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Gonzalez-Vacarezza N.,Ministry of Public Health | Aleman A.,Ministry of Public Health | Gonzalez G.,National Institute of Rheumatology | Perez A.,Ministry of Public Health
International Journal of Technology Assessment in Health Care | Year: 2014

Objectives: The aim of this study was to evaluate the efficacy and safety of rituximab and tocilizumab compared with adalimumab, etanercept, and infliximab, in patients with rheumatoid arthritis not responding to first-line treatment, and to compare the efficacy and safety of rituximab versus tocilizumab in patients not responding to anti-tumor necrosis factor α (anti-TNF) therapy. Methods: A literature search of randomized controlled trials, controlled clinical trials, and systematic reviews was performed to evaluate efficacy and safety of rituximab and tocilizumab. Results: Twenty-four RCTs were included in this systematic review with 6,357 participants; 3,450 treated with biological DMARD and 2,907 with standard care. In patients not responding to first-line treatment, rituximab shows lower response rate in at least 50 percent improvement in the American College of Rheumatology criteria (ACR50) and ACR70 compared with etanercept, at 6 months of follow-up. Tocilizumab shows higher ACR70 response rate compared with infliximab, at the same follow-up time. Other results showed no significant differences. Indirect comparisons between rituximab and tocilizumab in patients not responding for at least one anti-TNF, shows higher ACR20 response rate for tocilizumab at 6 months of follow-up. Regarding safety, adalimumab and etanercept were associated with significant fewer withdrawals due to adverse events compared with infliximab. Conclusions: Considering efficacy, safety, and the availability of 3 anti-TNFs in the National Medicines Formulary (adalimumab, etanercept, and infliximab), it seems appropriate to remove infliximab from the coverage, and introduce tocilizumab for patients not responding for at least one anti-TNF. © Cambridge University Press 2014. Source


Veres K.,Debrecen University | Szodoray P.,Debrecen University | Szodoray P.,University of Oslo | Szekanecz Z.,Debrecen University | And 10 more authors.
Lupus | Year: 2010

Antiphospholipid syndrome (APS) is a distinct clinical entity characterized by arterial and venous thromboembolic events, recurrent fetal loss and the presence of antiphospholipid antibodies in the patientsg' sera. In primary APS, there is no detectable underlying disease, while overlap APS is associated with clinical syndromes including systemic autoimmune diseases, infections, or malignancies. We carried out a retrospective analysis of serological and clinical manifestations as well as assessed outcome-measures in 165 patients with primary APS. Thrombotic manifestations and possible signs of autoimmune diseases were determined at the time of the diagnosis, followed by the analysis of recurrent thrombotic events and effects of therapy during the follow-up period. Among the 165 patients with primary APS at onset, 105 patients (63%) remained primary APS after a mean 5.2 years of follow-up. In 14% of the patients, subsequently APS became associated with various characteristics of undifferentiated connective tissue disease. Finally 23% of patients evolved into a definitive systemic autoimmune disease during a mean 9.75 years of follow-up. Recurrent thrombotic events were registered in 24% of patients. Our results suggest that primary APS may be considered as a potential early phase of a dynamic transition towards a well-defined systemic autoimmune disease. © The Author(s), 2010. Source


Zavada J.,Charles University | Pesickova S.S.,Charles University | Rysava R.,Charles University | Horak P.,Palacky University | And 13 more authors.
Lupus | Year: 2014

Objective: To evaluate the extended follow-up of the CYCLOFA-LUNE trial, a randomized prospective trial comparing two sequential induction and maintenance treatment regimens for proliferative lupus nephritis based either on cyclophosphamide (CPH) or cyclosporine A (CyA). Patients and methods: Data for kidney function and adverse events were collected by a cross-sectional survey for 38 of 40 patients initially randomized in the CYCLOFALUNE trial. Results: The median follow-up time was 7.7 years (range 5.0-10.3). Rates of renal impairment and end-stage renal disease, adverse events (death, cardiovascular event, tumor, premature menopause) did not differ between the CPH and CyA group, nor did mean serum creatinine, 24 h proteinuria and SLICC damage score at last follow-up. Most patients in both groups were still treated with glucocorticoids, other immunosuppressant agents and blood pressure lowering drugs. Conclusion: An immunosuppressive regimen based on CyA achieved similar clinical results to that based on CPH in the very long term. © The Author(s), 2013. Source


Borowiec A.,National Institute of Cardiology | Kontny E.,National Institute of Rheumatology | Smolis-Bak E.,National Institute of Cardiology | Kowalik I.,National Institute of Cardiology | And 6 more authors.
Cytokine | Year: 2015

Aims: Inflammatory state is considered a risk factor of atrial fibrillation (AF) occurrence. The aim of this study was a prospective evaluation of the inflammation parameters in patients with different forms of AF without structural heart disease. Methods and results: One hundred fifty-eight patients with paroxysmal/persistent AF (87; 55.1% men, mean age 65.8. ±. 9.6. years) without structural heart disease were enrolled in the study. Inflammatory parameters: WBC, ESR, hs-CRP, IL-6, IL-15 and TNF-alpha were measured at baseline and after one year follow-up. Despite frequent AF episodes median values of WBC, ESR and C-reactive protein at baseline and after follow up were within normal ranges. There were no significant differences between WBC, ESR and hs-CRP regarding AF types. In patients who developed permanent AF form (. n=. 14) hs-CRP concentrations were higher at baseline: 0.35 (IQR1: 0.09 IQR: 0.61) vs 0.15 (IQR1: 0.07 IQR: 0.29), p<. 0.01. Nevertheless, after one year's observation these differences were not significant. Among all cytokines were studied only IL-15 was significantly correlated with the number of AF episodes (. r=. 0.26), mean (IQ1-IQ3): 10 (3-30) vs 60 (50-100), p=. 0.00681. Conclusion: Basic inflammatory markers were not changed in patients with refractory atrial fibrillation episodes in prospective one year's observation. Only cytokine IL-15 was correlated to numbers of AF episodes. It's potential role as a marker of arrhythmia deserves further evaluation. © 2015 Elsevier Ltd. Source


Barbera A.,Center for Genetic Engineering and Biotechnology | Lorenzo N.,Center for Genetic Engineering and Biotechnology | Mazola Y.,Center for Genetic Engineering and Biotechnology | Falcon V.,Center for Genetic Engineering and Biotechnology | And 11 more authors.
International Immunopharmacology | Year: 2013

Rheumatoid arthritis (RA) is a chronic T-cell mediated autoimmune disease that affects primarily the joints. The induction of immune tolerance through antigen-specific therapies for the blockade of pathogenic CD4 + T cells constitutes a current focus of research. In this focus it is attempted to simultaneously activate multiple regulatory mechanisms, such as: apoptosis and regulatory T cells (Tregs). APL-1 is an altered peptide ligand derived from a novel CD4 + T-cell epitope of human heat-shock protein of 60 kDa, an autoantigen involved in the pathogenesis of RA. Previously, we have reported that APL-1 induces CD4 + CD25highFoxp3 + Tregs in several systems. Here, we investigated the ability of APL-1 in inducing apoptosis in PBMCs from RA patients, who were classified as active or inactive according to their DAS28 score. APL-1 decreased the viability of PBMCs from active but not from inactive patients. DNA fragmentation assays and typical morphological features clearly demonstrated that APL-1 induced apoptosis in these cells. Activated CD4 + CD25 + T cells but not resting CD4 + CD25 - T cells were identified as targets of APL-1. Furthermore, CD4 + T-cell responses to APL-1 were found to be dependent on antigen presentation via the HLA-DR molecule. Thus, APL-1 is a regulatory CD4 + T cell epitope which might modulate inflammatory immune responses in PBMCs from RA patients by inducing CD4 + CD25highFoxp3 + Tregs and apoptosis in activated CD4 + T cells. These results support further investigation of this candidate drug for the treatment of RA. © 2013 Elsevier B.V. Source

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