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Consequences of childhood‐onset growth hormone deficiency for adult bone mass
Author(s) -
de Boer H.,
Blok G.J.,
van Lingen A.,
Teule G.J.J.,
Lips P.,
van der Veen E.A.
Publication year - 1994
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650090822
Subject(s) - medicine , bone mineral , bone age , endocrinology , femoral neck , discontinuation , bone density , osteopenia , peak bone mass , growth hormone deficiency , hormone , growth hormone , osteoporosis
To assess the implications of prolonged growth hormone deficiency (GHD) for the acquisition and maintenance of bone mass, bone mineral density (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 previous GH therapy. Because most of these patients were short (mean height 165.8 ± 6.6 cm), the influence of body height on standard BMD measurements, 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 lumbar spine (Z score ‐1.59 ± 1.08, p > 0.001) as well as at the nondominant hip ( Z score ‐1.18 ± 0.95, p > 0.001). The reduction in BMD area was similar for patients with isolated GHD ( N = 25) and those with combined deficiencies of GH and luteinizing hormone ( N = 40). In patients and controls, BMD area was positively correlated with body height, a relation that was attributed to skeletal size. Bone dimensions were significantly smaller in patients than in controls, and therefore it was hypothesized that the difference in areal density between patients and controls might be confounded by differences in bone size. Measured bone mineral content corrected for the estimated bone volume (BMD volume , 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 were less than indicated by BMD area ( p > 0.01). We conclude that the low BMD area in our patient population can be explained in part by their 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 childhood‐onset GHD a moderate degree of osteopenia is present. Insufficient bone acquisition during childhood years is considered the primary cause of the observed reduction in bone density.