Glucocorticoid-induced osteoporosis: an overview

Abstract

Glucocorticoid-induced osteoporosis: an overviewGlucocorticoid-induced osteoporosis (GIOP) is one of the most serious adverse effects of glucocorticoids. Despite guidelines on the management of GIOP, effective medications and fracture outpatient clinics, this condition remains under-recognized and under-treated. This review covers recent insights into mechanisms involved in GIOP, monitoring for adverse effects of glucocorticoids on bone and prevention and treatment of GIOP. Recent guidelines on GIOP are discussed and a research agenda is proposed. EpidemiologyDespite development of many immunosuppressive nonbiological and biological drugs, glucocorticoids (GCs) still are widely used in the treatment of chronic allergic, inflammatory and autoimmune diseases and vasculitides, for their antiallergic, anti-inflammatory and immunosuppressive effects. A study showed that in the UK oral GCs were used by 0.9% of the adult population, with the highest use (2.5%) among elderly of 70-79 years of age; the most frequent indications overall for long-term GC treatment were respiratory diseases (40%) and arthropathies (19%) [1]. A recent study estimated that the prevalence of GC use, mostly of a long duration, in the USA is 1.2%, with infrequent use of a concomitant bisphosphonate [2].Since their introduction in the 1950s by Hench and collaborators [3], adverse effects are recognized, but their management and prevention still are very actual issues nowadays, approximately 60 years later [4,5]. Of these adverse effects, glucocorticoid-induced osteoporosis (GIOP) is a frequent and potentially disabling condition. In a meta-analysis on oral GC therapy and loss of bone mineral density (BMD) or fracture risk, including 66 papers on bone density and 23 on fractures, the risk of fracture was found to increase rapidly already within 3-6 months after the start of oral GC therapy more than 5 mg prednisone-equivalent per day, independently of disease treated, age and gender [6]. In that study, strong correlations were observed between cumulative dose of GCs and loss of BMD and between daily dose of GCs and risk of fracture. In another study, the combined effect of higher daily dose (>10 mg per day), longer duration of therapy (≥90 days of use) and continuous GC intake was associated with a relative risk for hip fracture of 7.16 (95% CI: 2.13-24.0) and for vertebral fracture of 16.94 (95% CI: 8.17-35.11) [7]. These data indicate a rapid deleterious effect, especially on trabecular bone, in line with the clinical observation that the prevalence of vertebral fractures during GC treatment is higher than that of other common sites for osteoporotic fracture, such as femur, humerus, forearm and wrist, ribs and other nonvertebral sites [8]. Nonvertebral fractures, especially of the femur, cause acute pain and loss of function, and nearly always lead to hospitalization, with serious mortality and morbidity, for example, slow recovery and often incomplete rehabilitation, leading to decreased physical and social functioning For reprint orders, please...

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