Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
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33231330 | Metabolic syndrome in rheumatoid arthritis patients: Relationship among its clinical compo | 2021 Mar | BACKGROUND: Metabolic syndrome (MetS) prevalence in rheumatoid arthritis (RA) patients is known to vary considerably across the world. This study aimed to determine the prevalence of MetS in RA patients from western Mexico and to analyze the interrelation of the MetS components with the clinical variables of RA. METHODS: This case-control study included 216 RA patients and 260 control subjects (CS). MetS prevalence was determined according to the NCEP/ATP III and the Latin American Consensus of the Latin American Diabetes Association (ALAD) criteria. RESULTS: MetS was observed in 30.6% RA patients and 33.3% of controls (p > 0.05) according to NCEP/ATP III and 28.7% in RA patients and 31.1% for controls using ALAD criteria. Total cholesterol, LDL-C, and Castelli's I-II indexes were lower in RA (p < 0.001) than in CS. The RA patients with MetS had more swollen joints than those without MetS (p = 0.018). In RA patients with MetS, DAS-28 score correlated with smoking index (rho = 0.4601, p = 0.0004) and VLDL-C (rho = 0.3108, p = 0.0056); similarly, rheumatoid factor (RF) correlated with age (rho = 0.2031, p = 0.0027), smoking index (rho = 0.3404, p < 0.0001), triglycerides (rho = 0.1958, p = 0.0039), and VLDL-C (rho = 0.1761, p = 0.0162). CONCLUSIONS: The MetS prevalence in RA patients from western Mexico is not higher than controls; however, in RA patients with MetS, some inflammatory markers are associated with MetS components; thus, the control of MetS in RA could be beneficial to regulate disease activity. | |
32798648 | The immunomodulatory role of PDEs inhibitors in immune cells: therapeutic implication in r | 2020 Nov | Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by inflammatory synovitis and progressive joint. Although the etiology is extremely complex, overwhelming evidence suggests that dysregulation or imbalance of the immune system plays a central role in disease pathogenesis. The bone loss and joint destruction are immunological insults mediated by infiltration and abnormal activation of various immune cells. Since pharmacological inhibition of cyclic nucleotide phosphodiesterases (PDEs), which degrade cyclic AMP and cyclic GMP, can regulate the activity of multiple immune cells, which are considered as a potential strategy for treating RA. Therefore, this review attempted to summarize the modulating effects of PDEs on immune cells and described the molecular underpinnings and potential clinical application of PDEs inhibitors for RA. | |
31711804 | Rheumatoid Arthritis Is Associated With Thromboembolic Complications Following Primary Tot | 2020 Apr | BACKGROUND: Recent studies have demonstrated patients with rheumatoid arthritis (RA) have deranged coagulation parameters predisposing them to venous thromboembolisms (VTEs). Therefore, the purpose of this study was to investigate whether patients who have RA undergoing primary TKA have higher rates of (1) VTEs; (2) readmission rates; and (3) costs of care. METHODS: Patients who have RA undergoing primary TKA were identified and matched to controls in a 1:5 ratio by age, sex, and comorbidities. Exclusions included patients with a history of VTEs and hypercoagulable states. Primary outcomes analyzed included rates of 90-day VTEs, along with lower extremity deep vein thromboses and pulmonary embolisms, 90-day readmission rates, in addition to day of surgery, and 90-day costs of care. A P-value less than .05 was considered statistically significant. RESULTS: Patients who have RA were found to have significantly higher incidence and odds (OR) of VTEs (1.9 vs 1.3%; OR: 1.51, P < .0001), deep vein thromboses (1.6 vs 1.1%; OR: 1.55, P < .0001), and pulmonary embolisms (0.4 vs 0.3%; OR: 1.26, P= .0001). Study group patients also had significantly higher incidence and odds of readmissions (21.6 vs 14.1%; OR: 1.67, P < .0001) compared to controls. In addition, RA patients incurred significantly higher day of surgery ($12,475.17 vs $11,428.96; P < .0001) and 90-day costs of care ($15,937.34 vs $13,678.85; P < .0001). CONCLUSION: After adjusting for age, sex, and comorbidities, the study found patients who have RA undergoing primary TKA had significantly higher rates of VTEs, readmissions, and costs. | |
32983422 | Health effects of a low-inflammatory diet in adults with arthritis: a systematic review an | 2020 | The aim is to systematically assess the health impact of a low-inflammatory diet intervention (full-diet or supplement), compared to usual diet or other dietary interventions, on weight change, inflammatory biomarkers, joint symptoms, and quality of life in adults with osteoarthritis, rheumatoid arthritis or seronegative arthropathy (psoriatic, reactive, ankylosing spondylitis or IBD-related), on outcomes assessed in prospective studies within 6 months of intervention commencement (PROSPERO CRD42019136567). Search of multiple electronic library databases from inception to July 2019, supplemented by grey literature searches, for randomised and prospective trials assessing the above objective. After exclusion of 446 ineligible studies, five randomised and two prospective trials involving 468 participants with either osteoarthritis or rheumatoid arthritis were included. GRADE assessment for all outcomes was very low. Meta-analyses produced the following standardised mean differences (SMD) and 95 % confidence interval (CI) 2-4 months following commencement of the diets favouring the low-inflammatory diet: weight SMD -0â‹…45 (CI -0â‹…71, -0â‹…18); inflammatory biomarkers SMD -2â‹…33 (CI -3â‹…82, -0â‹…84). No significant effects were found for physical function (SMD -0â‹…62; CI -1â‹…39, 0â‹…14), general health (SMD 0â‹…89; CI -0â‹…39, 2â‹…16) and joint pain (SMD -0â‹…98; CI -2â‹…90, 0â‹…93). In most studies, the quality of dietary intervention (dietitian input, use of validated dietary compliance tool) could not be gauged. In conclusion, very low-level evidence suggests that low-inflammatory diets or supplements compared to usual diets are associated with greater weight loss and improvement in inflammatory biomarkers. More high-quality trials are needed to assess the health effects of a low-inflammatory diet more comprehensively and conclusively in arthritic conditions. | |
30880553 | Rac1 regulates platelet microparticles formation and rheumatoid arthritis deterioration. | 2020 | Platelets play important roles in blood clotting, hemostasis and wound repair, while more and more research show that platelets also have significant contributions in the process of inflammation. Rheumatoid arthritis is a chronic systemic inflammatory autoimmune disease. Platelet microparticles, which are membrane vesicles shed by activated platelets, are reported to amplify inflammation in Rheumatoid arthritis. Here we show that either platelet-specific deletion of Rac1 (Rac1(-/-)) or Rac1-specific inhibitor NSC23766 dramatically inhibit platelet-derived microparticles formation. As we all know, collagen-induced arthritis (CIA) mouse model is the most common autoimmune model of rheumatoid arthritis. Interestingly, NSC23766 alleviated the process of collagen-induced arthritis of DBA mice in vivo, including the reduced hind paw thickness and ankle stiffness, the reduction of arthritic scores and incidence of arthritis. Our work also found that NSC23766-treated CIA mouse spleen is less swollen and contains less enlarged white pulp than PBS control. The histological analysis shows that NSC23766-treated but not solvent control improve the cartilage erosion symptom in the joint of CIA mouse. Interestingly, platelet microparticles in the peripheral blood of NSC23766-treated CIA mice were decreased significantly compared with PBS-treated CIA mice. In conclusion, our work demonstrated that Rac1 inhibition alleviates collagen-induced arthritis through the decrease of platelet microparticles' release. In short, Rac1 aggravate the rheumatoid arthritis deterioration through the regulation of platelet microparticles formation. | |
33210179 | Efficacy of methotrexate in reducing the risk of bone erosion in patients with rheumatoid | 2021 May | Even though new drugs for the treatment of rheumatoid arthritis (RA) have been developed, methotrexate (MTX) remains a commonly used drug for RA management. In addition to monitoring disease activity during RA treatment, bone erosion should be closely assessed throughout long-term RA management. In this review article, we present a systematic review of MTX effectiveness in reducing the risk of bone erosion. We reviewed randomized controlled trial studies that involved MTX monotherapy or MTX in combination with placebo. Evaluation of the progression of bone erosion was examined by radiographic assessment such as total Sharp score (TSS) or van der Heijde score (SvdH or vdH TSS), joint space narrowing (JSN), erosion score (ERO), and proportion of radiographic nonprogressors. Several key factors were found to influence the response to MTX treatment, such as gene polymorphism. The exact mechanism of the prevention of bone erosion by MTX remains unclear, which warrants future investigations. The variability of RA disease activity in study subjects resulted in variations in the results reported by individual studies. Collective analysis suggests that MTX could slow down the progression of bone erosion based on a radiographic score of less than 0.5-1/year. | |
31802391 | Tapering Biologic Therapy for Rheumatoid Arthritis: A Qualitative Study of Patient Perspec | 2020 Apr | BACKGROUND AND OBJECTIVE: Biologic therapies are cost effective for active rheumatoid arthritis but have adverse effects and are costly. Tapering of biologics is emerging as an important consideration when sustained remission is achieved. Recent trials have highlighted the clinical feasibility of tapering, but there is little evidence on how proposed tapering would be received by patients. The aim of this study was to explore factors influencing hypothetical decisions of patients with rheumatoid arthritis on tapering their biologics and their perspectives on remission and flare when considering the possibility of tapering. METHODS: Patients with rheumatoid arthritis with diverse experiences of biologics with different modes of administration were purposively sampled to participate in one of six focus groups (n = 43) or an individual interview (n = 2). Transcripts were analyzed using inductive thematic analysis. RESULTS: Five overarching themes on what influences a participant's decision to taper their biologic were identified. First, participants were fearful of uncertain outcomes of tapering, especially flare and joint damage. Second, participants prioritized quality of life from continuing biologics over the risk of adverse effects. Third, tapering biologics was seen as providing relief from the inconvenience of taking biologics regularly. Fourth, participants wanted assurance of prompt access to healthcare if their rheumatoid arthritis were to flare when tapering. Fifth, preferences for involvement in decision making varied, but fulfilling information needs was desired to aid a patient's preferred role in decision making on tapering. CONCLUSIONS: This study provides novel insight into the perspectives of patients with rheumatoid arthritis on tapering biologics when sustained remission is achieved at a crucial juncture in global affordability for healthcare systems. These patient perspectives can inform the planning of decision aids and clinical trials of decision-making processes when tapering is proposed. | |
31656153 | Rheumatoid Arthritis: Seropositivity versus Seronegativity; A Comparative Cross-sectional | 2020 | INTRODUCTION: Rheumatoid arthritis (RA) is biologically marked by a positive serum rate of rheumatoid factor (RA) and/or anti-citrullinated protein antibodies (ACPA). Nevertheless, 20% of RA cases remain seronegative. OBJECTIVE: The main purpose of this study, is to bring out the clinical, biological, imaging, therapeutic, and evolutionary distinctions between seropositive RA and seronegative one. METHODS: This is an observational cross-sectional study that involves patients with RA admitted in the rheumatology department, from the period between January 2012 and January 2018. RA seronegativity is described as the absence of both RF and ACPA, while seropositivity is recognized by the presence of at least one of the two antibodies. RESULTS: 294 patients were included, of which 90% were seropositive and 10% seronegative. Therefore, RA in this study is seropositive most often. The bivariate analysis underscored plenty of differences, statistically notable, according to the RA immune status. In fact, patients with seropositive RA had more synovitis (p=0.049), more deformities (p=0.01), and more bone destruction on radiographs (p=0.04). Furthermore, RA in this Moroccan study was quite severe (p=0.006) and got more complicated by systemic manifestations (p=0.02). Whereas, no distinction was brought up between the two groups, concerning the use of biotherapy. As for the multivariate study, seropositive RA in these patients, had greater severity (p=0.009, OR=4.53) and was more deforming (p=0.03 OR=2.45). CONCLUSION: RA in our Moroccan context is dominated by the seropositive form. This seropositivity is often coupled with clinical severity and joint destruction, resulting in more deformities. | |
33191792 | Differential mitochondrial genome in patients with Rheumatoid Arthritis. | 2021 Feb | BACKGROUND: Mitochondria play an important role in cell survival, function and lineage differentiation. Changes in mitochondrial DNA (mtDNA) may control mitochondrial functions and thus may impart an alternative cellular state thereby leading to a disease condition in the body. Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease wherein immune cells become self-reactive causing joint inflammation, swelling and pain in patients. The changes in mtDNA may alter cellular functions thereby directing the immune cells towards an inflammatory phenotype in RA. Therefore, it becomes pertinent to identify changes in mtDNA sequence in immune cells of RA patients to understand the pathogenesis and progression of RA. METHODS: mtDNA from peripheral blood mono-nuclear cells (PBMCs) of 23 RA patients and 17 healthy controls (HCs) were sequenced using next-generation sequencing (NGS). Further, single nucleotide polymorphisms (SNPs) and other variable changes in mtDNA hypervariable and coding regions, amino acid changes with a putative impact on disease, levels of heteroplasmy, copy number variations and haplogroup analysis in RA patients and HCs were analysed and compared to identify any association of mtDNA changes and RA disease. RESULTS: A total of 382 single nucleotide mtDNA variants were observed, 91 (23.82%) were present in hypervariable region and 291 (76.18%) in coding region of patients and HC. The variant 513 GCA > ACA, with G present in HVR-III, known to control the mitochondrial translation function, was significantly present in RA patients. The CYTB gene had larger number of SNPs in HC samples while RNR2 was more variable in RA patients. A non-synonymous heteroplasmy in ND1 gene was found at a single nucleotide position 3533 in an increased number of RA patients as compared to the controls. A significant increase in mtDNA duplication and a higher frequency of the haplogroup U was also characteristic of RA. Also, the presence of SNPs in mitochondrial tRNA genes at two positions 12308 A > G and 15924 A > G were found to be pathogenic. CONCLUSION: We herein observed an altered mtDNA sequence in immune cells of RA patients and thus a possible role of mitochondrial genome in the development of RA. The observed nucleotide changes in mtDNA control region, RNR2 gene, increased heteroplasmy and mtDNA duplication in RA patients may alter sites for transcription factor binding thereby influencing mtDNA gene expression, as well as copy numbers thereby affecting the mitochondrial proteins and their functions. These changes in mtDNA could be one of the probable reasons among many leading to the progression of RA. | |
32820183 | Dry eye in rheumatoid arthritis patients under TNF-inhibitors: conjunctival goblet cell as | 2020 Aug 20 | Dry eye disease (DED) is common in Rheumatoid Arthritis (RA) patients. The application of conjunctival goblet cell count as a clinical biomarker to diagnose and respond to treatment can take place in rheumatoid arthritis patients under TNF-inhibitors (TNFi) therapy. This study aimed to investigate the ocular surface parameters and the long-term effects of TNFi therapy on ocular surface features and goblet cell count of rheumatoid arthritis patients. At baseline, rheumatoid arthritis patients eligible to TNFi were compared to healthy controls (similar age/gender), regarding Ocular Surface Disease Index (OSDI) questionnaire, Schirmer I test, tear break-up time test, vital dye staining of the ocular surface, and conjunctival impression cytology. DED severity grade, impression cytology score, and goblet cell count were analyzed. Rheumatoid arthritis patients were followed after three (3 M) and 12 months (12 M), during TNFi treatment. Sixteen rheumatoid arthritis patients and 24 controls were compared: a higher frequency of abnormal OSDI (68.8% vs. 16.7%, p = 0.002), Schirmer's test < 10 mm (37.5% vs. 8.3%, p = 0.042), meibomian gland dysfunction (50% vs. 8.3%, p = 0.007), abnormal impression cytology (75% vs. 8.3%, p < 0.001), and mild to moderate DED (81.3% vs. 4.2%, p < 0.001) were observed in rheumatoid arthritis patients, who also had lower goblet cell count [325 (274-707) cells/mm(2) vs. 742 (562-863) cells/mm(2), p = 0.004]. The presence of Meibomian gland dysfunction was associated with higher disease activity scores (p < 0.05). The prospective early observation of these patients at 3 M showed an increase improvement in tear production by Schirmer's test [13 (7.5-17.5) vs. 23.5 (16-35); p = 0.001], and an improvement in impression cytology score [1 (0.5-2) vs. 1 (0-1), p = 0.031] and in goblet cell count [325 (274-707) vs. 931 (656-1,244), p < 0.001]. Eight RA responders to TNFi were also re-evaluated at 12 M with further improvement in goblet cell count [393 (275-827) vs. 872 (502-1,185) vs. 1,079 (867-1,244), p = 0.047]. Multifactorial DED is frequent in RA patients, comprising aqueous, lipid, and mucin components. TNFi prompt improves tear production and recovers the goblet cells, which can be a biomarker of the pathological process and response to therapy in this population. | |
32447598 | Cachexia in patients with rheumatoid arthritis: a cohort study. | 2020 Dec | BACKGROUND: Rheumatoid arthritis (RA) is an inflammatory disease that leads to altered body composition. The loss of lean mass with a preservation or increase in fat mass has been termed rheumatoid cachexia (RC), to contrast with classic cachexia, which is characterized by severe weight loss. There are limited data on the prevalence and progression of cachexia in RA over time, as well as on associated factors. Our aim was to determine the prevalence of cachexia and to determine associations with potential factors. METHODS: This prospective cohort study recruited consecutively patients diagnosed with RA and followed for 1 year. The assessments were performed: clinical features, body composition, and physical function. RC and classic cachexia were assessed by several established diagnostic criteria. The pairwise Student's t test, Chi-square test, and GEE were performed (accepted at p ≤ 0.05). RESULTS: Of 90 patients recruited, 81 completed the study. Most patients were women (88.9%), and the mean age was 56.5 ± 7.3 years. At baseline, the median DAS28-CRP was 3.0 (IQR, 1.0-3.0), 13.3-30.0% of the included patients had RC, while none met criteria for classic cachexia. The prevalence of cachexia did not change after 12 months. Disease activity status and treatment with biologic disease-modifying antirheumatic drugs were significantly associated with changes on body composition and physical function (p < 0.05). CONCLUSIONS: In this cohort, RC was common, while classic cachexia was absent. Disease activity and use of biologic therapies were associated with changes on body composition and physical function, underscoring the importance of aiming for remission when treating RA. | |
32192063 | Abberant Immunoglobulin G Glycosylation in Rheumatoid Arthritis by LTQ-ESI-MS. | 2020 Mar 17 | Aberrant glycosylation has been observed in many autoimmune diseases. For example, aberrant glycosylation of immunoglobulin G (IgG) has been implicated in rheumatoid arthritis (RA) pathogenesis. The aim of this study is to investigate IgG glycosylation and whether there is an association with rheumatoid factor levels in the serum of RA patients. We detected permethylated N-glycans of the IgG obtained in serum from 44 RA patients and 30 healthy controls using linear ion-trap electrospray ionization mass spectrometry (LTQ-ESI-MS), a highly sensitive and efficient approach in the detection and identification of N-glycans profiles. IgG N-glycosylation and rheumatoid factor levels were compared in healthy controls and RA patients. Our results suggested that total IgG purified from serum of RA patients shows significantly lower galactosylation (p = 0.0012), lower sialylation (p < 0.0001) and higher fucosylation (p = 0.0063) levels compared with healthy controls. We observed a positive correlation between aberrant N-glycosylation and rheumatoid factor level in the RA patients. In conclusion, we identified aberrant glycosylation of IgG in the serum of RA patients and its association with elevated levels of rheumatoid factor. | |
32856510 | Disease activity trajectories in rheumatoid arthritis: a tool for prediction of outcome. | 2021 Jan | Objective: Predicting treatment response and disease progression in rheumatoid arthritis (RA) remains an elusive endeavour. Identifying subgroups of patients with similar progression is essential for understanding what hinders improvement. However, this cannot be achieved with response criteria based on current versus previous Disease Activity Scores, as they lack the time component. We propose a longitudinal approach that identifies subgroups of patients while capturing their evolution across several clinical outcomes simultaneously (multi-trajectories). Method: For exploration, the RA cohort BARFOT (n = 2829) was used to identify 24 month post-diagnosis simultaneous trajectories of 28-joint Disease Activity Score and its components. Measurements were available at inclusion (0), 3, 6, 12, 24, and 60 months. Multi-trajectories were found with latent class growth modelling. For validation, the TIRA-2 cohort (n = 504) was used. Radiographic changes, assessed by the modified Sharp van der Heijde score, were correlated with trajectory membership. Results: Three multi-trajectories were identified, with 39.6% of the patients in the lowest and 18.9% in the highest (worst) trajectory. Patients in the worst trajectory had on average eight tender and six swollen joints after 24 months. Radiographic changes at 24 and 60 months were significantly increased from the lowest to the highest trajectory. Conclusion: Multi-trajectories constitute a powerful tool for identifying subgroups of RA patients and could be used in future studies searching for predictive biomarkers for disease progression. The evolution and shape of the trajectories in TIRA-2 were very similar to those in BARFOT, even though TIRA-2 is a newer cohort. | |
33139676 | Early retirement attributed to rheumatoid arthritis and its predictors. | 2020 Jul | OBJECTIVE: To evaluate the rate of early retirement due to rheumatoid arthritis (RA) in Portugal. METHODS: Prospective cohort study involving 11 Portuguese centers, including patients with a clinical diagnosis of RA, based on Reuma.pt registry, enrolled between 2008 and 2019. RESULTS: 3231 patients were included (81.5% female, aged 60.8 ± 13.0 years, mean disease duration 18.0 ± 10.3 years). Until the present time, 37.6% of these patients retired, 59.6% due to RA. Early retirement due to RA translated into losing 7 years of active work when compared to patients retired to other causes. Compared to professionally active patients, retired patients due to RA were diagnosed later in the disease process (p=0.003), had longer disease duration (p < 0.001), were more frequently positive for rheumatoid factor (p=0.043), had more frequently erosive disease (p < 0.001), had a blue-collar occupation (p < 0.001) and had a lower educational level (p < 0.001). Independent predictors for early retirement due to RA were: delayed diagnosis (OR: 2.23; 95% CI 1.18-4.21/year, p=0.013), erosive disease (OR: 2.21 95% CI 1.54-3.16, p < 0.001), need for biologic therapy (OR: 1.32; 95%CI 1.01-1.73, p=0.045) and lower educational level (OR: 0.83; 95%CI 0.79-0.86/year, p < 0.001). CONCLUSION: RA is, itself, the leading cause of early retirement in RA patients, accounting for the loss of an average of 7 years of active work. Delayed diagnosis, erosive disease and lower educational level are the main predictors of early retirement associated with RA in this population. | |
32195966 | The association between Bell's palsy and rheumatoid arthritis: A longitudinal study. | 2020 Mar | This study aimed to evaluate the relationship between Bell's palsy and rheumatoid arthritis in a national sample cohort from Korea.Data were collected for individuals ≥20 years old from 2002 to 2013 in the Korean National Health Insurance Service-National Sample Cohort. We extracted data for patients with rheumatoid arthritis (n = 7628) and 1:4-matched controls (n = 30,512) and analyzed the occurrence of Bell's palsy in both groups. Matching was performed based on age, sex, income, and region of residence. Rheumatoid arthritis was diagnosed according to International Classification of Disease-10 (ICD-10) codes (M05-M06) and the prescription of biological agents and/or disease-modifying antirheumatic drugs. Bell's palsy patients were diagnosed according to ICD-10 code H912 and treatment ≥2 times with steroids. Adjusted hazard ratios (HRs) were calculated using stratified Cox proportional hazard models for the Charlson comorbidity index and 95% confidence intervals (CIs). Subgroup analyses based on age and sex were also performed.The rates of Bell's palsy were similar between the rheumatoid arthritis group (0.5% [38/7628]) and the control group, with no significant difference (0.4% [124/30,512], P = .270). The adjusted HR for Bell's palsy was 1.12 (95% CI, 0.78-1.62) in the rheumatoid arthritis group (P = .540). In the subgroup analyses according to age and sex, the relationship between Bell's palsy and rheumatoid arthritis did not reach statistical significance.The risk of Bell's palsy was not increased in patients with rheumatoid arthritis. | |
32140775 | Analysis of a mathematical model of rheumatoid arthritis. | 2020 May | Rheumatoid arthritis is an autoimmune disease characterized by inflammation in the synovial fluid within the synovial joint connecting two contiguous bony surfaces. The inflammation diffuses into the cartilage adjacent to each of the bony surfaces, resulting in their gradual destruction. The interface between the cartilage and the synovial fluid is an evolving free boundary. In this paper we consider a two-phase free boundary problem based on a simplified model of rheumatoid arthritis. We prove global existence and uniqueness of a solution, and derive properties of the free boundary. In particular it is proved that the free boundary increases in time, and the cartilage shrinks to zero as [Formula: see text], even under treatment by a drug. It is also shown in the reduced one-phased problem, with cartilage alone, that a larger prescribed inflammation function leads to a faster destruction of the cartilage. | |
32238080 | Relationship between periodontitis and rheumatoid arthritis in Vietnamese patients. | 2020 Oct | Objective: This study aimed to survey periodontal status of Vietnamese patients with rheumatoid arthritis (RA) and investigates the association between periodontitis and RA in these patients.Materials and methods: We conducted a cross-sectional descriptive study on 150 RA patients and another 150 patients with osteoarthritis (OA). RA was evaluated using the DAS28 disease activity score based on C-reactive protein levels (DAS28-CRP), disease activity classification, and serum levels of RA biomarkers. Periodontal status was determined using periodontal indices.Results: The proportion of periodontitis cases in the RA group was significantly higher than the OA group (67 and 28%, respectively). The rate of severe periodontitis observed in the RA group was also significantly higher than that in the OA group (22.7 and 8%, respectively). RA patients with periodontitis had higher DAS28-CRP scores, disease activity levels, ACPA positivity and higher serum levels of CRP and ACPAs. Periodontitis is associated with an increased risk for RA (odds ratio [OR]: 5.14, 95% confidence interval [CI]: 3.14 - 8.41) and with higher disease activity classification (OR: 2.7, 95% CI: 1.14 - 6.42).Conclusions: Vietnamese RA patients often presented with a more serious periodontal condition than OA patients. We observed an association between periodontal disease (PD) status and clinic symptoms and biochemical/immunological characteristics of RA. | |
32562092 | Is There a Brain/Heart Interaction in Rheumatoid Arthritis and Seronegative Spondyloartrop | 2020 Jun 19 | PURPOSE OF REVIEW: To present the interaction between brain/heart and emphasize the role of combined brain/heart magnetic resonance imaging (MRI) in patients with rheumatoid arthritis (RA) and other seronegative spondyloarthropathies (SNA). RECENT FINDINGS: Both traditional cardiovascular disease (CVD) risk factors and intrinsic RA/SNA features contribute to the increased CVD-related morbidity/mortality. CVD in RA usually occurs a decade earlier than age- and sex-matched controls, and RA patients are twice more likely to develop myocardial infarction irrespective of age, history of prior CVD, and traditional CVD risk factors. RA also increases risk of non-ischemic heart failure (HF), valvular disease, and myo-pericarditis. CVD in SNA affects more commonly patients with long-standing disease. Ascending aortitis, aortic/mitral insufficiency, conduction defects, and diastolic dysfunction are the commonest findings in ankylosing spondylitis (AS). CVD is also the leading cause of death in psoriatic arthritis (PsA), due to myopericarditis, diastolic dysfunction, and valvular disease. Brain damage, due to either ischemic or hemorrhagic stroke and silent vascular damage, such as white matter hyperenhancement (WMH), is increased in both RA/SNA and may lead to cognitive dysfunction, depression, and brain atrophy. Magnetic resonance imaging (MRI) is ideal for serial brain/heart evaluation of patients with systemic diseases. RA/SNA patients are at high risk for brain/heart damage at early age, irrespectively of classic risk factors. Until more data will be obtained, a combined brain/heart MRI evaluation can be proposed in RA/SNA with new onset of arrhythmia and/or HF, cognitive dysfunction and/or depression. | |
32698072 | The endocannabinoid signaling pathway as an emerging target in pharmacotherapy, earmarking | 2020 Sep 15 | Rheumatoid arthritis is an inflammatory autoimmune disease, characterized by synovial proliferation, destruction to articular cartilage and severe pain. The cannabinoids obtained from Cannabis sativa exhibited their actions via cannabinoid-1 and -2 receptors, which also provides a platform for endocannabinoids to act. The endocannabinoid system comprises endocannabinoid molecules involved in signaling processes, along with G-protein coupled receptors and enzymes associated with ligand biosynthesis, activation and degradation. The action of endocannabinoid system in immune system regulation, via primary CB2 activation, followed by inhibition of production of pro-inflammatory cytokines, auto-antibodies and MMPs, FLSs proliferation and T-cell mediated immune response, are elaborated as potential therapeutic regimes in rheumatoid arthritis. The involvement of endocannabinoid system in immune cells like, B cells, T cells and macrophages, as well as regulatory actions on sensory noniceptors to ameliorate pain is significantly highlighted in the review, elaborating the actions of endocannabinoid signaling in mitigating the disease events. The review also focuses on enhancement of endocannabinoid tone, either by inhibiting the degradation enzymes, like FAAH, MAGL, COX, CytP450, LOX, etc. or by retarding cellular uptake processes. Moreover, the review portrays the optimizing role of endocannabinoid system, in abbreviating the symptoms and complications of rheumatoid arthritis in patients and mitigating inflammation, pain and immune mediated effects significantly. | |
33084415 | Icariin alleviates rheumatoid arthritis via regulating miR-223-3p/NLRP3 signalling axis. | 2020 Dec | Rheumatoid arthritis (RA) is considered to be a chronic autoimmune disease, pathogenesis of RA is complex and effective treatments for RA is still lacking. Previous studies found that microRNAs (miRNAs) play important roles in the pathogenesis of RA, and miR-223-3p is considered to be one of the possible biomarkers of RA. Recent studies have revealed that icariin alleviates RA in murine models, but the underlying mechanism needs to be further investigated. MiR-223-3p expression levels in fibroblast-like synoviocyte (RA-FLS) and patients with RA were quantified by qRT-PCR, cell proliferation was analyzed by CCK-8 and BrdU assay. Cell apoptosis was assessed by flow cytometry and western blotting. TNF-α, IL-1β and IL-6 concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Dual luminescence-based reporter gene assay was conducted to confirm the possible interaction between miR-223-3p and NLRP3. Icariin inhibits proliferation and inflammation cytokines secretion, promotes apoptosis of RA-FLS cells and upregulated the expression of miR-223-3p. MiR-223-3p targets to 3'-UTR of NRLP3 and regulates its expression. MiR-223-3p inhibitor reversed the effect of icariin on RA-FLS cells function. Additionally, anti-RA activity of icariin was restored by NLRP3 inhibitor MCC950 in miR-223-3p knockdown RA-FLS cells. Icariin inhibits proliferation and inflammation, promotes apoptosis of RA-FLS cells by regulating miR-223-3p/NLRP3 signalling, which may serve as a potential therapeutic target to alleviate RA. |