Increased frequency of osteoporosis and BMD below the expected range for age among South Korean women with rheumatoid arthritis
ABSTRACT To compare the frequency of osteoporosis and bone mineral density (BMD) below the expected range for age between female patients with rheumatoid arthritis (RA) and healthy subjects and to determine risk factors for bone loss in female patients with RA.
Two hundred and ninety-nine patients with RA and 246 age-matched healthy subjects were included in this study. BMD in the lumbar spine, femoral neck and total hip were measured with dual-energy X-ray absorptiometry. A T-score of -2.5 or lower in postmenopausal women was defined as osteoporosis, and a Z-score -2.0 or lower in females prior to menopause was defined as below the expected range for age.
The frequency of osteoporosis in the RA patients (22.1%) was significantly higher than in healthy subjects (11.4%) at either the spine or hip (P = 0.014). The occurrence of BMD below the expected range for age in RA patients (7.8%) was also significantly higher than in healthy subjects (1.0%, P = 0.015). In 299 female patients with RA, higher age, lower body mass index and postmenopausal status were significantly associated with the lumbar spine and hip BMD reduction. Of disease-related variables, glucocorticoid use was independently associated with reduction of hip BMD.
The prevalence of osteoporosis in the RA patients was 1.9 times higher than in healthy subjects. Glucocorticoid use was a risk factor for generalized bone loss in female RA patients.
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ABSTRACT: Methotrexate (MTX) is a nonbiological disease-modifying antirheumatic drug that has shown both a good control of clinical disease and a good safety. Usually drug-drug interactions (DDIs) represent the most limiting factor during the clinical management of any disease, in particular when several drugs are coadministered to treat the same disease. In this paper, we report the interactions among MTX and the other drugs commonly used in the management of rheumatoid arthritis. Using Medline, PubMed, Embase, Cochrane libraries, and Reference lists, we searched for the articles published until June 30, 2012, and we reported the most common DDIs between MTX and antirheumatic drugs. In particular, clinically relevant DDIs have been described during the treatment with MTX and NSAIDs, for example, diclofenac, indomethacin, or COX-2 inhibitors, and between MTX and prednisone or immunosuppressant drugs (e.g., leflunomide and cyclosporine). Finally, an increase in the risk of infections has been recorded during the combination treatment with MTX plus antitumor necrosis factor- α agents. In conclusion, during the treatment with MTX, DDIs play an important role in both the development of ADRs and therapeutic failure.Advances in Pharmacological Sciences 05/2013; 2013:313858. DOI:10.1155/2013/313858
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ABSTRACT: The study was to investigate the outcomes of rheumatoid arthritis (RA) patients with hip fractures with a large-scale, population-based, nationwide, case-cohort study using the Taiwan National Health Insurance database. The group has hip fractures at a younger age, higher complication, and mortality rate, which indicate that early intervention is necessary. This study seeks to evaluate the incidence, mortality, and complication rates in RA patients with hip fractures, using a nationwide database. Data were collected from the National Health Insurance Research Database of Taiwan. The study group included 117,129 patients with hip fractures diagnosed from January 2004 to December 2010. Matching based on the propensity of RA patients was used. In total, 1,088 hip fractures were reported among patients with RA. Patients with hip fractures were divided into two groups: those without RA (controls) and those with RA (RA group). The incidence of hip fracture and mortality and complication rates after the hip fracture were then compared between the two groups. RA patients had a significantly higher incidence of hip fracture (3,260/100,000 person-years) compared with the general population (72/100,000 person-years). Hip fractures occurred significantly earlier among RA patients (70.6 ± 5.3 years) compared with the control group (76.1 ± 6.2 years). Cumulative mortality rates at 6-month and 1-year follow-up were significantly higher among patients in the RA group (9.47 and 18.47 %) compared to the controls (8.47 and 13.62 %) and among RA patients without hip fractures (3.24 and 6.16 %). There was a significantly higher incidence of osteomyelitis after hip fracture among the RA group than among the body mass index-, comorbidity-, age-, and sex-matched patients in the control group. Compared to patients without RA, those with RA have a higher incidence of hip fractures at a relatively younger age and with higher complication and mortality rates. Steroid and disease-modifying anti-rheumatic drugs, the most common medicine in Taiwanese RA patients, might contribute to the high incidence of fracture and post-op infection. Appropriate early intervention to prevent hip fractures in RA patients is a critical issue in rheumatology care.Osteoporosis International 11/2014; 26(2). DOI:10.1007/s00198-014-2968-y · 4.17 Impact Factor
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ABSTRACT: Chronic inflammation affects bone metabolism leading to disequilibrium in the rates of bone resorption and repair and subsequently to local and generalized bone loss. Osteoporosis represents an important co-morbidity of Rheumatoid Arthritis (RA) patients, which exhibit increased fracture risk. Osteoclasts play a pivotal role in the development and progression of bone loss, while resident synovial cells such as T cells, monocytes and synovial fibroblasts have been identified as sources of osteoclast differentiation signals in RA. This process is mainly mediated through the receptor activator of nuclear-κappa B ligand (RANKL) signalling system, which is upregulated by numerous proinflammatory cytokines involved in the pathogenesis of RA. Improved knowledge of the association between cells and cytokines of the immune system and their relationship to bone remodelling has revealed several promising targets for the treatment of inflammatory bone loss in RA. In this respect, initiation of biologic therapies targeting inflammatory cytokines and/or lymphocyte activation have modified RA therapy not only by blocking local and systemic inflammatory cascades but also by providing beneficial effects against bone and joint degradation. In this article we briefly present the modern view of the mechanisms that govern inflammatory bone loss, highlighting the role of cytokine-induced molecular pathways, and discuss in detail the effects of different biologic treatment strategies on bone mass in RA patients.Autoimmunity reviews 03/2013; DOI:10.1016/j.autrev.2013.03.015 · 7.10 Impact Factor