The pre-clinical phase of rheumatoid arthritis: From risk factors to prevention of arthritis

Petrovská, Nora; Prajzlerová, Klára; Vencovský, Jiří; Šenolt, Ladislav; Filková, Mária

doi:10.1016/j.autrev.2021.102797

Cited by 93 publications

(51 citation statements)

References 245 publications

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“…RA is a multifactorial disease caused by genetic, environmental and stochastic factors [ 39 ]. The genetic risk for RA that has been estimated by scientific studies is about 50% [ 40 , 41 ]. The presence or absence of rheumatoid factor (RF) and ACPAs can divide RA into two types (seropositive and seronegative) and there are also differences between the risk factors involved [ 42 , 43 ].…”

Section: Epidemiologic Overviewmentioning

confidence: 99%

Management of Rheumatoid Arthritis: An Overview

Radu

Bungău

2021

Cells

495

185

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Rheumatoid arthritis (RA) is a multifactorial autoimmune disease of unknown etiology, primarily affecting the joints, then extra-articular manifestations can occur. Due to its complexity, which is based on an incompletely elucidated pathophysiological mechanism, good RA management requires a multidisciplinary approach. The clinical status of RA patients has improved in recent years due to medical advances in diagnosis and treatment, that have made it possible to reduce disease activity and prevent systemic complications. The most promising results were obtained by developing disease-modifying anti-rheumatic drugs (DMARDs), the class to which conventional synthetic, biologic, and targeted synthetic drugs belong. Furthermore, ongoing drug development has led to obtaining molecules with improved efficacy and safety profiles, but further research is needed until RA turns into a curable pathology. In the present work, we offer a comprehensive perspective on the management of RA, by centralizing the existing data provided by significant literature, emphasizing the importance of an early and accurate diagnosis associated with optimal personalized treatment in order to achieve better outcomes for RA patients. In addition, this study suggests future research perspectives in the treatment of RA that could lead to higher efficacy and safety profiles and lower financial costs.

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Section: Epidemiologic Overviewmentioning

confidence: 99%

Management of Rheumatoid Arthritis: An Overview

Radu

Bungău

2021

Cells

495

185

View full text Add to dashboard Cite

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“…Rheumatoid arthritis is a wide spread autoimmune disease with a high incidence and causes significant disability to those it affects (Petrovská et al, 2021). It is commonly recognized that the pathogenesis of RA involves the infiltration of interstitial inflammatory cells, the tumor-like proliferation of synovial cells, pannus formation, the erosion of bones and articular cartilage (Josef et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Anti-Rheumatoid Arthritic Effects of Paris Saponin VII in Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes and Adjuvant-Induced Arthritis in Rats

Meng

Yue

et al. 2021

Front. Pharmacol.

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In the pathogenesis of rheumatoid arthritis (RA), rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) have tumor-like characteristics, mainly manifested by hyperproliferation and resistance to apoptosis and then it will erode the bone and cartilage, eventually leading to joint destruction. Paris saponin VII (PS VII) is an active compound derived from a traditional herbal medicine named Trillium tschonoskii Maxim, which has anti-tumor, analgesic, and immunomodulatory effects. However, its anti-RA effect has not yet been reported. This study was to investigate the effect of PS VII on two rheumatoid arthritis fibroblast-like synoviocytes lines (RA-FLS and MH7A) and adjuvant-induced arthritis (AIA) in rats. In vitro, the effects of PS VII on the proliferation, cell cycle, and apoptosis of RA-FLS and MH7A cells were detected by MTT, flow cytometry, and western blot analysis. In vivo, the effect of PS VII on the weight of the rat, paw swelling, ankle joint diameter, arthritis index, serum inflammatory cytokines (TNF-α, IL-6, and IL-1β), histopathological assessment and apoptosis proteins in the synovial tissues were evaluated in AIA rats. The in vitro studies showed that PS VII inhibited the proliferation of RA-FLS and MH7A cells, induced S phase arrest and triggered cell apoptosis mainly through the mitochondrial apoptotic pathway and the regulation of JNK and p38 MAPK pathways. The in vivo studies revealed that PS VII could improve ameliorate body weight, paw swelling, ankle joint diameter, reduce the spleen and thymus index, suppress the production of TNF-α, IL-6 and IL-1β, improve histopathological changes and regulate the expressions of apoptosis proteins in AIA Rats. In conclusion, PS VII could inhibit the proliferation and trigger apoptosis of RA-FLS and MH7A cells by regulating the mitochondrial apoptosis pathway and the JNK and p38 MAPK pathways, and alleviate the symptoms of RA, signifying it to be one of the potential anti-RA therapeutics.

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“…However, further investigations are required to determine whether RA is one of the adverse effects of long-acting GLP-1 receptor agonists. Finally, it was difficult to eliminate the possibility that GLP-1 receptor agonist uncovered a preclinical phase of RA in our case [17]. Similarly, as we do not have previous clinical data, we could not determine whether our patient had already suffered from RA before administering GLP-1 receptor agonist.…”

Section: Discussion/conclusionmentioning

confidence: 84%

Long-Acting Glucagon-Like Peptide-1 Receptor Agonist-Induced Rheumatoid Arthritis in a Patient with Type 2 Diabetes Mellitus

Kikkawa

Hoshi²,

Isoda³

et al. 2021

Dubai Diabetes Endocrinol J

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Case Presentation: We report a case of a male patient with rheumatoid arthritis (RA) diagnosed during treatment with a long-acting glucagon-like peptide-1 (GLP-1) receptor agonist (once-weekly dulaglutide injection). At 3 months after dulaglutide initiation, he began experiencing left shoulder pain that continued despite treatment by an acupuncturist, indicating that the pain was not due to periarthritis scapulohumeralis. His HbA1c level was 7.3% at the 3-month follow-up. At the 6-month follow-up visit, the HbA1c level was 8.2%, the low-density lipoprotein cholesterol level was 132 mg/dL, and he expressed right shoulder pain. After 3 months, the HbA1c level was 9.0%, and his bilateral shoulder pain worsened, due to which he could not use his arms well. Routine laboratory testing revealed no other abnormalities at that time. However, several inflammatory and serological RA markers were detected, including an erythrocyte sedimentation rate of 73 (normal range, <10) mm/h, a C-reactive protein level of 1.89 (normal range, 0.0–0.14) mg/dL, a rheumatoid factor level of 26 (normal range, 0–15) IU/mL, and an anti-cyclic citrullinated protein antibody level of 195 (normal range, <4.5) U/mL. However, tests for antinuclear antibodies, anti-SS-A/Ro antibodies, and anti-RNP antibodies showed negative results. He was diagnosed with RA, and salazosulfapyridine (500 mg/day) was started. At 1 month after RA treatment initiation, his shoulder pain began showing improvement and improved HbA1c levels from 9.0% to 8.0%. Discussion: Thus, this case report suggests an association between RA and GLP-1. Based on a literature search in PubMed, we believe that this case report is the first to demonstrate that a patient with type 2 diabetes mellitus treated with a long-acting GLP-1 receptor agonist had RA. However, further research is needed to determine whether RA is one of the adverse effects of long-acting GLP-1 receptor agonists. Conclusion: During treatment with long-acting GLP-1 receptor agonists, it is necessary to consider the possibility of RA as a differential diagnosis when patients complain of persistent joint pain.

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The pre-clinical phase of rheumatoid arthritis: From risk factors to prevention of arthritis

Cited by 93 publications

References 245 publications

Management of Rheumatoid Arthritis: An Overview

Management of Rheumatoid Arthritis: An Overview

Anti-Rheumatoid Arthritic Effects of Paris Saponin VII in Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes and Adjuvant-Induced Arthritis in Rats

Long-Acting Glucagon-Like Peptide-1 Receptor Agonist-Induced Rheumatoid Arthritis in a Patient with Type 2 Diabetes Mellitus

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