103 research outputs found
Risk of serious infections during rituximab, abatacept and anakinra treatments for rheumatoid arthritis: meta-analyses of randomised placebo-controlled trials
Linking genotype to cell function in chronic inflammation: analysis of the IL-23/Th17 axis in spondylarthropathy
Complete genome sequence of Mycobacterium xenopi type strain RIVM700367
Item does not contain fulltextMycobacterium xenopi is a slow-growing, thermophilic, water-related Mycobacterium species. Like other nontuberculous mycobacteria, M. xenopi more commonly infects humans with altered immune function, such as chronic obstructive pulmonary disease patients. It is considered clinically relevant in a significant proportion of the patients from whom it is isolated. We report here the whole genome sequence of M. xenopi type strain RIVM700367.1 juni 201
Community-acquired necrotizing pneumonia due to methicillin-sensitive Staphylococcus aureus secreting Panton-Valentine leukocidin: a review of case reports
Risk of infections in bronchiectasis during disease-modifying treatment and biologics for rheumatic diseases
<p>Abstract</p> <p>Background</p> <p>Bronchiectasis is frequently associated (up to 30%) with chronic inflammatory rheumatic diseases and leads to lower respiratory tract infections. Data are lacking on the risk of lower respiratory tract infections in patients treated with biologic agents.</p> <p>Methods</p> <p>Monocenter, retrospective systematic study of all patients with a chronic inflammatory rheumatic disease and concomitant bronchiectasis, seen between 2000 and 2009. Univariate and multivariate analyses were performed to evidence predictive factors of the number of infectious respiratory events.</p> <p>Results</p> <p>47 patients were included (mean age 64.1 ± 9.1 years, 33 (70.2%) women), with a mean follow-up per patient of 4.3 ± 3.1 years. Rheumatoid arthritis was the main rheumatic disease (90.1%). The mean number of infectious events was 0.8 ± 1.0 event per patient-year. The factors predicting infections were the type of treatment (biologic vs. non biologic disease-modifying treatments), with an odds ratio of 8.7 (95% confidence interval: 1.7-43.4) and sputum colonization by any bacteria (odds ratio 7.4, 2.0-26.8). In multivariate analysis, both factors were independently predictive of infections.</p> <p>Conclusion</p> <p>Lower respiratory tract infectious events are frequent among patients receiving biologics for chronic inflammatory rheumatic disease associated with bronchiectasis. Biologic treatment and pre-existing sputum colonization are independent risk factors of infection occurrence.</p
Abatacept monotherapy compared with abatacept plus disease-modifying anti-rheumatic drugs in rheumatoid arthritis patients: data from the ORA registry
Rituximab versus an alternative TNF inhibitor in patients with rheumatoid arthritis who failed to respond to a single previous TNF inhibitor: SWITCH-RA, a global, observational, comparative effectiveness study.
OBJECTIVES: To compare the effectiveness of rituximab versus an alternative tumour necrosis factor (TNF) inhibitor (TNFi) in patients with rheumatoid arthritis (RA) with an inadequate response to one previous TNFi. METHODS: SWITCH-RA was a prospective, global, observational, real-life study. Patients non-responsive or intolerant to a single TNFi were enrolled ≤4 weeks after starting rituximab or a second TNFi. Primary end point: change in Disease Activity Score in 28 joints excluding patient's global health component (DAS28-3)-erythrocyte sedimentation rate (ESR) over 6 months. RESULTS: 604 patients received rituximab, and 507 an alternative TNFi as second biological therapy. Reasons for discontinuing the first TNFi were inefficacy (n=827), intolerance (n=263) and other (n=21). A total of 728 patients were available for primary end point analysis (rituximab n=405; TNFi n=323). Baseline mean (SD) DAS28-3-ESR was higher in the rituximab than the TNFi group: 5.2 (1.2) vs 4.8 (1.3); p<0.0001. Least squares mean (SE) change in DAS28-3-ESR at 6 months was significantly greater in rituximab than TNFi patients: -1.5 (0.2) vs -1.1 (0.2); p=0.007. The difference remained significant among patients discontinuing the initial TNFi because of inefficacy (-1.7 vs -1.3; p=0.017) but not intolerance (-0.7 vs -0.7; p=0.894). Seropositive patients showed significantly greater improvements in DAS28-3-ESR with rituximab than with TNFi (-1.6 (0.3) vs -1.2 (0.3); p=0.011), particularly those switching because of inefficacy (-1.9 (0.3) vs -1.5 (0.4); p=0.021). The overall incidence of adverse events was similar between the rituximab and TNFi groups. CONCLUSIONS: These real-life data indicate that, after discontinuation of an initial TNFi, switching to rituximab is associated with significantly improved clinical effectiveness compared with switching to a second TNFi. This difference was particularly evident in seropositive patients and in those switched because of inefficacy
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