Glucocorticoid-induced osteoporosis and Cushing’s syndrome



  • Glucocorticoid-induced osteoporosis (GIOP) remains the most common form of drug-induced osteoporosis. Patients may fracture at a different bone mineral density (BMD) threshold and absolute fracture risk using FRAX should be adjusted for glucocorticoid dose. Sufficient calcium and vitamin D are necessary but are generally insufficient for higher risk persons. The use of bone therapy in GIOP is motivated by an understanding of GIOP pathophysiology, including effects on heightened bone resorption and reduced bone formation. Osteoblast and osteocyte apoptosis contributes to both GIOP and glucocorticoid-associated osteonecrosis. Bisphosphonates, teriparatide, raloxifene, and denosumab stabilize or improve BMD more than placebo. Teriparatide, zoledronic acid, and denosumab increased BMD more so than an oral bisphosphonate. Teriparatide also reduced a small number of vertebral fractures more so than risedronate. All drugs tested in GIOP have had reasonable safety profiles, considering the significant comorbidity burden of those being treated with glucocorticoids. International guidelines advocate early and aggressive management of GIOP in order to lower fracture morbidity.
  • Authors

    Digital Object Identifier (doi)

    International Standard Book Number (isbn) 13

  • 9780128130735
  • Start Page

  • 1103
  • End Page

  • 1138