be responsible for an impairment in GH secretion.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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 micro g/l. Mean serum GH secretory peak after GHRH-Arg stimulation test was reduced in five subjects (mean 9.3 +/- 3.6 microg/l, P < 0.006 vs. Controls, mean 67.0 +/- 44.0 microg/l, cut-off, 16.0 microg/l) and normal in one subject (38.7 microg/l). However, serum IGF-I levels were reduced only in two patients (29 and 57 microg/l) and normal in four subjects (range 127-208 microg/l). The basal secretion of the other anterior pituitary hormones was within their normal ranges.
  
  
  CONCLUSIONS
  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.
authors: Department of Endocrinology and Metabolism, University of Pisa, Pisa, Italy.
authors: Elisabetta
authors: E
authors: Cecconi
authors: Fausto
authors: F
authors: Bogazzi
authors: Filomena
authors: F
authors: Cetani
authors: Lucia
authors: L
authors: Grasso
authors: Claudio
authors: C
authors: Marcocci
authors: Maura
authors: M
authors: Genovesi
authors: Massimo
authors: M
authors: Procopio
authors: Maurizio
authors: M
authors: Gasperi
authors: Aldo
authors: A
authors: Pinchera
authors: Ezio
authors: E
authors: Ghigo
authors: Enio
authors: E
authors: Martino
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000368:Aged; D001120:Arginine; D002118:Calcium / Q000652:urine*; D016022:Case-Control Studies; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D013007:Growth Hormone-Releasing Hormone; D019382:Human Growth Hormone / Q000097:blood / Q000172:deficiency*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006934:Hypercalcemia / Q000503:physiopathology*; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D011388:Prolactin / Q000097:blood; D011446:Prospective Studies; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D014284:Triiodothyronine; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013007:Growth Hormone-Releasing Hormone; D001120:Arginine; D013974:Thyroxine; D002118:Calcium; D006854:Hydrocortisone