Glucocorticoid-induced osteoporosis
Glucocorticoids can reduce bone mineral density (BMD) in both men and women. They reduce bone formation and increase bone resorption by reducing osteoblast function and intestinal calcium absorption, and causing osteocyte dysfunction, hypercalciuria and gonadal suppression. Glucocorticoids also increase fracture risk independent of BMD, so a patient taking a glucocorticoid has a higher fracture risk than a patient not taking a glucocorticoid who has the same BMD.
Before starting glucocorticoid therapy that is expected to continue long term, assess the patient’s risk of fracture, and measure their BMD. For all patients, ensure their calcium intake is sufficient and they are vitamin D replete. Also optimise the management of any other risk factors for fracture (see Risk factors for minimal-trauma fracture), and provide advice on prevention of minimal-trauma fracture.
Bisphosphonates prevent fractures in patients taking glucocorticoid therapy, and are considered first-line treatment. Denosumab can also prevent fracture in these patients, but at the time of writing it is not available on the Pharmaceutical Benefits Scheme (PBS) for this indication1. Teriparatide is more effective than alendronate in reducing vertebral fractures in patients taking glucocorticoids, but strict eligibility criteria for PBS funding apply2. Estrogen therapy can prevent or reduce glucocorticoid-induced bone loss in postmenopausal women.
If no other risk factors are present, preventive drug therapy may only be required for the duration of glucocorticoid treatment.
Consider measuring BMD every 12 to 24 months for the first few years of glucocorticoid treatment. If BMD results are stable and acceptable, further BMD measurement can be less frequent.