CONSEQUENCES OF CHILDHOOD-ONSET GROWTH-HORMONE DEFICIENCY FOR ADULT BONE MASS

Citation
H. Deboer et al., CONSEQUENCES OF CHILDHOOD-ONSET GROWTH-HORMONE DEFICIENCY FOR ADULT BONE MASS, Journal of bone and mineral research, 9(8), 1994, pp. 1319-1326
Citations number
30
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
08840431
Volume
9
Issue
8
Year of publication
1994
Pages
1319 - 1326
Database
ISI
SICI code
0884-0431(1994)9:8<1319:COCGDF>2.0.ZU;2-G
Abstract
To assess the implications of prolonged growth hormone deficiency (GHD ) for the acquisition and maintenance of bone mass, bone mineral densi ty (BMD) was measured in 70 adult males (mean age 26.7 +/- 4.5 years) with childhood-onset GHD, 7.4 +/- 4.2 years after discontinuation of p revious GH therapy. Because most of these patients were short (mean he ight 165.8 +/- 6.6 cm), the influence of body height on standard BMD m easurements, conventionally reported as the areal density (BMD(area), expressed in g/cm(2)), was analyzed in a group of age-matched healthy males. In GHD patients, BMD(area) was significantly reduced at the lum bar spine (Z score -1.59 +/- 1.08, p < 0.001) as well as at the nondom inant hip (Z score -1.18 +/- 0.95,p < 0.001). The reduction in BMD(are a) was similar for patients with isolated GHD (N = 25) and those with combined deficiencies of GH and luteinizing hormone (N = 40). In patie nts and controls, BMD(area) was positively correlated with body height , a relation that was attributed to skeletal size. Bone dimensions wer e significantly smaller in patients than in controls, and therefore it was hypothesized that the difference in areal density between patient s and controls might be confounded by differences in bone size. Measur ed bone mineral content corrected for the estimated bone volume (BMD(v olume), expressed in g/cm(3)) remained significantly reduced (Z score: lumbar spine, -0.90 +/- 1.08, p < 0.001; femoral neck, -0.74 +/- 1.00 , p < 0.001), but the differences between GHD patients and controls we re less than indicated by BMD(area) (p < 0.01). We conclude that the l ow BMD(area) in our patient population can be explained in part by the ir subnormal body height. However, after correction for the effect of body height-related differences in bone volume, bone density was still significantly reduced. This indicates that in adult males with childh ood-onset GHD a moderate degree of osteopenia is present. Insufficient bone acquisition during childhood years is considered the primary cau se of the observed reduction in bone density.