title: An update on glucocorticoid-induced osteoporosis.
abstract: In general, bone loss from glucocorticoid treatment occurs rapidly within the first 6 months of therapy. Glucocorticoids alter bone metabolism by multiple pathways; however, the bone loss is greatest in areas rich in trabecular bone. Preventive measures should be initiated early. It is the author's opinion that all subjects initiating treatment with prednisone at 7.5 mg or greater require calcium supplementation (diet plus supplement) at a dose of 1500 mg and vitamin D at a dose of 400 to 800 IU/d. If the patient is going to remain on this dose of glucocorticoid for more than 4 weeks, an antiresorptive agent should be started (e.g., estrogen, bisphosphonate, raloxifene). If a patient has established osteoporosis and is either initiating glucocorticoid therapy or is chronically treated with prednisone at 5 mg d or greater in addition to calcium and vitamin D supplementation, a potent antiresorptive agent (bisphosphonate) should be started. A bone mineral density measurement of either the lumbar spine or the hip may be helpful is assessing an individual's risk of osteoporosis, may improve compliance with treatment, and can be used to monitor the efficacy of the prescribed therapy. There is no reason to withhold treatment for glucocorticoid-induced bone loss until a bone mass measurement is taken, however. In motivated patients, a weight-bearing and resistance exercise program should be prescribed to help retain muscle strength and prevent depression. If hypercalciuria develops with glucocorticoid use, either thiazide diuretics or sodium restriction may be helpful. In patients who continue to lose bone or experience fracture's despite antiresorptive therapy while on glucocorticoids, bone-building anabolic agents (e.g., hPTH 1-34 or PTH 1-84) may be available someday soon.
authors: Division of Rheumatology, University of California at San Francisco, San Francisco, California, USA. nelane@itsa.ucsf.edu
authors: N E
authors: NE
authors: Lane
mesh_terms: D000818:Animals; D015519:Bone Density / Q000187:drug effects; D016723:Bone Remodeling / Q000187:drug effects; D004164:Diphosphonates / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D004967:Estrogens / Q000627:therapeutic use; D050723:Fractures, Bone / Q000139:chemically induced / Q000517:prevention & control; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D010024:Osteoporosis / Q000139:chemically induced* / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy; D010281:Parathyroid Hormone / Q000627:therapeutic use; D020849:Raloxifene Hydrochloride / Q000627:therapeutic use; D012969:Sodium Fluoride / Q000627:therapeutic use; D006113:United Kingdom / Q000453:epidemiology
chemical_list: D004164:Diphosphonates; D004967:Estrogens; D005938:Glucocorticoids; D010281:Parathyroid Hormone; D020849:Raloxifene Hydrochloride; D012969:Sodium Fluoride