The “Treat to Target” Approach to Rheumatoid Arthritis

Salomon-Escoto, Karen; Kay, Jonathan

doi:10.1016/j.rdc.2019.06.001

Cited by 20 publications

(27 citation statements)

References 106 publications

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“…Treatment targets in RA involve low disease activity as well as remission. For monitoring disease activity, in order to make it quantifiable, defined measures are available as guidelines for treatment [ 333 ]. This strategy can help to gain control of the active disease as quickly as possible, and the number of treatment options have grown remarkably.…”

Section: Treatment Strategies In Ramentioning

confidence: 99%

Recent Advances in Understanding the Pathogenesis of Rheumatoid Arthritis: New Treatment Strategies

Mueller

Payandeh

Mohammadkhani

et al. 2021

Cells

104

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Rheumatoid arthritis (RA) is considered a chronic systemic, multi-factorial, inflammatory, and progressive autoimmune disease affecting many people worldwide. While patients show very individual courses of disease, with RA focusing on the musculoskeletal system, joints are often severely affected, leading to local inflammation, cartilage destruction, and bone erosion. To prevent joint damage and physical disability as one of many symptoms of RA, early diagnosis is critical. Auto-antibodies play a pivotal clinical role in patients with systemic RA. As biomarkers, they could help to make a more efficient diagnosis, prognosis, and treatment decision. Besides auto-antibodies, several other factors are involved in the progression of RA, such as epigenetic alterations, post-translational modifications, glycosylation, autophagy, and T-cells. Understanding the interplay between these factors would contribute to a deeper insight into the causes, mechanisms, progression, and treatment of the disease. In this review, the latest RA research findings are discussed to better understand the pathogenesis, and finally, treatment strategies for RA therapy are presented, including both conventional approaches and new methods that have been developed in recent years or are currently under investigation.

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Section: Treatment Strategies In Ramentioning

confidence: 99%

Recent Advances in Understanding the Pathogenesis of Rheumatoid Arthritis: New Treatment Strategies

Mueller

Payandeh

Mohammadkhani

et al. 2021

Cells

104

View full text Add to dashboard Cite

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“…Rheumatoid arthritis (RA), as a chronic and autoimmune disease, is featured by increased systematic autoantibody, inflammation, and synovial hyperplasia, which affects many populations especially females 1,2 . Along with the development of biopharmaceutics (such as tumor necrosis factor inhibitor, interleukin‐6 inhibitor, and JAK inhibitor) and more standardized management (such as treat‐to‐target strategy), the outcome of RA is much improved 3–6 . However, there are still a proportion of RA patients lack response to the current treatment, giving rise to the deeper exploration of RA pathology and biomarkers to improve its management 7…”

Section: Introductionmentioning

confidence: 99%

Measurement of synovium and serum dual specificity phosphatase 22 level: Their inter‐correlation and potency as biomarkers in rheumatoid arthritis

Chen

et al. 2021

Clinical Laboratory Analysis

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Background Dual specificity phosphatase 22 (DUSP22), also named as Jun N‐terminal kinase pathway associated phosphatase recently, is reported to be closely engaged in immune and inflammation regulation. This study aimed to investigate the interaction between synovium DUSP22 and serum DUSP22 levels and to explore their correlation with rheumatoid arthritis (RA) risk, inflammation, and disease activity. Methods Synovium and serum samples from 42 RA patients with knee involvement underwent arthroscopy, and 20 knee trauma patients were collected. Besides, serum samples from 40 healthy controls were also obtained. Synovium DUSP22 expression was detected by reverse transcription quantitative polymerase chain reaction, while serum DUSP22 level was detected by enzyme‐linked immunosorbent assay. Results Synovium DUSP22 level was greatly decreased in RA patients compared to trauma controls (p < 0.001), and it was negatively correlated with tender joint count (TJC) (r = −0.318, p = 0.040), C‐reactive protein (CRP) (r = −0.330, p = 0.033), and Lysholm score (r = −0.423, p = 0.005) in RA patients. Serum DUSP22 level was lowest in RA patients, followed by trauma controls, then highest in healthy controls (p < 0.001). Serum DUSP22 level was negatively associated with TJC (r = −0.438, p = 0.004), swollen joint count (SJC) (r = −0.372, p = 0.015), CRP (r = −0.391, p = 0.011), and disease activity score in 28 joints (DAS28ESR) score (r = −0.406, p = 0.008), and it increased after treatment (p = 0.001) in RA patients. In addition, serum DUSP22 level positively related to synovium DUSP22 level in RA patients (r = 0.394, p = 0.010). Conclusion Synovium and serum DUSP22 are intercorrelated and insufficiently expressed in RA patients; meanwhile, their deficiency correlates with increased systemic inflammation, disease activity, and joint dysfunction.

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“…Rheumatoid arthritis (RA) is among the most common debilitating joint conditions in the United States, affecting up to 1% of the population [ 1 – 4 ]. In recent decades, therapeutic advances in disease-modifying antirheumatic drugs (DMARDs) have enabled inhibition of disease progression and made clinical remission an achievable goal [ 5 – 8 ]. However, a challenge remains in optimizing treatment regimens to reach such a state in the shortest duration of time, to minimize damage to the joints caused by elevated disease activity.…”

Section: Introductionmentioning

confidence: 99%

Non-invasive monitoring of arthritis treatment response via targeting of tyrosine-phosphorylated annexin A2 in chondrocytes

et al. 2021

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Background The development and optimization of therapies for rheumatoid arthritis (RA) is currently hindered by a lack of methods for early non-invasive monitoring of treatment response. Annexin A2, an inflammation-associated protein whose presence and phosphorylation levels are upregulated in RA, represents a potential molecular target for tracking RA treatment response. Methods LS301, a near-infrared dye-peptide conjugate that selectively targets tyrosine 23-phosphorylated annexin A2 (pANXA2), was evaluated for its utility in monitoring disease progression, remission, and early response to drug treatment in mouse models of RA by fluorescence imaging. The intraarticular distribution and localization of LS301 relative to pANXA2 was determined by histological and immunohistochemical methods. Results In mouse models of spontaneous and serum transfer-induced inflammatory arthritis, intravenously administered LS301 showed selective accumulation in regions of joint pathology including paws, ankles, and knees with positive correlation between fluorescent signal and disease severity by clinical scoring. Whole-body near-infrared imaging with LS301 allowed tracking of spontaneous disease remission and the therapeutic response after dexamethasone treatment. Histological analysis showed preferential accumulation of LS301 within the chondrocytes and articular cartilage in arthritic mice, and colocalization was observed between LS301 and pANXA2 in the joint tissue. Conclusions We demonstrate that fluorescence imaging with LS301 can be used to monitor the progression, remission, and early response to drug treatment in mouse models of RA. Given the ease of detecting LS301 with portable optical imaging devices, the agent may become a useful early treatment response reporter for arthritis diagnosis and drug evaluation.

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The “Treat to Target” Approach to Rheumatoid Arthritis

Cited by 20 publications

References 106 publications

Recent Advances in Understanding the Pathogenesis of Rheumatoid Arthritis: New Treatment Strategies

Recent Advances in Understanding the Pathogenesis of Rheumatoid Arthritis: New Treatment Strategies

Measurement of synovium and serum dual specificity phosphatase 22 level: Their inter‐correlation and potency as biomarkers in rheumatoid arthritis

Non-invasive monitoring of arthritis treatment response via targeting of tyrosine-phosphorylated annexin A2 in chondrocytes

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