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ID PMID Title PublicationDate abstract
34016483 Triggers of Cardiovascular Diseases in Rheumatoid Arthritis. 2022 Jun The risk of cardiovascular disease (CVD) in patients with rheumatoid arthritis (RA) is higher than that in patients without RA, and it is even higher than that in patients with diabetes. Autoimmune-mediated inflammation is observed in patients with RA, resulting in endothelial dysfunction, oxidative stress and activation, and vascular migration of white blood cells. Traditionally, RA-associated CVD was assumed to be mediated by disease-related inflammation, resulting in atherosclerosis (AS). However, this concept has been challenged because treatment with anti-rheumatic drugs, such as methotrexate or proinflammatory cytokine antagonists, such as tumor necrosis factor-alpha (TNF-α) inhibitors, did not reduce the risk of CVD in patients with RA. Current cardiovascular guidelines recommend screening and treatment of CVD risk factors in patients with RA but without clear biomarkers and treatment goals. There is no scientific basis for establishing therapeutic targets for cardiovascular risk factors in RA. Numerous studies have shown that the mechanism of early cardiac dysfunction in patients with RA may occur prior to AS. Therefore, it is crucial to explore the related mechanisms to prevent early cardiac dysfunction in patients with RA.
35215538 Nutrition and Diet in Rheumatoid Arthritis. 2022 Feb 19 Rheumatic and musculoskeletal diseases (RMDs) are chronic systemic immune/inflammatory conditions characterized by the interaction between gene predisposition, autoimmunity and environmental factors [...].
34997270 [Innovative strategies for treatment of rheumatoid arthritis]. 2022 Mar Besides excellent guidelines and newly developed highly effective drugs, evidence-based strategic use of these new drugs has especially contributed to enormous advances in rheumatoid arthritis treatment, apparent especially since 2000. Currently, the treat-to-target (T2T) strategy has proven to be the most successful in several studies and systematic reviews. The target is to achieve remission, which should be reached and sustained for an optimal outcome (i.e. stable over a long time period). If the initial disease-modifying antirheumatic drug (DMARD) treatment fails, the best strategy for continuing treatment is controversial, with swap or switch being open to debate (change within a class of drugs or change in the mechanism of action). Recent studies seem to indicate that switching to another mechanism of action is the most successful approach. A hotly discussed topic is the question whether DMARD treatment can or should be tapered when sustained remission has been achieved? Many patients wish for a reduction of drugs in cases of stable remission; however, the stable disease control might become destabilized by tapering. The main priority is the reduction or tapering of glucocorticoid treatment. When the decision for reduction of DMARD treatment is made together with the patient, a complete cessation bears a high risk of a flare, therefore, a careful step by step reduction of DMARD treatment should be preferred. In the case of a running combination, the question whether the conventional DMARD (mostly methotrexate), the biological (b)DMARD or targeted synthetic (ts)DMARD should be reduced first, must be decided on an individual basis. Most patients prefer to first reduce methotrexate and transfer to a monotherapy.
35090806 Rheumatoid arthritis: From synovium biology to cell-based therapy. 2022 Apr Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects the synovial joints and, if not treated properly, can lead to multiple progressive articular and extra-articular damage. Its pathogenesis is primarily associated with an inadequate immune response and dysregulated cytokine production. However, RA is also linked to disruption in oxygen metabolism, impaired redox signaling, acidosis and aberrant intercellular communication. Even though treatment modalities have made RA a manageable disease, a significant number of patients still do not respond satisfactorily or suffer considerably from the adverse events of conventional therapy. In recent years, cell-based strategies, especially the administration of the mesenchymal/medicinal stem/signaling cells (MSCs), have been proposed as a novel and very promising therapeutic approach. RA patients may benefit from the potent anti-inflammatory and immunomodulatory properties and tissue-repair potential of MSCs. Furthermore, the satisfactory safety profile of MSC therapy has been already demonstrated in several clinical studies. This review summarizes current understanding of the pathomechanism behind RA at the molecular and cellular level and focuses on MSC-based clinical research and applications of MSCs for RA treatment.
35085197 Rheumatoid arthritis and DVT risk. 2022 Feb 1 Studies show that patients with rheumatoid arthritis (RA) have an increased risk for deep vein thrombosis (DVT) compared with the general population. This article discusses the pathophysiology and clinical manifestations of RA, explores the DVT risk in patients with RA, and outlines critical nursing actions to care for these patients.
35031874 Rheumatoid arthritis and myasthenia gravis: a case-based review of the therapeutic options 2022 Apr INTRODUCTION: Myasthenia gravis is an autoimmune disease affecting the neuromuscular junction, often associated with other autoimmune diseases, including rheumatoid arthritis. Patients with rheumatoid arthritis present an increased prevalence of myasthenia gravis compared to the general population. While these two diseases share some therapeutic options, such as glucocorticoids, methotrexate, and rituximab, there are no guidelines for treating concomitant disease. We aim to review the available evidence and to discuss the efficacy and safety of the therapeutic options in patients with rheumatoid arthritis associated with myasthenia gravis. METHOD: We described three patients with rheumatoid arthritis associated with myasthenia gravis and we performed a systematic review of the associated literature. RESULTS: A 48-year-old man and two women (48 and 55 years old) with concomitant diagnoses of active rheumatoid arthritis and well-controlled myasthenia gravis are described. They were treated with methotrexate, leflunomide, upadacitinib, and adalimumab. None of them experienced changes in their myasthenic symptoms. We found 9 additional cases from our literature review. Methotrexate, rituximab, upadacitinib, diphenyl sulfone, auranofin, and loxoprofen sodium did not show an impact on the seven patients with previously well-controlled myasthenia. Glucocorticoids, methotrexate, and rituximab proved effective in active myasthenia gravis and arthritis. Conflicting data emerged for Tumor-necrosis factor inhibitors. CONCLUSIONS: Although the available evidence remains scarce, we consider glucocorticoids, methotrexate, and rituximab as safe and effective options. The role of tumor-necrosis factor inhibitors remains uncertain. Eventually, Janus Kinase inhibitors are a novel interesting option for these patients. Key Points • To date, the only evidence on the treatment of patients with rheumatoid arthritis and concomitant myasthenia gravis derives from case reports. • Based on the review of the available case reports and on the cases we described, we consider glucocorticoids, methotrexate, and rituximab as safe and effective options, while the role of Tumor-necrosis factor inhibitors remains uncertain. • Based on the cases we described, Janus Kinase inhibitors are a novel interesting option for patients with concomitant rheumatoid arthritis and myasthenia gravis.
34942050 Some important inhibitors and mechanisms of rheumatoid arthritis. 2022 Jun Rheumatoid arthritis (RA) is a chronic disease that seriously affects human health and quality of life, and it is one of the main causes of labor loss and disability. Many countries have listed rheumatoid arthritis as one of the national a key diseases to tackle. The pathogenesis of RA in humans is still unknown, and medical researchers believe that the pathogenesis of RA may be the result of a combination of genetic and environmental factors. RA is an incurable condition that can only be controlled and treated with conventional drugs. In this paper, the pathologic features and pathogenesis of RA were introduced, and the research progress of new anti-rheumatoid arthritis chemical drugs in recent years was reviewed.
35029702 [Treatment of rheumatoid arthritis and spondylarthritis with biologics]. 2022 Feb Biologics are an integral part of modern strategies for treatment of rheumatoid arthritis (RA) and spondylarthritis (SpA), including psoriatic arthritis (PsA). Biologics are biotechnologically produced proteins that have inhibiting effects on humoral and cellular components of rheumatic inflammation. Substance classes used in rheumatology are tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, IL‑6, IL-12, IL-17 and IL-23 inhibitors effective against cytokines as well as the T lymphocyte activation inhibitor abatacept and the B lymphocyte-depleting rituximab. There are clear recommendations for the use of biologics for RA patients inadequately responding to one or more conventional synthetic disease-modifying antirheumatic drugs and for ankylosing spondylitis (AS) and nonradiographical axial SpA patients with an inadequate response to at least two nonsteroidal antirheumatic drugs. For PsA the recommended use depends on the most prominent manifestations in each case. Treatment with biologics should follow the treat to target principle, with a defined and validated treatment target. Treatment in cases of RA and SpA should target remission or at least a low or minimum disease activity. The safety of treatment with biologics has been intensively investigated. There are very specific contraindications for individual substance classes with a focus on an increased risk of infections. The standard procedure before starting treatment with biologics includes the exclusion of latent tuberculosis and hepatitis B. The TNF-alpha inhibitors have a protective effect with respect to myocardial infarction, stroke and venous thromboembolism.
35185879 Ferroptosis in Rheumatoid Arthritis: A Potential Therapeutic Strategy. 2022 Ferroptosis is one of the newly discovered forms of cell-regulated death characterized by iron-dependent lipid peroxidation. Extensive research has focused on the roles of ferroptosis in tumors, blood diseases, and neurological diseases. Some recent findings have indicated that ferroptosis may also be related to the occurrence and development of inflammatory arthritis. Ferroptosis may be a potential therapeutic target, and few studies in vitro and animal models have shown implications in the pathogenesis of inflammatory arthritis. This mini review discussed the common features between ferroptosis and the pathogenesis of rheumatoid arthritis (RA), and evaluated therapeutic applications of ferroptosis regulators in preclinical and clinical research. Some critical issues worth paying attention to were also raised to guide future research efforts.
34998696 Rheumatoid arthritis and HIV-associated arthritis: Two sides of the same coin or different 2022 Mar The relationship between rheumatoid arthritis (RA) and human immunodeficiency virus (HIV)-associated arthritis is a complex one that was first described more than three decades ago. There are many similarities and some differences in the clinical presentations of both diseases. In addition, treatment options and long-term monitoring can be challenging in the presence of both disorders, as HIV causes an immunocompromised state and medications used to treat RA are immunosuppressive. In this chapter, we discuss the clinical presentation and the use of conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) and biologic disease-modifying antirheumatic drugs (bDMARDs) in the management of these conditions.
35121639 Long-term safety and efficacy of upadacitinib or adalimumab in patients with rheumatoid ar 2022 Feb OBJECTIVES: To assess the long-term safety and efficacy of the Janus kinase inhibitor upadacitinib versus adalimumab over 3 years in the ongoing long-term extension (LTE) of SELECT-COMPARE, a randomised controlled phase 3 trial of patients with active rheumatoid arthritis and inadequate response to methotrexate (MTX). METHODS: Patients on stable background MTX were randomised 2:2:1 to upadacitinib 15 mg, placebo or adalimumab 40 mg. Patients with an insufficient response were switched by week 26 from placebo to upadacitinib, upadacitinib to adalimumab or adalimumab to upadacitinib. Patients who completed the 48-week double-blind period could enter an LTE for up to 10 years. Safety and efficacy results were analysed here through 3 years. Treatment-emergent adverse events (AEs) were summarised based on exposure to upadacitinib and adalimumab. Efficacy was analysed by original randomised groups (non-responder imputation), as well as separately by treatment sequence (as observed). RESULTS: Rates of several AEs were generally comparable between upadacitinib and adalimumab, including AEs leading to discontinuation, serious infections and serious AEs, malignancies, major adverse cardiac events, venous thromboembolism and deaths. Consistent with earlier results, herpes zoster, lymphopaenia, hepatic disorder and CPK elevation were reported at higher rates with upadacitinib versus adalimumab. In terms of efficacy, upadacitinib continued to show numerically better clinical responses than adalimumab over 3 years across all endpoints, including low disease activity and remission. CONCLUSION: The safety profile of UPA 15 mg was consistent with previous study-specific and integrated safety reports. Higher levels of clinical response continued to be observed with upadacitinib versus adalimumab through 3 years of treatment.
35101111 Role of the S100 protein family in rheumatoid arthritis. 2022 Jan 31 Rheumatoid arthritis is a chronic systemic autoimmune disease characterized by synovial hyperplasia, inflammatory cell infiltration, and proliferation of inflammatory tissue (angiogranuloma). The destruction of joints and surrounding tissues eventually causes joint deformities and dysfunction or even loss. The S100 protein family is one of the biggest subtribes in the calcium-binding protein family and has more than 20 members. The overexpression of most S100 proteins in rheumatoid arthritis is closely related to its pathogenesis. This paper reviews the relationship between S100 proteins and the occurrence and development of rheumatoid arthritis. It will provide insights into the development of new clinical diagnostic markers and therapeutic targets for rheumatoid arthritis.
34553824 Rheumatoid arthritis is a preventable disease: 11 ways to reduce your patients' risk. 2022 May New evidence shows that up to 40% of rheumatoid arthritis (RA) cases are attributable to exposure to potentially modifiable factors. We can now identify people at higher risk of RA (pre-RA) through their family history, risk factors, autoantibodies and symptoms. Counselling these patients to act to modify factors known to be associated with RA risk could prevent the development of RA, and evidence shows that informing individuals of their risk and of ways to reduce it leads to positive behavioural change and is not harmful. This consumer-focussed narrative review is targeted at primary care providers and physicians to describe 11 changes that can be made, based on current evidence linking potentially modifiable factors to RA risk. These evidence-based recommendations are: (i) cease smoking; (ii) reduce exposure to inhaled silica, dusts and occupational risks; (iii) maintain a healthy weight; (iv) increase leisure time physical activity; (v) maintain good dental hygiene; (vi) maximise breastfeeding if able; (vii) maximise dietary quality and avoid high-salt diets; (viii) consume high levels of omega-3 fatty acids and fish; (ix) reduce consumption of sugar-sweetened soft drinks; (x) consume moderate levels of alcohol; and (xi) remain vitamin D replete.
35184919 Perioperative Management of Immunosuppressive Medications for Rheumatoid Arthritis. 2022 Apr Operations in patients with rheumatoid arthritis are complicated by the fact that most drugs used in medical management have immunosuppressive mechanisms of action, including corticosteroids and conventional synthetic and biologic disease-modifying antirheumatic drugs. In deciding to continue or discontinue these medications perioperatively, surgeons must weigh the relative risk of infection from immunosuppression against the risk of rheumatoid arthritis symptom flares from reduced medical disease control. The objective of this article is to review the existing evidence regarding perioperative management of immunosuppressive rheumatoid arthritis medications, with a specific focus on relevance to hand and upper-extremity procedures.
34526397 Radiographic Progression of Structural Joint Damage Over 5 Years of Baricitinib Treatment 2022 Feb OBJECTIVE: To evaluate the effect of baricitinib on inhibiting radiographic progression of structural joint damage over 5 years in patients with active rheumatoid arthritis (RA). METHODS: Patients completed 1 of 3 phase III baricitinib trials (ClinicalTrials.gov: NCT01711359, NCT01710358, or NCT01721057) and entered the long-term extension RA-BEYOND (NCT01885078), in which patients received once-daily 4 mg or 2 mg baricitinib. Across these trials, patients initially receiving methotrexate (MTX) or adalimumab (ADA) switched to baricitinib 4 mg at Week 52. Patients initially receiving placebo (PBO) switched to baricitinib 4 mg at Week 24. Radiographs were scored at baseline and Years 2, 3, 4, and 5. Change from baseline in van der Heijde modified total Sharp score (ΔmTSS) was computed. RESULTS: Overall, 2125 of 2573 (82.6%) randomized patients entered RA-BEYOND; 1837 of 2125 (86.4%) entered this analysis. From Years 3 to 5, higher proportions of disease-modifying antirheumatic drug (DMARD)-naïve patients on initial baricitinib (monotherapy or with MTX) had no progression vs initial MTX (ΔmTSS ≤ 0 at Year 5: 59.6% baricitinib 4 mg; 66.2% baricitinib 4 mg + MTX; 40.7% MTX). Higher proportions of patients with inadequate response (IR) to MTX on initial baricitinib or ADA vs PBO had no progression (ΔmTSS ≤ 0 at Year 5: 54.8% baricitinib 4 mg; 55.0% ADA; 50.3% PBO). Higher proportions of patients with conventional synthetic DMARD-IR on initial baricitinib 4 mg had less progression vs initial PBO or baricitinib 2 mg (ΔmTSS ≤ 0 at Year 5: 66.7% baricitinib 4 mg; 58.2% baricitinib 2 mg; 60.0% PBO). CONCLUSION: Oral baricitinib maintained lower levels of radiographic progression than initial conventional synthetic DMARD or PBO through 5 years in patients with active RA.
34906416 Implications of a diagnosis of rheumatoid arthritis in resource-poor countries. 2022 Mar Rheumatoid arthritis (RA) is a multisystemic autoimmune disease that predominantly affects synovial joints. It causes marked disability, reduces health-related quality of life, and leads to high mortality. The diagnosis of RA is often made by standard criteria, and the management of this condition is usually undertaken according to the established guidelines. In resource-poor settings, the diagnosis and management of RA are hampered by diverse factors such as late presentation, inadequate trained personnel, poor healthcare infrastructure, low socioeconomic status, poor access to both conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) and biologics, and a high burden of infectious diseases such as tuberculosis, hepatitis, and human immunodeficiency virus. There is a need to establish registries in these settings to provide adequate information on the pattern, medication, and long-term outcome of RA in resource-poor countries in order to provide a practical and evidence-based management guide for rheumatologists, which is appropriate for these settings.
35095918 Inflammasome and Its Therapeutic Targeting in Rheumatoid Arthritis. 2021 Inflammasome is a cytoplasmic multiprotein complex that facilitates the clearance of exogenous microorganisms or the recognition of endogenous danger signals, which is critically involved in innate inflammatory response. Excessive or abnormal activation of inflammasomes has been shown to contribute to the development of various diseases including autoimmune diseases, neurodegenerative changes, and cancers. Rheumatoid arthritis (RA) is a chronic and complex autoimmune disease, in which inflammasome activation plays a pivotal role in immune dysregulation and joint inflammation. This review summarizes recent findings on inflammasome activation and its effector mechanisms in the pathogenesis of RA and potential development of therapeutic targeting of inflammasome for the immunotherapy of RA.
35401513 Epigenetic Regulation in the Pathogenesis of Rheumatoid Arthritis. 2022 Rheumatoid arthritis (RA) is an autoimmune disease. The etiology of RA remains undetermined and the pathogenesis is complex. There remains a paucity of ideal therapeutic drugs and treatment strategies. The epigenetic modifications affect and regulate the function and characteristics of genes through mechanisms, including DNA methylation, histone modification, chromosome remodeling, and RNAi, thereby exerting a significant impact on the living state of the body. Recently, the phenomenon of epigenetic modification in RA has garnered growing research interest. The application of epigenetically modified methods is the frontier field in the research of RA pathogenesis. This review highlights the research on the pathogenesis of RA based on epigenetic modification in the recent five years, thereby suggesting new methods and strategies for the diagnosis and treatment of RA.
35333708 Pathogenesis of rheumatoid arthritis: one year in review 2022. 2022 Mar The mechanisms underlying the pathogenesis of rheumatoid arthritis (RA) involve different components of the immune system. In subjects with genetic predisposition to develop RA, a tight interaction between cells and mediators of the innate and adaptive immune system leads to the amplification and perpetuation of inflammation and tissue remodelling. The research carried out in the last year in the field of RA has improved the current knowledge on the pathogenesis of the disease, and is potentially useful to develop new therapeutic approaches. Thus, in this review we provide an overview on the new insights into RA pathogenesis, resulting from a literature search of the data published in the last year.
33978821 IL-23R gene polymorphisms in rheumatoid arthritis. 2022 Mar Rheumatoid arthritis (RA) is a common autoimmune disease in which many different genetic variants of functional gene polymorphisms may play a culprit role in the underlying pathogenetic mechanism. The recent studies suggest that interleukin-23 receptor (IL-23R) gene polymorphisms may increase susceptibility to the development of various autoimmune diseases. We aimed to examine the possible relationship of nine single nucleotide polymorphisms (SNPs) in the IL-23R gene to susceptibility to rheumatoid arthritis and their associations with disease characteristics in the South Aegean region of Turkey. We enrolled 100 rheumatoid arthritis patients and age- and sex-matched 96 healthy subjects in the study. After deoxyribonucleic acid (DNA) isolation was performed, a 'Restriction Fragment Length Polymorphism' (RFLP) method was used for the investigation of polymorphisms associated with the IL-23R gene. Allele identification and genotyping were obtained from polymerase chain reaction (PCR) products using gel electrophoresis. Allele frequencies and detected genotypes were compared between groups. All statistical analyses were performed using SPSS 25.0 (IBM SPSS Statistics 25 software (Armonk, NY: IBM Corp.)). Continuous variables were defined by the mean ± standard deviation and categorical variables were defined by number and percent. Logistic Regression Analysis was used for determining which variables affect the presence of RA. Differences between categorical variables were analyzed with Chi-square analysis. Statistical significance was determined as p < 0.05. The mean age was 53.48 ± 11.7 years in the RA group, whereas 52.55 ± 12.7 years in the healthy control group. The genotypes of IL-23R with rs11805303(TT), rs10889677(AA), rs1004819(AA), and rs7530511(CT) polymorphisms were seen more often in RA patients than healthy controls. Having the AA genotype of IL-23R rs1004819 and the CT genotype of Il-23R rs7530511 increase the development risk of RA with a statistical significance (OR: 3.416 p = 0.003 and OR: 4.899 p = 0.0001, respectively). RA patients with the CC genotype of Il-23R with rs11805303, the CC genotype with rs10889677, and the TT genotype with rs2201841 of the IL-23R gene had higher erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels than with other genotypes. RA patients with the CC genotype rs11805303 and the GG genotype rs1004819 of the IL-23R gene had more active disease. Our findings suggest that all of the nine analyzed IL-23R gene polymorphisms are seen more frequently than healthy controls in our study population. Besides, some SNPs were related to higher acute phase reactants and higher disease activity scores.