Increased frequency of osteoporosis and BMD below the expected range for age among South Korean women with rheumatoid arthritis
Department of Internal Medicine, Pusan National University School of Medicine, Busan, South Korea. International Journal of Rheumatic Diseases
(Impact Factor: 1.47).
06/2012; 15(3):289-96. DOI: 10.1111/j.1756-185X.2012.01729.x
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.
Available from: Emilio Russo
- "Glucocorticoids (e.g., dexamethasone and prednisone) are anti-inflammatory and immune suppressor agents that are able to reduce the inflammation and the progression of RA, through the inhibition of cytokines secretion and osteoclasts activation          . However, even if they represent a first-line treatment in patients with RA, their use is limited for the development of serious ADRs such as loss of bone mass, increased risk of fractures, infections, diabetes and hypertension   . The DMARDs group, includes both nonbiological and biological drugs; between the DMARDs, methotrexate (MTX) due to "
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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-
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(7):313858. DOI:10.1155/2013/313858
Available from: Theodoros Dimitroulas
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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; 12(10). DOI:10.1016/j.autrev.2013.03.015 · 7.93 Impact Factor
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Clear information is still lacking on the safety of corticosteroids (GCs) therapy in RA despite six decades of clinical experience.
We performed a literature search in Ovid MEDLINE from January 2000 to December 2012. Our Population Intervention Comparator Outcomes (PICO) strategy search was: rheumatoid arthritis [Population], corticosteroids or glucocorticoids [Intervention], any comparison [Comparator], adverse effects [Outcome]. Studies were selected if they reported any measure of association between GCs intake and potential adverse effects in RA patients.
We identified 1030 papers and selected for analysis 26 observational studies and six systematic reviews. The major side effects of GCs in RA are bone loss, risk of cardiovascular events and risk of infections as evidenced by large observational studies and not necessarily RCTs. Others associations were reported with herpes zoster, tuberculosis, hyperglycemia, cutaneous abnormalities, gastrointestinal perforation, respiratory infection and self-reported health problems such as cushingoid phenotype, ecchymosis, parchment-like skin, epistaxis, weight gain and sleep disturbance. Other potential adverse effects of GCs were studied but no association was found. These included psychological disorders, dermatophytosis, brain diseases, interstitial lung disease, memory deficit, metabolic syndrome, lymphoma, non-Hodgkin's lymphoma, renal function and cerebrovascular accidents. Most of the evidence emanates from observational researches and the inherent limitations of such data should be kept in mind.
Recent observational data and systematic reviews suggest that GCs can lead to relatively alarming and burdensome side effects in RA. This is particularly true for patients who have longer term and higher dose therapies. GCs are largely used in RA and knowing their safety profile is essential to improve patients care. The design of new therapeutic strategies intended to minimize the daily dosing of GCs while conserving their beneficial effect should be encouraged.
Current Medical Research and Opinion 06/2013; 29(9). DOI:10.1185/03007995.2013.818531 · 2.65 Impact Factor
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