Short-term studies (3-6 mo) of GH replacement have failed to demonstrate an increase in bone mass (13,31-33). In several studies reduced BMD has been recorded following six months GH therapy (32,34), but after more than 12 mo treatment increases of 4-10% above baseline have been demonstrated (30,32).
Markers of serum bone formation (osteocalcin, bone alkaline phosphatase, bone Gla protein, carboxyterminal propeptide of type 1 procollagen = PICP) and urinary bone resorption markers (deoxypyridinoline, pyridinoline, crosslinked telopetide of type 1 collagen = ICTP) increased in both short-term and long-term studies indicating an activation of bone remodelling (13,30-34).
In summary, adult GH-deficiency is associated with reduced bone mass as assessed by bone mineral density measurements. The available data provide evidence that GH is an osteo-anabolic hormone when given to GH-deficient adults. The findings in most of the trials suggest that GH has a biphasic effect: following an initial predominance of bone resorption, stimulation of bone formation leads to a net gain in bone mass after 12-24 mo of treatment.
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