13
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Glucocorticoid‐induced osteoporosis in rheumatic diseases

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The aim of this article is to review rheumatological diseases that are associated with glucocorticoid‐induced osteoporosis or fractures and to perform a critical analysis of the current guidelines and treatment regimens. The electronic database MEDLINE was searched using the date range of July 1986 to June 2009 and the following search terms: osteoporosis, bone mineral density, fractures, systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, vasculitis, juvenile rheumatoid arthritis, juvenile idiopathic arthritis and juvenile dermatomyositis. Osteopenia and osteoporosis respectively account for 1.4 to 68.7% and 5.0 to 61.9% of adult rheumatological diseases. Among juvenile rheumatological disorders, the frequency of low bone mass ranges from 38.7 to 70%. In general, fracture rates vary from 0 to 25%. Although glucocorticoid‐induced osteoporosis has a high rate of prevalence among rheumatic diseases, a relatively low number of patients on continuous glucocorticoid treatment receive adequate diagnostic evaluation or preventive therapy. This deficit in patient care may result from a lack of clear understanding of the attributed risks by the patients and physicians, the high complexity of the treatment guidelines and poor patient compliance.

          Related collections

          Most cited references229

          • Record: found
          • Abstract: found
          • Article: not found

          Teriparatide or alendronate in glucocorticoid-induced osteoporosis.

          Bisphosphonate therapy is the current standard of care for the prevention and treatment of glucocorticoid-induced osteoporosis. Studies of anabolic therapy in patients who are receiving long-term glucocorticoids and are at high risk for fracture are lacking. In an 18-month randomized, double-blind, controlled trial, we compared teriparatide with alendronate in 428 women and men with osteoporosis (ages, 22 to 89 years) who had received glucocorticoids for at least 3 months (prednisone equivalent, 5 mg daily or more). A total of 214 patients received 20 microg of teriparatide once daily, and 214 received 10 mg of alendronate once daily. The primary outcome was the change in bone mineral density at the lumbar spine. Secondary outcomes included changes in bone mineral density at the total hip and in markers of bone turnover, the time to changes in bone mineral density, the incidence of fractures, and safety. At the last measurement, the mean (+/-SE) bone mineral density at the lumbar spine had increased more in the teriparatide group than in the alendronate group (7.2+/-0.7% vs. 3.4+/-0.7%, P<0.001). A significant difference between the groups was reached by 6 months (P<0.001). At 12 months, bone mineral density at the total hip had increased more in the teriparatide group. Fewer new vertebral fractures occurred in the teriparatide group than in the alendronate group (0.6% vs. 6.1%, P=0.004); the incidence of nonvertebral fractures was similar in the two groups (5.6% vs. 3.7%, P=0.36). Significantly more patients in the teriparatide group had at least one elevated measure of serum calcium. Among patients with osteoporosis who were at high risk for fracture, bone mineral density increased more in patients receiving teriparatide than in those receiving alendronate. (ClinicalTrials.gov number, NCT00051558 [ClinicalTrials.gov].). Copyright 2007 Massachusetts Medical Society.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis.

            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.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Zoledronic acid and risedronate in the prevention and treatment of glucocorticoid-induced osteoporosis (HORIZON): a multicentre, double-blind, double-dummy, randomised controlled trial.

              Persistent use of glucocorticoid drugs is associated with bone loss and increased fracture risk. Concurrent oral bisphosphonates increase bone mineral density and reduce frequency of vertebral fractures, but are associated with poor compliance and adherence. We aimed to assess whether one intravenous infusion of zoledronic acid was non-inferior to daily oral risedronate for prevention and treatment of glucocorticoid-induced osteoporosis. This 1-year randomised, double-blind, double-dummy, non-inferiority study of 54 centres in 12 European countries, Australia, Hong Kong, Israel, and the USA, tested the effectiveness of 5 mg intravenous infusion of zoledronic acid versus 5 mg oral risedronate for prevention and treatment of glucocorticoid-induced osteoporosis. 833 patients were randomised 1:1 to receive zoledronic acid (n=416) or risedronate (n=417). Patients were stratified by sex, and allocated to prevention or treatment subgroups dependent on duration of glucocorticoid use immediately preceding the study. The treatment subgroup consisted of those treated for more than 3 months (272 patients on zoledronic acid and 273 on risedronate), and the prevention subgroup of those treated for less than 3 months (144 patients on each drug). 62 patients did not complete the study because of adverse events, withdrawal of consent, loss to follow-up, death, misrandomisation, or protocol deviation. The primary endpoint was percentage change from baseline in lumbar spine bone mineral density. Drug efficacy was assessed on a modified intention-to-treat basis and safety was assessed on an intention-to-treat basis. This trial is registered with ClinicalTrials.gov, number NCT00100620. Zoledronic acid was non-inferior and superior to risedronate for increase of lumbar spine bone mineral density in both the treatment (least-squares mean 4.06% [SE 0.28] vs 2.71% [SE 0.28], mean difference 1.36% [95% CI 0.67-2.05], p=0.0001) and prevention (2.60% [0.45] vs 0.64% [0.46], 1.96% [1.04-2.88], p<0.0001) subgroups at 12 months. Adverse events were more frequent in patients given zoledronic acid than in those on risedronate, largely as a result of transient symptoms during the first 3 days after infusion. Serious adverse events were worsening rheumatoid arthritis for the treatment subgroup and pyrexia for the prevention subgroup. A single 5 mg intravenous infusion of zoledronic acid is non-inferior, possibly more effective, and more acceptable to patients than is 5 mg of oral risedronate daily for prevention and treatment of bone loss that is associated with glucocorticoid use.
                Bookmark

                Author and article information

                Journal
                Clinics (Sao Paulo)
                Clinics
                Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo
                1807-5932
                1980-5322
                November 2010
                : 65
                : 11
                : 1197-1205
                Affiliations
                [I ]Rheumatology Division, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
                [II ]Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT, USA; and The University of Connecticut School of Medicine, Farmington, CT, USA.
                Author notes
                E-mail: rosamariarp@ 123456yahoo.com Tel.: 55 11 3061‐7490
                Article
                cln_65p1197
                10.1590/S1807-59322010001100024
                2999719
                21243296
                1afff235-b95b-46e9-9922-2b1d47145178
                Copyright © 2010 Hospital das Clínicas da FMUSP

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 July 2010
                : 11 August 2010
                : 11 August 2010
                Page count
                Pages: 9
                Categories
                Review

                Medicine
                glucocorticoids,bone mineral density,fractures, rheumatic diseases,osteoporosis
                Medicine
                glucocorticoids, bone mineral density, fractures, rheumatic diseases, osteoporosis

                Comments

                Comment on this article