2016
DOI: 10.1097/bor.0000000000000267
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Comorbidities in rheumatoid arthritis

Abstract: Several comorbidities are frequently observed in rheumatoid arthritis because of the persistent activity of the disease and/or because of the administered antirheumatic therapies. Programs to adequately collect these comorbidities and/or prevent them are resulting in a better outcome for rheumatoid arthritis patients.

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Cited by 108 publications
(75 citation statements)
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“…Lung disease, certain malignancies, osteoporosis, and psychiatric disorders have all been associated with RA [2, 8, 11-13]. Apart from the considerable disease burden of RA, patients often are affected by concomitant comorbidities, many of which are age dependent [2].…”
Section: Introductionmentioning
confidence: 99%
“…Lung disease, certain malignancies, osteoporosis, and psychiatric disorders have all been associated with RA [2, 8, 11-13]. Apart from the considerable disease burden of RA, patients often are affected by concomitant comorbidities, many of which are age dependent [2].…”
Section: Introductionmentioning
confidence: 99%
“…Increased osteoclastogenesis promotes joint destruction and early onset osteoporosis in patients with RA [20]. Treatment of early onset osteoporosis is important in these patients, because their chronic in ammatory status (due to long-term use of glucocorticoids) can exacerbate osteoporosis [38]. Osteoclasts are the main effector cells in osteoporosis, and a therapeutic modality that acts on both arthritis and osteoporosis would likely be effective for patients RA.…”
Section: Discussionmentioning
confidence: 99%
“…Rheumatoid arthritis (RA) is a chronic systemic disease, which is characterized as a symmetric polyarticular inflammation of synovia-lined joints and progressive loss of articular cartilage and subchondral bone (Bilthariya et al, 2015;Gasparyan et al, 2011;Dougados, 2016). Although the exact molecular pathogenesis of RA remains elucidated, evidence suggests that the pathogenesis of RA was associated with the imbalance of cellular and humoral immunity, which were mediated by diverse inflammatory cells such as lymphocytes and synovial cells via various signal transduction cascades involving the signal transduction of G protein-adenylyl cyclase-3 0 ,5 0 -cyclic adenosine monophosphate (cAMP) and Ras-mitogen-associated protein kinases (Findlay and Haynes, 2005;Chang et al, 2009;Bollmann, 2012;Mauri and Ehrenstein, 2007;Bae and Park, 2016;Loetscher, 2005;Tanaka, 2005;Chen, 2010).…”
Section: Introductionmentioning
confidence: 99%