Glucocorticoid-induced osteoporosis: who to treat with what agent?

Abstract

Among the adverse events of glucocorticoid treatment are bone loss and fractures. Despite available, effective preventive measures, many patients receiving or initiating glucocorticoid therapy are not appropriately evaluated and treated for bone health and fracture risk. Populations with, or at risk of, glucocorticoid-induced osteoporosis (GIOP) to target for these measures are defined on the basis of dose and duration of glucocorticoid therapy and bone mineral density. That patients with GIOP should be treated as early as possible is generally agreed upon; however, diversity remains in intervention thresholds and management guidelines. The FRAX(®) algorithm provides a 10-year probability of fracture that can be adjusted according to glucocorticoid dose. There is no evidence that GIOP and postmenopausal osteoporosis respond differently to treatments. Available anti-osteoporotic therapies such as anti-resorptives including bisphosphonates and the bone anabolic agent teriparatide are effective for the management of GIOP. Prevention with calcium and vitamin D supplementation is less effective than specific anti-osteoporotic treatment. Anti-osteoporotic treatment should be stopped at the time of glucocorticoid cessation, unless the patient remains at increased risk of fracture.

The Prediction and Monitoring of Toxicity Associated with Long-Term Systemic Glucocorticoid Therapy

“…Bone mineral density (BMD) decreases even with low-dose GCs [ 54 , 55 ] and fracture risk increases with cumulative GC therapy [ 13 ]. Fractures are associated with substantial http://eproofing.springer.com/journals/printpage.php?token=tied1_9h6GfkA1bz4BdhSLmRr-9cVV1LwfAgIK7u4rw morbidity and associated healthcare costs [ 56 ], particularly in the elderly [ 57 ]. Current recommendations advise assessment of risk factors for osteoporosis/fracture, for example by using the FRAX tool; while there is good evidence for several pharmacological treatments such as bisphosphonates [ 58 ••], this type of high-level evidence was not available recommendations regarding monitoring and for non-pharmacological treatments [ 59 ].…”

MicroRNA-29a mitigates glucocorticoid induction of bone loss and fatty marrow by rescuing Runx2 acetylation

“…Glucocorticoid excess impairs bone metabolism and microarchitecture integrity, and thereby increases the morbidity of osteoporotic disorders [1]. Impeded bone formation [2] and capacious marrow adipogenesis [3] are prominent detrimental reactions that occur in glucocorticoid-mediated skeletal deterioration.…”

Inactivation of autophagy ameliorates glucocorticoid-induced and ovariectomy-induced bone loss

“…The most common form of primary osteoporosis is postmenopausal osteoporosis, which results from decreased oestrogen production after menopause in women. Among the secondary forms of osteoporosis, glucocorticoid-induced osteoporosis induced by prolonged use of glucocorticoids, for example, for the treatment of rheumatic diseases, is common 3. Despite the different underlying aetiologies, glucocorticoid osteoporosis and postmenopausal osteoporosis share the activation of osteoclast-induced bone resorption at the expense of bone formation as the underlying pathomechanism.…”