Comparative effectiveness of cycling of tumor necrosis factor-α (TNF-α) inhibitors versus switching to non-TNF biologics in rheumatoid arthritis patients with inadequate response to TNF-α inhibitor using a Bayesian approach

2014 ◽  
Vol 37 (5) ◽  
pp. 662-670 ◽  
Author(s):  
Hye-Lin Kim ◽  
Min-Young Lee ◽  
Sun-Young Park ◽  
Sun-Kyeong Park ◽  
Ji-Hye Byun ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Bayesian Approach ◽  
Comparative Effectiveness ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Inadequate Response ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor Necrosis Factor-α Inhibitor Use Is Not Associated with Lipid Changes in Rheumatoid Arthritis

2012 ◽  
Vol 39 (5) ◽  
pp. 946-948 ◽  
Author(s):  
ANDRONIKI BILI ◽  
STEPHANIE J. MORRIS ◽  
JENNIFER A. SARTORIUS ◽  
H. LES KIRCHNER ◽  
JANA L. ANTOHE ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Levels ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.To determine the association of use of tumor necrosis factor-α (TNF-α) inhibitors with differences in lipid levels in patients with rheumatoid arthritis (RA).Methods.We studied 807 patients with incident RA to compare differences in lipid levels in TNF-α inhibitor users versus nonusers, with adjustment for relevant covariables.Results.TNF-α inhibitor use was not associated with differences in levels of low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), triglycerides, LDL:HDL, or TC:HDL compared to nonusers.Conclusion.Use of TNF-α inhibitor was not associated with differences in lipid levels in patients with RA.

TUMOR NECROSIS FACTOR-α CONVERTING ENZYME EXPRESSION IN THE JOINTS OF RHEUMATOID ARTHRITIS PATIENTS

2002 ◽  
Vol 06 (02) ◽  
pp. 63-71 ◽  
Author(s):  
Koichiro Takahi ◽  
Tetsuya Tomita ◽  
Takanobu Nakase ◽  
Motoharu Kaneko ◽  
Hiroshi Takano ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Subchondral Bone ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mononuclear Cells ◽  
Converting Enzyme ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

The purpose of this study is to investigate the expression of tumor necrosis factor-α converting enzyme (TACE) in the synovium and subchondral bone region of patients with rheumatoid arthritis (RA) and to determine the contribution of the enzyme to the pathogenesis of RA. Joint tissues were obtained during total knee arthroplasty from patients with RA and osteoarthritis (OA). The expression of TACE and TNF-α mRNA was detected by in situ hybridization. Characterization of TACE expressing cells was performed by immunohistochemistry using serial sections. We found that TACE mRNA was expressed in both synovium and subchondral bone region and co-localized with TNF-α mRNA in RA. On the other hand, TACE mRNA expression was scarcely detectable in OA samples. TACE was expressed in mononuclear cells, such as CD3 and CD14 positive cells in RA samples. In conclusion, the expression of TACE is up-regulated in the rheumatoid synovium and subchondral bone region, and the results in this study demonstrate that TACE may be involved and play a role in the pathogenesis of RA.

Tumor necrosis factor-α -308 polymorphism in North Indian rheumatoid arthritis patients and association with mRNA and serum TNF-α

2017 ◽  
Vol 36 (10) ◽  
pp. 2209-2216 ◽  
Author(s):  
Mohd Jahid ◽  
Rehan-Ul-Haq ◽  
Puja Kumari Jha ◽  
Diwesh Chawla ◽  
Rajnish Avasthi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

The Risk of Tuberculosis in Patients with Rheumatoid Arthritis Treated with Tumor Necrosis Factor-α Antagonist: A Metaanalysis of Both Randomized Controlled Trials and Registry/Cohort Studies

2015 ◽  
Vol 42 (12) ◽  
pp. 2229-2237 ◽  
Author(s):  
Jing-Wen Ai ◽  
Shu Zhang ◽  
Qiao-Ling Ruan ◽  
Yi-Qi Yu ◽  
Bing-Yan Zhang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Cohort Studies ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Controlled Trials ◽  
Randomized Controlled ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.Tumor necrosis factor-α (TNF-α) antagonists have significantly improved treatment results in rheumatoid arthritis (RA), but have also increased the risk of tuberculosis (TB). Etanercept (ETN), adalimumab (ADA), infliximab (IFX), golimumab, and certolizumab pegol are the 5 drugs currently available on the market. This article aimed to evaluate the risk of TB infection from these 5 drugs for patients with RA.Methods.We searched PubMed, EMBASE, COCHRANE library, OVID, and EBSCO for randomized controlled trials (RCT) of TNF-α antagonist versus control and registry/longitudinal cohort studies of 1 TNF-α antagonist versus another. The Mantel-Haenszel test was adopted to analyze risk ratio (RR) in this metaanalysis.Results.Fifty RCT and 13 non-RCT were included in this study. No significant difference in TB risk was found in the RCT because of the short observational periods. In the non-RCT, TNF-α antagonist was associated with a higher TB risk in patients with RA (RR 4.03, 95% CI 2.36–6.88), and the TB incidence rates of IFX and ADA were 2.78 and 3.88 times, respectively, higher than that of ETN. Further, preventive treatment for latent TB infection (LTBI) was shown to reduce the TB risk by 65% (RR 0.35, 95% CI 0.15–0.82).Conclusion.This study demonstrated a significant increase in TB risk in patients with RA treated with TNF-α antagonists; among them, ETN is least likely to cause active TB. The study also proposes the necessity of LTBI prophylaxis in patients with RA.

Disease Activity Improvement in Rheumatoid Arthritis Treated with Tumor Necrosis Factor-α Inhibitors Correlates with Increased Soluble Fas Levels

2014 ◽  
Vol 41 (10) ◽  
pp. 1961-1965 ◽  
Author(s):  
Eloisa Romano ◽  
Riccardo Terenzi ◽  
Mirko Manetti ◽  
Francesca Peruzzi ◽  
Ginevra Fiori ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Soluble Fas ◽  
Tnf Α ◽  
Before And After ◽  
Factor Α ◽  
Necrosis Factor

Objective.Rheumatoid arthritis (RA) is characterized by chronic synovial inflammation and hyperplasia. Tumor necrosis factor-α (TNF-α) plays a pivotal role in RA by interfering with the Fas–Fas ligand (FasL) proapoptotic pathway. We investigated the circulating levels of soluble Fas (sFas) and soluble FasL (sFasL), and their possible correlation with disease activity and improvement after anti-TNF-α treatment in RA.Methods.Serum levels of sFas and sFasL were measured by quantitative ELISA in 52 patients with RA before and after 3 months of anti-TNF-α treatment (adalimumab, n = 32; infliximab, n = 20). Disease activity measures [Disease Activity Score at 28 joints-erythrocyte sedimentation rate (DAS28-ESR), C-reactive protein (CRP)] were recorded before and after treatment. Forty age-matched and sex-matched healthy subjects served as controls.Results.No significant differences in serum sFas levels were detected between anti-TNF-α-naive patients with RA and controls. After anti-TNF-α treatment, serum sFas levels significantly increased in patients with RA compared to both anti-TNF-α-naive patients and controls. Increased sFas levels inversely correlated with disease activity variables (DAS28-ESR: r = −0.739, CRP: r = −0.636, both p < 0.001). No significant differences in sFasL levels were detected in patients with RA before and after anti-TNF-α treatment.Conclusion.In RA, an increase in sFas levels closely correlates with improvement in disease activity induced by TNF-α inhibitors, suggesting their ability to modulate Fas-mediated synoviocyte apoptosis.

Interleukin 10 and Tumor Necrosis Factor-α Genotypes in Rheumatoid Arthritis — Association with Clinical Response to Glucocorticoids

2010 ◽  
Vol 37 (3) ◽  
pp. 503-511 ◽  
Author(s):  
BANESA de PAZ ◽  
MERCEDES ALPERI-LÓPEZ ◽  
FRANCISCO J. BALLINA-GARCÍA ◽  
CATUXA PRADO ◽  
LOURDES MOZO ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Clinical Response ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 10 ◽  
Functional Polymorphisms ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.There are dysregulated levels of interleukin 10 (IL-10) and tumor necrosis factor-α (TNF-α) in rheumatoid arthritis (RA), and their role in the disease is controversial. We analyzed the association of functional polymorphisms of IL-10 and TNF-α with susceptibility and disease characteristics at the time of diagnosis, and we also evaluated their possible use as predictors of clinical response to treatments.Methods.Patients with recent-onset RA (n = 162) and healthy controls (n = 373) were genotyped for −1082 IL-10 and −308 TNF-α polymorphisms and data were related to clinical and immunological measurements of patients at the time of diagnosis. Response to treatment after 6 months was determined in 125 patients by the absolute change in Disease Activity Score (DAS28) and the American College of Rheumatology criteria for improvement.Results.We found a reduced frequency of the low IL-10 producer genotype (−1082AA) in patients with RA compared to controls (26.5% vs 38.9%; p = 0.006), while it is a risk factor for anticyclic citrullinated peptide antibodies (anti-CCP) positivity (p = 0.028). Evaluation of clinical response to treatments indicated that carriage of the high IL-10 genotype was associated with a favorable outcome (p = 0.009), specifically to prednisone therapy (p = 0.0003). No significant effects were observed with TNF-α polymorphism alone; however, in combination with the IL-10 genotype, it increased the strength of these associations.Conclusion.Results show an association between the low IL-10 producer genotype and protection from RA; nevertheless, when other specific genetic and/or environmental factors trigger onset of RA, this genotype may predispose to development of anti-CCP+ RA disease with reduced response to prednisone treatment.

Associations Between Tumor Necrosis Factor-α (TNF-α) −308 and −238 G/A Polymorphisms and Shared Epitope Status and Responsiveness to TNF-α Blockers in Rheumatoid Arthritis: A Metaanalysis Update

2010 ◽  
Vol 37 (4) ◽  
pp. 740-746 ◽  
Author(s):  
YOUNG HO LEE ◽  
JONG DAE JI ◽  
SANG-CHEOL BAE ◽  
GWAN GYU SONG
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Shared Epitope ◽  
Tnf Blockers ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Se Status

Objective.To investigate whether tumor necrosis factor-α (TNF-α) promoter −308 A/G and −238 A/G polymorphisms and shared epitope (SE) status are associated with responsiveness to anti-TNF therapy in patients with rheumatoid arthritis (RA).Methods.A comparative metaanalysis was conducted on A allele carriers (genotypes A/A + A/G) of the TNF-α promoter −308 and −238 A/G polymorphisms and SE status in responders and nonresponders to anti-TNF therapy.Results.A total of 13 studies were included in the metaanalysis. Metaanalysis showed that the TNF-α −308 A/G polymorphism is not associated with responsiveness to TNF blockers in RA patients. Studies with a small number of subjects (< 100) showed that the odds ratio for the A allele carrier state was significantly lower among responders (OR 0.344, 95% CI 0.152–0.779, p = 0.01). Studies with a higher number of subjects (≥ 100) found no association between the TNF-α −308 A/G polymorphism and responsiveness to TNF blockers. The overall metaanalysis showed that the TNF-α −238 A/G polymorphism was not associated with the responsiveness of RA patients to TNF blockers, and stratification by TNF blocker revealed that the TNF-α −238 A/G polymorphism was associated with response of infliximab (OR 0.441, 95% CI 0.203–0.609, p = 0.039). SE status was found not to be associated with response to TNF blockers.Conclusion.Metaanalysis of available data revealed an association between treatment response to infliximab and the TNF-α −238 A/G polymorphism, but no associations between treatment response and the TNF-α −308 A/G polymorphism or SE status.

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