Conclusions

A broad range of experimental data confirm that GH plays an important role in preserving the skeleton. GHD attributable to pituitary disease is associated with osteoporosis. Because of this it has been hypothesized that the decline in bone density seen in aging is attributable to declining GH secretion. In vitro, GH stimulates osteoblast proliferation and collagen production. Evidence from clinical studies indicates that GH replacement in GH-deficient adults improves bone density, though it is unclear whether this finding will be applicable to the relative GHD of aging.

Although the clinical use of GH in adults with GHD has been approved in the United States and Europe, a number of important questions remain unanswered. First, standards regarding the diagnosis of GHD must be established. Second, the best parameter to determine physiologic versus pharmacologic GH dosing is unknown. Third, the role, if any, of GH therapy in the treatment of osteoporosis in GH sufficient patients remains to be determined. Studies of GH administration to date have evaluated the hormone's effect on markers of bone turnover and bone density. The principal functional consequence of osteoporosis, however, is pathologic fracture, a potentially disabling or fatal condition. Larger studies of more prolonged duration will be required to determine whether GH administration affects this critical clinical endpoint.

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