The Epidemiology of Corticosteroid-Induced Osteoporosis: a Meta-analysis

Abstract

Abstract. Studies of oral corticosteroid dose and loss of bone mineral density have reported inconsistent results. In this meta-analysis, we used information from 66 papers on bone density and 23 papers on fractures to examine the effects of oral corticosteroids on bone mineral density and risk of fracture. Strong correlations were found between cumulative dose and loss of bone mineral density and between daily dose and risk of fracture. The risk of fracture was found to increase rapidly after the start of oral corticosteroid therapy (within 3 to 6 months) and decrease after stopping therapy. The risk remained independent of underlying disease, age and gender. We conclude that oral corticosteroid treatment using more than 5 mg (of prednisolone or equivalent) daily leads to a reduction in bone mineral density and a rapid increase in the risk of fracture during the treatment period. Early use of preventive measures against corticosteroid-induced osteoporosis is recommended.

Prednisone affects inflammation, glucose tolerance, and bone turnover within hours of treatment in healthy individuals

“…Certainly, GC-induced osteoporosis is a well-known adverse consequence of chronic GC therapy, and several groups have reported that daily prednisone doses as little as 10 mg or lower result in clinically significant bone loss (16,32). In the present investigation, circulating concentrations of the bone formation marker osteocalcin decreased dramatically within hours of administration of all prednisone doses and remained suppressed for at least 24 h. Of the bone formation markers analysed, osteocalcin was the most sensitive to GC treatment.…”

“…GCs reduce osteoblast function and replication as well as increase osteoblast apoptosis (1,8,9,10). Although the specific mechanism by which GCs interfere with osteoblast function remains unclear, reductions in bone formation markers have been reported to occur within days of treatment with prednisone (11,12,13,14,15), and increases of about two-or three-fold in the relative risk of hip and vertebral fractures in patients receiving GCs have been reported (16,17).…”

Glucocorticoids maintain human osteoclasts in the active mode of their resorption cycle

“…(3) However, lack of bone formation and function of OB lineage cells cannot be responsible alone for some of the most important effects that GCs have on bone. These include rapid increase in fracture risk within the first 3 to 6 months of treatment, (2,4) which could be explained best by an effect of GCs on bone resorption itself. In addition, bone-resorption markers increase immediately in patients receiving intravenous GCs, and the maximum increase in serum cross-linked C-telopeptide (CTX) was already reached 24 hours after the very first infusion.…”

Review of American College of Rheumatology (Acr) Clinical Guidelines for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis

“…Одним из осложне-ний терапии ГК является потеря костной массы и сопутст-вующие этому переломы [9]. Переломы костей скелета имеют различную локализацию, однако наиболее высокий риск отмечался для переломов позвонков, которые, как правило, протекают бессимптомно [10].…”