scholarly journals Relapsing Polychondritis in a Patient with Ankylosing Spondylitis Using Etanercept

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Valderilio Feijó Azevedo ◽  
Natalia Bassalobre Galli ◽  
Alais Daiane Fadini Kleinfelder ◽  
Julia Farabolini D’Ippolito ◽  
Andressa Gulin Tolentino ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Autoimmune Disease ◽  
Tumor Necrosis ◽  
Biological Therapy ◽  
Relapsing Polychondritis ◽  
Tracheobronchial Tree ◽  
Substantial Improvement ◽  
Autoantibody Production ◽  
Cartilaginous Tissues ◽  
Necrosis Factor

Relapsing polychondritis (RP) is an autoimmune disease characterized by recurrent episodes of inflammation and progressive destruction of cartilaginous tissues, especially of the ears, nose, joints, and tracheobronchial tree. Its etiology is not well understood, but some studies have linked its pathophysiology with autoimmune disease and autoantibody production. We described a case of a 46-year-old male patient with ankylosing spondylitis who developed RP after the use of etanercept. Few similar cases have been described in the literature. However, they show a possible association between the use of biological inhibitors of tumor necrosis factor (anti-TNFα), which potentially produces autoantibodies, and the development of RP. The treatment was based on data in the literature and included the cessation of biological therapy and the addition of corticosteroids with substantial improvement.

scholarly journals Pathogenetic mechanisms of biological agents in managing of relapsing polychondritis

2018 ◽  
Vol 17 (2) ◽  
pp. 167-174
Author(s):  
E. G. Khaleva ◽  
G. A. Novik ◽  
F. V. Rokhlina
Keyword(s):  
Autoimmune Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Relapsing Polychondritis ◽  
Necrosis Factor Alpha ◽  
Pathogenetic Mechanisms ◽  
Cartilaginous Tissues ◽  
Factor Alpha ◽  
Necrosis Factor

Relapsing polychondritis (RPC) is an autoimmune disease characterized by the inflammation of cartilaginous tissues and other proteoglycan rich tissues. A concomitant disease, particularly myelodysplasia or systemic autoimmune disease can be detected in one-third of the patients with RPC. Unlike adults in children, RPC is less often associated with other autoimmune diseases. The diagnosis of RPC is established using the criteria of Mc Adam (1976) or Damiani (1979). The basis of the pathogenesis of RPC is an autoimmune reaction, which is initially directed against cartilage and then spreads to non-cartilaginous tissues. One of the elements in the pathogenesis of RPC is the mechanical trauma of cartilage, resulting in the release of pro-inflammatory cytokines (tumor necrosis factor alpha, interferon-γ, interleukin-8, and macrophage inflammatory protein 1) and local inflammation followed by the formation of autoantibodies in a patient with a genetic predisposition. In the treatment of RPC, steroids, non-steroidal anti-inflammatory drugs, colchicine are used and, if they are ineffective, immunosuppressants are prescribed. The most effective anti-cytokine drugs used in the treatment of RPC are tumor necrosis factor-alpha (TNF-α) inhibitors, IL-1 receptor antagonists, an inhibitor of the costimulatory pathway of T-lymphocyte activation, monoclonal antibodies against the IL-6 receptor. Given the fact that management of these patients is very complex, the aim of the study is to review available data on pathogenetic mechanisms of biological agents in managing of relapsing polychondritis.

scholarly journals Low BASDAI score alone is not a good predictor of anti-tumor necrosis factor treatment efficacy in ankylosing spondylitis: a retrospective cohort study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Bora Nam ◽  
Bon San Koo ◽  
Tae-Han Lee ◽  
Ji-Hui Shin ◽  
Jin-Ju Kim ◽  
...  
Keyword(s):  
Cohort Study ◽  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Retrospective Cohort Study ◽  
Retrospective Cohort ◽  
Tumor Necrosis ◽  
Activity Index ◽  
Rank Test ◽  
Necrosis Factor

Abstract Background The purpose of this study was to determine the prevalence of high disease activity as measured using the Ankylosing Spondylitis Disease Activity Score (ASDAS) in ankylosing spondylitis (AS) patients who nonetheless have low Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores after anti-tumor necrosis factor (TNF) treatment. Its clinical impact on anti-TNF survival was also investigated. Methods We conducted a single-centre retrospective cohort study of AS patients having low BASDAI scores (< 4) and available ASDAS-C-reactive protein (CRP) data after 3 months of first-line anti-TNF treatment. Patients were grouped into high-ASDAS (≥ 2.1) and low-ASDAS (< 2.1) groups according to the ASDAS-CRP after 3 months of anti-TNF treatment. Their characteristics were compared. And survival analyses were carried out using Kaplan–Meier curves and log-rank test with the event being discontinuation of anti-TNF treatment due to lack/loss of efficacy. Results Among 116 AS patients with low BASDAI scores after 3 months of anti-TNF treatment, 38.8% were grouped into the high-ASDAS group. The high-ASDAS group tended to have greater disease activity after 9 months of treatment (BASDAI 2.9 ± 1.1 vs. 2.3 ± 1.4, p=0.007; ASDAS-CRP 1.8 ± 0.6 vs. 1.5 ± 0.7, p=0.079; proportion of high ASDAS-CRP 27.8% vs. 13.8%, p=0.094) and greater risk of discontinuing anti-TNF treatment due to lack/loss of efficacy than the low-ASDAS group (p=0.011). Conclusions A relatively high proportion of AS patients with low BASDAI scores had high ASDAS-CRP. These low-BASDAI/high-ASDAS-CRP patients also had a greater risk for discontinuation of anti-TNF treatment due to low/lack of efficacy than the low-ASDAS group. The use of the ASDAS-CRP alone or in addition to the BASDAI may improve the assessment of AS patients treated with anti-TNF agents.

Polymorphism within the tumor necrosis factor α (TNF) promoter region in patients with ankylosing spondylitis

1999 ◽  
Vol 60 (2) ◽  
pp. 140-144 ◽  
Author(s):  
Eric L Kaijzel ◽  
Brigitta M.N Brinkman ◽  
Michiel V van Krugten ◽  
Louise Smith ◽  
Tom W.J Huizinga ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
Promoter Region ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor-α (TNFα) inhibitors in the treatment of nonradiographic axial spondyloarthritis: current evidence and place in therapy

2017 ◽  
Vol 9 (8) ◽  
pp. 197-210 ◽  
Author(s):  
Valeria Rios Rodriguez ◽  
Denis Poddubnyy
Keyword(s):  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Axial Spondyloarthritis ◽  
Efficacy And Safety ◽  
Tnfα Inhibitors ◽  
Factor Α ◽  
Nonradiographic Axial Spondyloarthritis ◽  
Necrosis Factor

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.

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