1,721,101 research outputs found
Bone status in children and adolescents with growth hormone deficiency: effect of growth hormone treatment
No full textEffect of GH treatment on bone mass in children with GH deficiency.
No full textChildren with GH deficiency have reduced bone mass and mineral density in comparison with normal individuals. GH treatment improves the accrual of bone mass during childhood and adolescence, but suboptimal GH treatment may cause a reduced bone mass in adulthood. At final height, treated patients with GH deficiency have normal mean values of bone mass, but some patients showed reduced lumbar bone mineral density (BMD) values. Lumbar peak bone mass (PBM) in treated patients who discontinued the treatment at final height is delayed and reduced. GH treatment during the transition from late adolescence to young adulthood can increase bone mass and mineral density. In patients with GH deficiency a possible strategy for avoiding acquisition of a suboptimal bone mass in the young-adult, could be to continue GH treatment during the transition to adulthood up to the acquisition of PBM
Hypophosphataemic rickets
No full textX-Linked hypophosphataemic rickets (XLH) is frequently associated with short stature even when conventional treatment (1,25-dihydroxyvitamin D-3 or 1 alpha-hydroxyvitamin D-3 plus inorganic phosphate salts) is administered for a long time. The pathogenesis of growth retardation is probably multifactorial. Affected patients usually show normal growth hormone (GH) secretion. in some poorly growing XLH patients, long-term GH treatment associated with conventional therapy improves linear growth. GH treatment also increases phosphate retention but th is effect is transient. Copyright (C) 2000 S. Karger AG, Basel
Critical ages and stages of puberty in the accumulation of spinal and femoral bone mass: The validity of bone mass measurements
No full textIn growing children, lumbar and femoral areal bone mineral density (aBMD), as measured by dual-energy X-ray absorptiometry (DXA), is influenced by skeletal growth and bone size. Correction of lumbar bone mineral density (BMD) for bone volume (volumetric BMD [vBMD]), by the use of mathematical extrapolations, reduces the confounding effect of bone size, but vBMD remains dependent on age and bone size during growth. Femoral (neck and mid-shaft) vBMD, assessed by DXA, is independent of age prior to puberty, but a slight increase occurs in late puberty and after menarche. Femoral (mid-shaft) cortical bone density and radial cortical and trabecular bone densities, assessed by quantitative computed tomography (QCT), show no peak during childhood or adolescence. Bone strength index, calculated by peripheral QCT, increases with age and correlates with handgrip strength, bone cross-sectional area and cortical area. Puberty is one of the main factors that influences lumbar bone mineral content and aBMD accumulation, but a high incidence of fractures occurs during this period of life, which may be associated with a reduced aBMD. Copyright (C) 2000 S. Karger AG. Basel
Bone mineral density and biochemical parameters of bone turnover in children with growth hormone deficiency
No full textGrowth hormone (GH) is a crucial factor in the build-up and in the maintenance of peak bone mass. Children with GH deficiency have osteopenia and a concomitant reduction in bone turnover. On the other hand, GH therapy improves bone mineral density and stimulates bone turnover. These data suggest that GH treatment may have a beneficial effect on peak bone mass. In children with GH deficiency, the values of some biochemical markers of bone turnover may be closely related to growth response during GH therapy. However, further studies are needed to define the usefulness of bone markers in order to optimize the treatment and to predict the growth outcome in GH-treated children
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