New therapeutic approaches in rheumatoid arthritis

2016 ◽  
Vol 45 (6) ◽  
pp. e179-e192 ◽  
Author(s):  
Ronald F. van Vollenhoven
2010 ◽  
Vol 10 ◽  
pp. 2248-2253 ◽  
Author(s):  
Xiao Hua Pan ◽  
Jianxin Zhang ◽  
Xiaowei Yu ◽  
Ling Qin ◽  
Ligeng Kang ◽  
...  

Due to the complex etiology of rheumatoid arthritis (RA), it is difficult to be completely cured at the current stage although many approaches have been applied in clinics, especially the wide application of nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs). New drug discovery and development via the recently discovered cholinergic anti-inflammatory and antinociceptive pathways should be promising. Based on the above, the nicotinic acetylcholine receptor agonists maintain the potential for the treatment of RA. Therefore, new therapeutic approaches may rise from these two newly discovered pathways. More preclinical experiments and clinical trials are required to confirm our viewpoint.


2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Céline Coppard ◽  
Francis Bonnefoy ◽  
Dalil Hannani ◽  
Françoise Gabert ◽  
Olivier Manches ◽  
...  

Abstract Background Despite major advances in rheumatoid arthritis outcome, not all patients achieve remission, and there is still an unmet need for new therapeutic approaches. This study aimed at evaluating in a pre-clinical murine model the efficacy of extracorporeal photopheresis (ECP) in the treatment of rheumatoid arthritis, and to provide a relevant study model for dissecting ECP mechanism of action in autoimmune diseases. Methods DBA/1 mice were immunized by subcutaneous injection of bovine collagen type II, in order to initiate the development of collagen-induced arthritis (CIA). Arthritic mice received 3 ECP treatments every other day, with psoralen + UVA-treated (PUVA) spleen cells obtained from arthritic mice. Arthritis score was measured, and immune cell subsets were monitored. Results ECP-treated mice recovered from arthritis as evidenced by a decreasing arthritic score over time. Significant decrease in the frequency of Th17 cells in the spleen of treated mice was observed. Interestingly, while PUVA-treated spleen cells from healthy mouse had no effect, PUVA-treated arthritic mouse derived-spleen cells were able to induce control of arthritis development. Conclusions Our results demonstrate that ECP can control arthritis in CIA-mice, and clarifies ECP mechanisms of action, showing ECP efficacy and Th17 decrease only when arthritogenic T cells are contained within the treated sample. These data represent a pre-clinical proof of concept supporting the use of ECP in the treatment of RA in Human.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2019 ◽  
Author(s):  
David L. Scott

The management of rheumatoid arthritis has changed dramatically over the last three decades. Improvements in clinical assessment have been a key driver of these changes. However, in the last five years, three areas of unresolved uncertainty have dominated specialist thinking in the field. These challenges comprise identifying the optimal management target, determining how best to reach this target by using intensive treatments, and individualising management because not all patients need or respond to identical treatments. The key problem that links each of these areas is balancing different types of evidence and is most readily appreciated in relation to treatment intensity. Giving more intensive therapy improves outcomes but also increases risks and, with biologic treatments, substantially increases drug costs. Specialists and healthcare funders need to agree on how best to rationalise optimal care for patients with what is most effective and safe and what is affordable.


2019 ◽  
Vol 20 (6) ◽  
pp. 1332 ◽  
Author(s):  
Shyi-Jou Chen ◽  
Gu-Jiun Lin ◽  
Jing-Wun Chen ◽  
Kai-Chen Wang ◽  
Chiung-Hsi Tien ◽  
...  

Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disease of unknown etiology. It is characterized by the presence of rheumatoid factor and anticitrullinated peptide antibodies. The orchestra of the inflammatory process among various immune cells, cytokines, chemokines, proteases, matrix metalloproteinases (MMPs), and reactive oxidative stress play critical immunopathologic roles in the inflammatory cascade of the joint environment, leading to clinical impairment and RA. With the growing understanding of the immunopathogenic mechanisms, increasingly novel marked and potential biologic agents have merged for the treatment of RA in recent years. In this review, we focus on the current understanding of pathogenic mechanisms, highlight novel biologic disease-modifying antirheumatic drugs (DMRADs), targeted synthetic DMRADs, and immune-modulating agents, and identify the applicable immune-mediated therapeutic strategies of the near future. In conclusion, new therapeutic approaches are emerging through a better understanding of the immunopathophysiology of RA, which is improving disease outcomes better than ever.


2011 ◽  
Vol 152 (39) ◽  
pp. 1552-1559 ◽  
Author(s):  
Katalin Dankó ◽  
Melinda Vincze

Inflammatory myopathies are chronic, immune-mediated diseases characterized with progressive proximal muscle weakness. They encompass a variety of syndromes with protean manifestations. The aims of therapy are to increase muscle strength, prevent the development of contractures, and to manage the systemic manifestations of the disease. This is a complex treatment which requires routine and wide knowledge. The most important task is to recognize the disease and guide the patient to immunologic center. Although the first line of therapy continues to include corticosteroids, there are a multitude of agents available for treating patients with myositis. There are several different immunosuppressive agents which may be applied alone or in combination with each other, as well as an increasing number of novel and exciting biologic agents targeting molecules participating in the pathogenesis of inflammatory myopathy. Physiotherapy and rehabilitation in the remission period may significantly improve the functional outcome of patients with these disorders. Orv. Hetil., 2011, 152, 1552–1559.


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