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Necrosis Factor Blockers (necrosis + factor_blocker)

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Medical Sciences100%

Selected Abstracts

Different response to rituximab in tumor necrosis factor blocker,naive patients with active ankylosing spondylitis and in patients in whom tumor necrosis factor blockers have failed: A twenty-four,week clinical trial,

ARTHRITIS & RHEUMATISM, Issue 5 2010
I.-H. Song
Objective Histologic studies have shown B cell clusters in the subchondral bone marrow of the spine of patients with ankylosing spondylitis (AS). An immunotherapy targeting B cells in AS is therefore of interest. We undertook this study to examine the efficacy and safety of rituximab in patients with AS refractory to nonsteroidal antiinflammatory drugs in whom previous treatment with tumor necrosis factor , (TNF,) blockers either had not been tried or had failed. Methods In this phase II clinical trial, 1,000 mg rituximab was administered intravenously at baseline and at week 2 in 20 patients with active AS. Ten of these patients had never received TNF blockers, and treatment with TNF blockers had failed in the other 10 patients. The primary end point was a 20% improvement in disease activity at week 24 according to the criteria of the Assessment of SpondyloArthritis international Society (an ASAS20 response). Results Seventy-five percent of the patients were male, 90% were HLA,B27 positive, their mean age was 39.7 years, and their mean disease duration was 16.8 years. Patients had active disease, defined as a Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) score ,4. While there was no clear response at week 24 in the group in whom TNF blockers had failed (30% had achieved an ASAS20 response, 10% had achieved an ASAS40 response, none had achieved partial remission according to the ASAS criteria, and none had achieved 50% improvement on the BASDAI [a BASDAI50 response] beyond an expected placebo response), we observed a good improvement in the TNF blocker,naive group at week 24 (50% had achieved an ASAS20 response, 40% had achieved an ASAS40 response, 30% had achieved partial remission according to the ASAS criteria, and 50% had achieved a BASDAI50 response). Conclusion Although rituximab does not seem to be effective in patients with AS that does not respond to TNF blockers, it had significant efficacy in TNF blocker,naive patients. Therefore, further controlled trials with B cell,directed therapies should be performed in TNF blocker,naive AS patients in the future. [source]

Clinical experience with tumor necrosis factor blockers in Korean rheumatoid arthritis patients

INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 2 2006
Jin-Wuk HUR
Abstract Tumor necrosis factor (TNF) blockers have become an important treatment in rheumatoid arthritis (RA) with its proven effectiveness. But it is not universally effective in all patients and it comes with a relatively high economic burden. We should use them effectively. Advances in pharmacoeconomics and pharmacogenetics may be able to help us reach this goal. This article will review our clinical experience of biological agents to treat RA at Hanyang University in Korea, with emphasis on the current therapies targeting TNF and the rational use of theses agents in RA. [source]

Different response to rituximab in tumor necrosis factor blocker,naive patients with active ankylosing spondylitis and in patients in whom tumor necrosis factor blockers have failed: A twenty-four,week clinical trial,

ARTHRITIS & RHEUMATISM, Issue 5 2010
I.-H. Song
Objective Histologic studies have shown B cell clusters in the subchondral bone marrow of the spine of patients with ankylosing spondylitis (AS). An immunotherapy targeting B cells in AS is therefore of interest. We undertook this study to examine the efficacy and safety of rituximab in patients with AS refractory to nonsteroidal antiinflammatory drugs in whom previous treatment with tumor necrosis factor , (TNF,) blockers either had not been tried or had failed. Methods In this phase II clinical trial, 1,000 mg rituximab was administered intravenously at baseline and at week 2 in 20 patients with active AS. Ten of these patients had never received TNF blockers, and treatment with TNF blockers had failed in the other 10 patients. The primary end point was a 20% improvement in disease activity at week 24 according to the criteria of the Assessment of SpondyloArthritis international Society (an ASAS20 response). Results Seventy-five percent of the patients were male, 90% were HLA,B27 positive, their mean age was 39.7 years, and their mean disease duration was 16.8 years. Patients had active disease, defined as a Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) score ,4. While there was no clear response at week 24 in the group in whom TNF blockers had failed (30% had achieved an ASAS20 response, 10% had achieved an ASAS40 response, none had achieved partial remission according to the ASAS criteria, and none had achieved 50% improvement on the BASDAI [a BASDAI50 response] beyond an expected placebo response), we observed a good improvement in the TNF blocker,naive group at week 24 (50% had achieved an ASAS20 response, 40% had achieved an ASAS40 response, 30% had achieved partial remission according to the ASAS criteria, and 50% had achieved a BASDAI50 response). Conclusion Although rituximab does not seem to be effective in patients with AS that does not respond to TNF blockers, it had significant efficacy in TNF blocker,naive patients. Therefore, further controlled trials with B cell,directed therapies should be performed in TNF blocker,naive AS patients in the future. [source]

How tumour necrosis factor blockers interfere with tuberculosis immunity

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2010
J. Harris
Summary Tumour necrosis factor (TNF) is a potent inflammatory cytokine that plays an important role in immunity to numerous bacterial infections, including Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB) in humans. Infliximab, adalimumab, certolizumab pegol and etanercept are anti-TNF agents used to treat a range of inflammatory/autoimmune diseases, such as rheumatoid arthritis. The use of some of these drugs has been linked to reactivation TB. In addition to blocking TNF-mediated immune responses, some anti-TNF drugs have been found to interfere with innate immune responses, such as phagolysosomal maturation and monocyte apoptosis, as well as cell-mediated responses, including interferon-, secretion by memory T cells, complement-mediated lysis of Mtb-reactive CD8+ T cells and increased regulatory T cell activity. This review summarizes some of the reported effects of TNF blockers on immune cell responses in the context of the observed clinical data on TB reactivation in patients on anti-TNF therapy. [source]