ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 P427

Is increase in bone mineral content caused by increase in skeletal muscle mass/strength in adult patients with growth hormone (GH) treated GH deficiency? A litterature analysis

Oliver Niels Klefter & Ulla Feldt-Rasmussen

National University Hospital, Copenhagen, Denmark.

Growth hormone (GH) has a well known anabolic effect on skeletal muscles, and patients with GH deficiency (GHD) are characterised by a reduced muscle mass, but also reduced bone mineral density (BMD) and content (BMC), which have been ascribed to GHD per se. Correspondingly, the increase in bone and muscle mass by GH therapy has been seen as separate GH influences on bones and muscles, respectively. The aim of this study was therefore to investigate if changes in BMD/BMC in adult patients with GHD could be due to a muscle modulating effect, and if treatment with GH would primarily increase muscle mass and strength with a secondary increase in BMD, thus supporting the current physiological concept that mass and strength of bones are mainly determined by dynamic loads from the skeletal muscles.

A literature review resulted in 34 clinical trials, published during the period 1996–2006, and fulfilling the criteria for investigating variables related to the development in muscle mass, muscle strength, and BMC/BMD in adult GHD patients treated with GH.

Three out of four trials found significant increases in muscle mass compared to baseline, while eight out of 11 trials found significant increases in one or more measures of muscle strength compared to baseline. The largest increase in muscle mass was observed during the first 12 months of treatment. Nineteen out of 26 trials found significant increases from baseline values in BMC or BMD in one or more body regions. The significant increases in BMD and BMC occurred after 12–18 months of treatment, i.e. usually later than the increase in the muscle measurements. Only 5 clinical trials studied both muscle and bone variables concomitantly in GH treated adult GHD patients. None of these studied the relationship between the changes in muscle and bone measurements.

In conclusion, although in vitro studies have shown that GH has a direct effect on bone remodelling, current physiological concepts and the results of clinical trials from the past 10 years suggest that the anabolic changes in muscle mass and muscle strength may also contribute to changes in BMC and BMD in the GH treated adult GHD patients. Studies addressing this particular issue are, however, needed to clarify the relative contribution of mechanisms.

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