scholarly journals Switching TNFα inhibitors: Patterns and determinants

2021 ◽  
Vol 9 (4) ◽  
Author(s):  
Rosanne W. Meijboom ◽  
Helga Gardarsdottir ◽  
Matthijs L. Becker ◽  
Mark C. H. de Groot ◽  
Kris L. L. Movig ◽  
...  
Keyword(s):  

2012 ◽  
Vol 20 (1) ◽  
pp. 2-5 ◽  
Author(s):  
Emmett T. Cunningham ◽  
Sirichai Pasadhika ◽  
Eric B. Suhler ◽  
Manfred Zierhut


2017 ◽  
Vol 9 (8) ◽  
pp. 197-210 ◽  
Author(s):  
Valeria Rios Rodriguez ◽  
Denis Poddubnyy

Nonradiographic axial spondyloarthritis (SpA) and radiographic SpA (also known as ankylosing spondylitis) are currently considered as two stages or forms of one disease (axial SpA). The treatment with tumor necrosis factor-α (TNFα) inhibitors has been authorized for years for ankylosing spondylitis. In recent years, most of the anti-TNFα agents have also been approved for the treatment of nonradiographic axial SpA by the European Medicines Agency (EMA) and similar authorities in many countries around the world (but not in the US), increasing the number of possible therapies for this indication. Data from several clinical trials have demonstrated the good efficacy and safety profiles from those anti-TNFα agents. Presently, a large number of patients achieve a satisfactory clinical control with the current therapies, however, there remains a percentage refractory to nonsteroidal anti-inflammatory drugs (NSAIDs) and TNFα inhibitors; therefore, several new drugs are currently under investigation. In 2015, the first representative of a new class of biologics [an interleukin (IL)-17 inhibitor] secukinumab, was approved for the treatment of ankylosing spondylitis; a clinical trial in nonradiographic axial SpA is currently underway. In this review, we discuss the recent data on efficacy and safety of TNFα-inhibitors focusing on the treatment of nonradiographic axial SpA.



2016 ◽  
Vol 51 (5) ◽  
pp. 388-393 ◽  
Author(s):  
María Henar García-Lagunar ◽  
María Rocío Gutiérrez-Cívicos ◽  
María Sergia García-Simón ◽  
Pablo Conesa-Zamora ◽  
Enrique Jimenez-Santos ◽  
...  

Background: The introduction of anti–tumor necrosis factor α (anti-TNFα) drugs has improved the clinical outcomes in rheumatoid arthritis (RA) and ankylosing spondylitis (AS). However, these drugs may cause adverse effects that motivate a change in or discontinuation of the treatment. Objective: To evaluate the causes of discontinuation or changes in the dosage regimen in a cohort of patients with RA and AS treated with infliximab, adalimumab, etanercept, and golimumab under clinical practice conditions. Methods: This was a retrospective observational study that included patients with RA or AS treated with anti-TNFα drugs between 2008 and 2013. Changes in the dosage regimen, reasons for treatment discontinuation, and adverse effects were recorded and analyzed. Time to discontinuation was estimated using Kaplan-Meier survival analysis. Results: A total of 123 patients with RA and 93 patients with AS were treated with anti-TNFα therapy. During the study, 55.3% of RA patients and 41.7% of AS patients had stopped the treatment. The most frequent changes were modifications in the dosing, and the most frequent adverse effects were reactions after the infusion or injection (53.8% and 66.7% in RA and AS, respectively). Drug survival of etanercept in RA (67.9%) is greater than for adalimumab and infliximab, whereas drug survival of infliximab in AS (70.0%) is greater than for etanercept and adalimumab at 5 years, although there were no significant differences ( P = 0.098 in RA and 0.194 in AS). Conclusions: The main cause of discontinuation of anti-TNFα is therapeutic failure in both diseases. Etanercept and infliximab have the best survival rates in RA and AS, respectively.



2020 ◽  
Vol 22 (3) ◽  
pp. 311-319 ◽  
Author(s):  
Quoc-Bao D. Nguyen ◽  
Caroline T. Starling ◽  
Adelaide A. Hebert


Immunotherapy ◽  
2015 ◽  
Vol 7 (6) ◽  
pp. 669-681 ◽  
Author(s):  
Éric Toussirot
Keyword(s):  


2008 ◽  
Vol 57 (5) ◽  
pp. 418-420 ◽  
Author(s):  
Evangelos M. Davas ◽  
Ioannis Alexiou ◽  
Mary Boulbou ◽  
Athanasios Koutroumpas ◽  
Konstantinos Makaritsis ◽  
...  


2017 ◽  
Vol 4 (3) ◽  
pp. 62
Author(s):  
David T. Dulaney ◽  
Wassem Juakiem ◽  
Katherine Cebe ◽  
Angelo H. Paredes

Behcet’s disease (BD) is a multisystem mucocutaneous inflammatory condition characterized by recurrent genital and oral ulcers, ocular inflammation, and can involve the gastrointestinal tract. Treatment involves the usage of immunosuppressive agents to control the disease with glucocorticoids utilized for treatment of flares. Tumor necrosis factor inhibitors are frequently used to control the disease as well. We present the case of a 40 years old African American female presenting with intestinal BD that was refractory to adalimumab therapy. In conjunction with glucocorticoids, the patient’s intestinal disease was controlled with infliximab therapy. Currently, there have been no studies comparing the efficacy of TNFα inhibitors on the treatment of BD. Future studies are needed to compare the efficacy of TNFα inhibitor agents in the treatment of intestinal manifestations of BD.



2019 ◽  
Vol 23 (2) ◽  
pp. 115-120
Author(s):  
Virginia E Duncan ◽  
Karen M Chisholm ◽  
M Cristina Pacheco

Background Antitumor necrosis alpha (TNFα) therapy is often used in the management of patients with inflammatory bowel disease (IBD) and may have effects on lymphoid tissue architecture and function. The goal of our study was to characterize the effects of TNFα inhibitors on mesenteric lymph node and mucosa-associated lymphoid tissue in patients with IBD. Methods We examined lymphoid tissue morphology in IBD patients treated with TNFα inhibitors compared to untreated controls. Intestinal resections from 19 patients (10 anti-TNFα treated and 9 controls) were reviewed. Immunohistochemistry for CD21, CD20, and CD3 was performed on ileocecal valve lymphoid tissue and mesenteric lymph nodes from the resection specimens to assess follicular architecture. Results Relative to control groups, TNFα-treated groups showed less preserved germinal center architecture, evidenced by lower overall semiquantitative scores for follicular architecture. Likewise, the percentage of secondary follicles to total follicles was decreased in patients treated with TNFα blockade. Conclusions Our results suggest that TNFα inhibitors may play a role in disruption of lymphoid germinal center architecture in patients with IBD. Awareness of this disrupted lymphoid morphology when examining histologic sections from patients with IBD treated with TNFα inhibitors may prevent unnecessary studies to exclude a lymphoproliferative disorder.



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