Prevention of bone demineralization by calcium supplementation in precocious puberty during gonadotropin-releasing hormone agonist treatment

Citation
F. Antoniazzi et al., Prevention of bone demineralization by calcium supplementation in precocious puberty during gonadotropin-releasing hormone agonist treatment, J CLIN END, 84(6), 1999, pp. 1992-1996
Citations number
43
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
84
Issue
6
Year of publication
1999
Pages
1992 - 1996
Database
ISI
SICI code
0021-972X(199906)84:6<1992:POBDBC>2.0.ZU;2-5
Abstract
We have previously demonstrated a negative impact on peak bone mass in girl s with precocious puberty treated with GnRH agonist (GnRHa). Several studie s have shown that a high calcium intake positively influences bone mass in prepubertal girls and leads to a higher peak bone mass. The aim of this stu dy was to evaluate the effect of calcium supplementation in girls with prec ocious puberty during GnRHa treatment. Forty girls affected by true central precocious puberty and treated with th e GnRHa triptorelin were studied for 2 yr. After diagnosis, the patients me re randomly assigned to three groups: group A, treated only with GnRHa; gro up B, treated for 12 months solely with GnRHa and then supplemented with ca lcium gluconolactate/carbonate (1 g calcium/day in two doses) for 12 months ; and group C, treated from the beginning with combined GnRHa and calcium. Bone mineral density (BMD) at the lumbar spine was measured by dual energy x-ray absorptiometry at the beginning of the study and after 12 and 24 mont hs and was expressed as the calculated true volumetric density (BMDv) in mi lligrams per cm(3). Group A showed a decrease in absolute BMDv levels, in so score for chronolo gical age (CA), and even more in so score for bone age (BA). Group B showed the same behavior during the first year, but this trend was reversed in th e second year, when calcium supplementation was added to GnRHa treatment. G roup C showed an increase in absolute BMDv levels and in so score for CA an d BA. BMDv variations (expressed as absolute values, so score for CA, and s o score for BA) became statistically significant at 24 months between group s C and A (P = 0.036, P = 0.032, and P = 0.025, respectively). The behavior of the lumbar spine BMDv in the three groups is consistent wit h a positive effect of calcium supplementation during GnRHa treatment. In c alcium-supplemented patients, the normal process of bone mass accretion at puberty is preserved despite GnRHa treatment. Therefore, the reduction in B MD during GnRHa treatment in girls with precocious puberty is at least comp letely reversible and preventable if calcium supplementation is associated from the beginning.