BENEFITS OF GROWTH-HORMONE TREATMENT ON BONE METABOLISM, BONE-DENSITYAND BONE STRENGTH IN GROWTH-HORMONE DEFICIENCY AND OSTEOPOROSIS

Bone mass is reduced in patients with GH deficiency (GHD) leading to a n increased vertebral fracture rate and clinically significant osteopo rosis. Patients with GHD of juvenile onset have reduced skeletal miner alization. When substituting GH in patients with GHD, bone turnover is increased and bone mineral density initially decreases during the fir st year due to the increase in remodelling space. From the experience in patients with acromegaly, cortical bone mass is increased and trabe cular bone mass is normal in eugonadal or decreased in the hypogonadal patients. However, bone mineral content and bone area are increased l eading to a higher biomechanical competence of bone as shown in rats. In patients with GHD of juvenile onset, mineralization and bone matura tion are achieved during treatment with GH in adult life after having reached final body height leading to an increase in bone mass. The GH/ IGF-I system is dysregulated in patients with post-menopausal osteopor osis. This is shown by reduced systemic IGF and IGFBP-3-levels in oste oporosis suggesting a decrease of endogenous GH-secretion or a dysregu lation of the GH receptor system which is beyond the normal ageing pro cess of the GH/IGF system, the ''somatopause''. A premature somatopaus e may be responsible for the dysregulation in some patients with osteo porosis. However, 24-h GH profiles do not differ between patients suff ering from osteoporosis or osteoarthritis. Treatment of osteoporosis w ith GH might be beneficial due to the increased bone metabolism and im proved bone geometry which occurs with GH. The substantial increase of bone remodelling achieved with GH may be helpful during late post-men opause with decreased bone turnover and impaired osteoblastic function . Using GH to prevent physiological bone loss that occurs with age see ms possible, but has to be discussed on an ethical and economic basis. (C) 1998 Churchill Livingstone.