title: [Glucocorticoid-induced osteoporosis and rheumatic diseases. Pathogenesis, prevention and treatment].
abstract: Glucocorticoids (GC) are diffusely used to treat a wide variety of inflammatory and autoimmune disorders, including rheumatic diseases. GC-induced osteoporosis (GIO) is the most common and serious side-effect for patients receiving GC. Loss of bone mineral density (BMD) is greatest in the first few months of GC use; fracture (Fx) risk is significantly increased at the spine and hip on doses even as low as 2.5 mg of prednisolone daily; Fx risk increases rapidly from the onset of therapy and, for a given BMD, is higher in GIO than in postmenopausal OP. General measures to reduce bone loss include use of the lowest effective dose; consideration of alternative routes of administration; adequate calcium and vitamin D supplementation. Today, results from large randomised controlled clinical trials provide evidence that bone loss and Fx may be prevented through the use of bone sparing agents (hormone therapy, bisphosphonates, PTH 1-34). Bisphosphonates (alendronate, risedronate) are first-choice therapy for the prevention and treatment of GIO; patients at high risk for Fx, for example those in post-menopausal status or aged > or =65 years and those with a prior fragility Fx, should be advised to start bone-protective therapy at the time of starting GC. Due to the prevalence of GC use, it is imperative that there be a greater awareness of GIO and of therapies that may be offered to patients both for prevention and treatment.
authors.affiliation: U.O. Reumatologia, Dipartimento di Medicina Interna, Università di Pisa, Italia. odimunno@int.med.unipi.it
authors.forename: Ombretta
authors.initials: O
authors.lastname: Di Munno
authors.forename: Andrea
authors.initials: A
authors.lastname: Delle Sedie
mesh_terms: D042842:11-beta-Hydroxysteroid Dehydrogenases / Q000502:physiology; D000293:Adolescent; D000328:Adult; D015519:Bone Density / Q000187:drug effects; D001842:Bone and Bones / Q000187:drug effects; D002118:Calcium / Q000627:therapeutic use; D016207:Cytokines / Q000502:physiology; D004164:Diphosphonates / Q000627:therapeutic use; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000139:chemically induced* / Q000188:drug therapy / Q000453:epidemiology / Q000517:prevention & control; D010281:Parathyroid Hormone / Q000502:physiology; D011965:Receptors, Glucocorticoid / Q000819:agonists / Q000502:physiology; D012216:Rheumatic Diseases / Q000150:complications / Q000188:drug therapy*; D014807:Vitamin D / Q000627:therapeutic use
chemical_list: D016207:Cytokines; D004164:Diphosphonates; D005938:Glucocorticoids; D010281:Parathyroid Hormone; D011965:Receptors, Glucocorticoid; D014807:Vitamin D; D042842:11-beta-Hydroxysteroid Dehydrogenases; D002118:Calcium