3 research outputs found

    Relevance of gastrointestinal manifestations in a large Spanish cohort of patients with systemic lupus erythematosus: what do we know?

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    SLE can affect any part of the gastrointestinal (GI) tract. GI symptoms are reported to occur in >50% of SLE patients. To describe the GI manifestations of SLE in the RELESSER (Registry of SLE Patients of the Spanish Society of Rheumatology) cohort and to determine whether these are associated with a more severe disease, damage accrual and a worse prognosis. METHODS: We conducted a nationwide, retrospective, multicentre, cross-sectional cohort study of 3658 SLE patients who fulfil =4 ACR-97 criteria. Data on demographics, disease characteristics, activity (SLEDAI-2K or BILAG), damage (SLICC/ACR/DI) and therapies were collected. Demographic and clinical characteristics were compared between lupus patients with and without GI damage to establish whether GI damage is associated with a more severe disease. RESULTS: From 3654 lupus patients, 3.7% developed GI damage. Patients in this group (group 1) were older, they had longer disease duration, and were more likely to have vasculitis, renal disease and serositis than patients without GI damage (group 2). Hospitalizations and mortality were significantly higher in group 1. Patients in group 1 had higher modified SDI (SLICC Damage Index). The presence of oral ulcers reduced the risk of developing damage in 33% of patients. CONCLUSION: Having GI damage is associated with a worse prognosis. Patients on a high dose of glucocorticoids are at higher risk of developing GI damage which reinforces the strategy of minimizing glucocorticoids. Oral ulcers appear to decrease the risk of GI damage. © The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology

    Impact of Comorbidity on Physical Function in Patients With Ankylosing Spondylitis and Psoriatic Arthritis Attending Rheumatology Clinics: Results From a Cross-Sectional Study

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    Objective: To evaluate the impact of comorbidities on physical function in patients with ankylosing spondylitis (AS) and psoriatic arthritis (PsA). Methods: This was a cross-sectional analysis of the baseline visit from the Cardiovascular in Rheumatology study. Multivariate models with physical function as the dependent variable (Bath Ankylosing Spondylitis Functional Index and Health Assessment Questionnaire for AS and PsA, respectively) were performed. Independent variables were a proxy for the Charlson Comorbidity Index (CCIp; range 0-27), sociodemographic data, disease activity (erythrocyte sedimentation rate [ESR] and Bath Ankylosing Spondylitis Disease Activity Index [BASDAI] in AS; Disease Activity Score in 28 joints [DAS28] using the ESR in PsA), disease duration, radiographic damage, and treatments. Results were reported as beta coefficients, 95% confidence intervals (95% CIs), and P values. Results: We included 738 patients with AS and 721 with PsA; 21% of patients had >1 comorbidity. Comorbidity burden (CCIp) was independently associated with worse adjusted physical function in patients with PsA (? = 0.11). Also, female sex (? = 0.14), disease duration (? = 0.01), disease activity (DAS28-ESR; ? = 0.19), and the use of nonsteroidal antiinflammatory drugs (? = 0.09), glucocorticoids (? = 0.11), and biologics (? = 0.15) were associated with worse function in patients with PsA. A higher education level was associated with less disability (? = -0.14). In patients with AS, age (? = 0.03), disease activity (BASDAI; ? = 0.81), radiographic damage (? = 0.61), and the use of biologics (? = 0.51) were independently associated with worse function on multivariate analyses, but CCIp was not. Conclusion: The presence of comorbidities in patients with PsA is independently associated with worse physical function. The detection and control of the comorbidities may yield an integral management of the disease.The CARMA project has been supported by an unrestricted Grant from Abbvie, Spain. The sponsor had no role in the study design, the collection, analysis or interpretation of the data; in the writing of the report; or in the decision to submit the article for publication. Dr. González-Gay’s studies have been supported by Grants from “Fondo de Investigaciones Sanitarias,” Spain PI06/0024, PI09/00748, PI12/00060, PI15/00525, PI18/00043 and RD12/0009/0013(RIER) and RD16/0012 (RIER) from “Instituto de Salud Carlos III” (ISCIII), Spain

    Switching TNF antagonists in patients with chronic arthritis: An observational study of 488 patients over a four-year period

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    The objective of this work is to analyze the survival of infliximab, etanercept and adalimumab in patients who have switched among tumor necrosis factor (TNF) antagonists for the treatment of chronic arthritis. BIOBADASER is a national registry of patients with different forms of chronic arthritis who are treated with biologics. Using this registry, we have analyzed patient switching of TNF antagonists. The cumulative discontinuation rate was calculated using the actuarial method. The log-rank test was used to compare survival curves, and Cox regression models were used to assess independent factors associated with discontinuing medication. Between February 2000 and September 2004, 4,706 patients were registered in BIOBADASER, of whom 68% had rheumatoid arthritis, 11% ankylosing spondylitis, 10% psoriatic arthritis, and 11% other forms of chronic arthritis. One- and two-year drug survival rates of the TNF antagonist were 0.83 and 0.75, respectively. There were 488 patients treated with more than one TNF antagonist. In this situation, survival of the second TNF antagonist decreased to 0.68 and 0.60 at 1 and 2 years, respectively. Survival was better in patients replacing the first TNF antagonist because of adverse events (hazard ratio (HR) for discontinuation 0.55 (95% confidence interval (CI), 0.34-0.84)), and worse in patients older than 60 years (HR 1.10 (95% CI 0.97-2.49)) or who were treated with infliximab (HR 3.22 (95% CI 2.13-4.87)). In summary, in patients who require continuous therapy and have failed to respond to a TNF antagonist, replacement with a different TNF antagonist may be of use under certain situations. This issue will deserve continuous reassessment with the arrival of new medications. © 2006 Gomez-Reino and Loreto Carmona; licensee BioMed Central Ltd
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