Endocrine Abstracts

Osteoporosis is a common complication of oral glucocorticoid therapy and is associated with significant morbidity. Glucocorticoid-induced osteoporosis is characterised by rapid bone loss and increased fracture risk during the first few months of therapy. The increase in fracture risk is dose-related and most prominent in the spine. Although awareness of glucocorticoid-induced osteoporosis has increased in recent years, the condition remains under-diagnosed and under-treated.

Recently there have been advances in fracture risk assessment and treatment in glucocorticoid-induced osteoporosis. The fracture risk algorithm FRAX includes glucocorticoid use as a risk factor but does not take account of the dose, thus underestimating fracture risk in individuals taking higher doses. A modification to FRAX has recently been developed that provides an adjustment for the dose of glucocorticoids.

The rapid increase in fracture risk following initiation of glucocorticoid therapy emphasises the importance of primary prevention of fracture in high-risk individuals. Bisphosphonates are anti-resorptive agents that prevent or reduce glucocorticoid-induced bone loss; vertebral fracture reduction has been demonstrated in secondary analyses. PTH 1–34 peptide (teriparatide) has been shown to increase bone mineral density and reduce vertebral fracture risk in glucocorticoid-treated patients when compared to alendronate treated patients. Bisphosphonates provide the first-line approach in most individuals, with teriparatide as an alternative in those unable to tolerate bisphosphonates. In patients with malabsorption, intravenous zoledronate, 5 mg by i.v. infusion once yearly, is an appropriate option. Calcium and vitamin D supplements should be co-prescribed with these treatments. New recommendations incorporating these advances have recently been issued by the American College of Rheumatology and a joint working group from the International Osteoporosis Foundation and the European Calcified Tissue Society.