Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2009) 20 S10.1

Secondary osteoporosis

Growth hormone deficiency: bone matters

Galina Götherström


Sahlgrenska University Hospital, Göteborg, Sweden.

Growth hormone (GH) plays a critical role for longitudinal bone growth in children, the achievement of a normal peak bone mass in young adults, and it also affects bone mass and bone remodelling in adults. Among the most reported features of severe growth hormone deficiency (GHD) are abnormal body composition, in particular, increased fat mass and reduced lean body mass, osteopenia and increased risk of fracture. Low bone mass has been reported using dual energy X-ray absorptiometry (DEXA) and other quantitative methodologies. Bone quality in GHD adults is not studied. Reduced serum concentrations of the markers of bone turnover and the scarce histomorphometry data suggest that GHD is, probably, a state of low bone turnover.

Clinical studies have shown that GH replacement therapy accelerates bone turnover within a few weeks, whereas changes in bone mineral density (BMD) and bone mineral content (BMC) were observed much later, 1–2 years after initiating of GH therapy because of initially negative bone remodelling balance.

There are few studies determining the effects of prolonged GH replacement. Seven years of GH replacement therapy in 20 adults resulted in increased lumbar spine and forearm BMD between 1 and 6 years. In our study, 10 years of GH therapy in 87 GHD adults produced sustained increases in bone mass and density with the maximum effect after 7–10 years.

T-scores were almost normalized. As t-score in lumbar spine and femur neck is strongly related to the risk of fractures in these regions, the 10-year replacement is likely to reduce the risk of fractures in GHD adults.

The differences in the treatment responses between genders, age groups and groups of adults with different onset of GHD will be discussed.

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