HYPERBARIC OXYGENATION IN COMPLEX THERAPY OF RHEUMATOID ARTHRITIS IN PATIENTS WITH CONCOMITANT ANEMIA

2020 ◽  
pp. 42-52
Author(s):  
T.S. Golubtsova ◽  
A.B. Peskov ◽  
S.V. Peskova ◽  
M.P. Markevich ◽  
V.V. Gnoevykh ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Chronic Inflammation ◽  
Hyperbaric Oxygenation ◽  
Joint Inflammation ◽  
Primary Objective ◽  
Hemoglobin Level ◽  
Standard Scheme ◽  
Comparison Results ◽  
Complex Therapy ◽  
Activity Indices

Anemia occurs in approximately 30–70 % of patients with rheumatoid arthritis (RA). The most common cause of low hemoglobin level is chronic inflammation. Hyperbaric oxygenation (HBO) reduces the chronic inflammatory process, hypoxia severity and stimulates erythropoiesis. Therefore, HBO can be considered as one of the promising methods for treating anemia of chronic inflammation. The primary objective of the study is to carry out the efficacy analysis of rheumatoid arthritis (RA) complex therapy using hyperbaric oxygenation (HBO) for comparison results in patients with anemia and with a normal hemoglobin level. Materials and Methods. To assess the advisability of HBO in patients with RA and concomitant anemia, we analyzed indicators of RA activity and local joint inflammation in 120 patients. 30 patients were treated according to the standard scheme, 30 patients underwent one and 60 patients – five additional HBO sessions (1.3 atm during 40 min). Patients who underwent HBO were divided into two subgroups with normal and low hemoglobin levels. Results. On the 14th day of inpatient hospitalization, we fixed decrease in RA activity indices in all groups. The decrease in the activity of RA and local joint inflammation in patients who underwent HBO was faster than in patients who were treated according to the standard scheme, and in patients who underwent only one HBO session. Better results were observed in patients with concomitant anemia compared with patients with normal hemoglobin level. It was confirmed by a significant decrease in acute-phase blood values (ESR and CRP) and RA activity indices (assessment of disease activity (by a doctor and by a patient), CDIA, SDIA and DAS28). Conclusion. Additional HBO in complex RA therapy contributes to the efficacy of inpatient treatment. The most pronounced effect is observed in patients with both RA and anemia. Keywords: hyperbaric oxygenation, rheumatoid arthritis, anemia. Анемия встречается у 30–70 % больных, страдающих ревматоидным артритом (РА). Наиболее частой причиной снижения уровня гемоглобина крови является хроническое воспаление. Гипербарическая оксигенация (ГБО) способствует уменьшению активности хронического воспалительного процесса, выраженности гипоксии и стимулирует эритропоэз, следовательно, применение ГБО можно рассматривать как один из перспективных методов лечения анемии хронического воспаления. Цель работы – провести сравнительный анализ эффективности комплексной терапии пациентов, страдающих ревматоидным артритом, с включением курса гипербарической оксигенации на фоне анемии и при нормальном значении уровня гемоглобина крови. Материалы и методы. Для оценки целесообразности проведения курса ГБО у больных, страдающих РА с сопутствующей анемией, проведен динамический анализ показателей активности РА и локального воспаления в суставе у 120 пациентов (30 пациентов получили лечение по стандартной схеме, 30 больных дополнительно прошли 1 сеанс ГБО и 60 пациентов прошли 5 сеансов ГБО при 1,3 атм в течение 40 мин). Пациенты, прошедшие курс ГБО, были разделены на две подгруппы: с нормальным и сниженным уровнем гемоглобина. Результаты. На 14-й день госпитализации у всех пациентов отмечали регресс клинических проявлений артрита. Снижение показателей активности РА и локального воспаления в суставе у пациентов, прошедших курс ГБО, происходило быстрее, чем у больных, получивших лечение по стандартной схеме, и пациентов, прошедших один сеанс ГБО. Более высокие результаты лечения получены у больных с сопутствующей анемией по сравнению с пациентами с нормальными значениями гемоглобина, что подтверждено значимым снижением острофазовых показателей крови (СОЭ и СРБ) и индексов активности РА (ООАВ, ООАБ, CDIA, SDIA и DAS28). Выводы. Включение курса ГБО в стандартную схему терапии РА повышает эффективность стационарного лечения. Наиболее выраженный эффект наблюдается у больных с РА и анемией. Ключевые слова: гипербарическая оксигенация, ревматоидный артрит, анемия.

scholarly journals Linkage of Periodontitis and Rheumatoid Arthritis: Current Evidence and Potential Biological Interactions

2019 ◽  
Vol 20 (18) ◽  
pp. 4541 ◽  
Author(s):  
Rafael Scaf de Molon ◽  
Carlos Rossa Jr. ◽  
Rogier M. Thurlings ◽  
Joni Augusto Cirelli ◽  
Marije I. Koenders
Keyword(s):  
Rheumatoid Arthritis ◽  
Chronic Inflammation ◽  
Structural Damage ◽  
Joint Inflammation ◽  
Periodontal Pathogen ◽  
Current Evidence ◽  
Biological Interactions ◽  
Loss Of Function ◽  
Synovial Joint ◽  
Chronic Inflammatory Condition

The association between rheumatoid arthritis (RA) and periodontal disease (PD) has been the focus of numerous investigations driven by their common pathological features. RA is an autoimmune disease characterized by chronic inflammation, the production of anti-citrullinated proteins antibodies (ACPA) leading to synovial joint inflammation and destruction. PD is a chronic inflammatory condition associated with a dysbiotic microbial biofilm affecting the supporting tissues around the teeth leading to the destruction of mineralized and non-mineralized connective tissues. Chronic inflammation associated with both RA and PD is similar in the predominant adaptive immune phenotype, in the imbalance between pro- and anti-inflammatory cytokines and in the role of smoking and genetic background as risk factors. Structural damage that occurs in consequence of chronic inflammation is the ultimate cause of loss of function and disability observed with the progression of RA and PD. Interestingly, the periodontal pathogen Porphyromonas gingivalis has been implicated in the generation of ACPA in RA patients, suggesting a direct biological intersection between PD and RA. However, more studies are warranted to confirm this link, elucidate potential mechanisms involved, and ascertain temporal associations between RA and PD. This review is mainly focused on recent clinical and translational research intends to discuss and provide an overview of the relationship between RA and PD, exploring the similarities in the immune-pathological aspects and the possible mechanisms linking the development and progression of both diseases. In addition, the current available treatments targeting both RA and PD were revised.

Body Mass Index Impact on Disease Activity, Clinical and Sonographic Remission Rates in Patients with Rheumatoid Arthritis

2019 ◽  
Vol 15 (3) ◽  
pp. 215-223
Author(s):  
Tanya Sapundzhieva ◽  
Rositsa Karalilova ◽  
Anastas Batalov
Keyword(s):  
Rheumatoid Arthritis ◽  
Body Mass Index ◽  
Disease Activity ◽  
Body Mass ◽  
Normal Weight ◽  
Clinical Disease ◽  
Clinical Disease Activity ◽  
Das 28 ◽  
Remission Rates ◽  
Activity Indices

Aim: To investigate the impact of body mass index (BMI) on clinical disease activity indices and clinical and sonographic remission rates in patients with rheumatoid arthritis (RA). Patients and Methods: Sixty-three patients with RA were categorized according to BMI score into three groups: normal (BMI<25), overweight (BMI 25-30) and obese (BMI≥30). Thirty-three of them were treated with conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs), and 30 with biologic DMARDs (bDMARDs). Patients underwent clinical and laboratory assessment and musculoskeletal ultrasound examination (MSUS) at baseline and at 6 months after initiation of therapy. We evaluated the rate of clinical and sonographic remission (defined as Power Doppler score (PD) = 0) and its correlation with BMI score. Results: In the csDMARDs group, 60% of the normal weight patients reached DAS28 remission; 33.3% of the overweight; and 0% of the obese patients. In the bDMARDs group, the percentage of remission was as follows: 60% in the normal weight subgroup, 33.3% in the overweight; and 15.8% in the obese. Within the csDMARDs treatment group, two significant correlations were found: BMI score–DAS 28 at 6th month, rs = .372, p = .033; BMI score–DAS 28 categories, rs = .447, p = .014. Within the bDMARDs group, three significant correlations were identified: BMI score–PDUS at sixth month, rs = .506, p =.004; BMI score–DAS 28, rs = .511, p = .004; BMI score–DAS 28 categories, rs = .592, p = .001. Sonographic remission rates at 6 months were significantly higher in the normal BMI category in both treatment groups. Conclusion: BMI influences the treatment response, clinical disease activity indices and the rates of clinical and sonographic remission in patients with RA. Obesity and overweight are associated with lower remission rates regardless of the type of treatment.

Evaluating the efficacy of intra-articular injections of platelet rich plasma (PRP) in rheumatoid arthritis patients and its impact on inflammatory cytokines, disease activity and quality of life.

2020 ◽  
Vol 16 ◽  
Author(s):  
Dalia S. Saif ◽  
Nagwa N. Hegazy ◽  
Enas S. Zahran
Keyword(s):  
Quality Of Life ◽  
Rheumatoid Arthritis ◽  
Disease Activity ◽  
Inflammatory Cytokines ◽  
Platelet Rich Plasma ◽  
Joint Inflammation ◽  
Monthly Interval ◽  
Post Injection ◽  
Tnf Α

Background: Among rheumatoid arthritis patients (RA), general disease activity is well regulated by diseasemodifying anti-rheumatic medications (DMARDS), but sometimes local inflammation still persists among a few joints. Adjuvant modern molecular interventions as Platelet Rich Plasma (PRP) with a suggested down regulating effect on inflammatory mediators has a proven effect in management of RA. We aim to evaluate the therapeutic effect of intra-articular PRP versus steroid in RA patients and their impact on inflammatory cytokines IL1B , TNF α, local joint inflammation, disease activity and quality of life (QL). Methods: Open labeled parallel randomized control clinical trial was carried out on 60 RA patients randomly divided into 2 groups, Group 1: included 30 patients received 3 intra-articular injections of PRP at monthly interval, Group 2: included 30 patients received single intra-articular injection of steroid. They were subjected to clinical, laboratory, serum IL1B and TNF α assessment at baseline and at 3, 6 months post injection. Results: Patients of both groups showed improvements in their scores of evaluating tools at 3months post injection and this improvement was persistent in the PRP group up to 6 months post injection while it was continued only for 3 months in the steroid group. Conclusions: PRP is a safe, effective and useful therapy in treating RA patients who had insufficient response and persistent pain and inflammation in just one or two joints through its down regulating effect on inflammatory cytokines IL1B, TNF α with subsequent improvement of local joint inflammation, disease activity and QL.

scholarly journals OP0326 ACPA-INDUCED PAIN-BEHAVIOR, BONE LOSS AND TENDON INFLAMMATION IN MICE: A NOVEL MODEL FOR THE PRE-DISEASE PHASES OF ACPA-POSITIVE RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 200.2-200
Author(s):  
A. Krishnamurthy ◽  
Y. Kisten ◽  
A. Circiumaru ◽  
K. Sakurabas ◽  
P. Jarvolli ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Bone Loss ◽  
Joint Inflammation ◽  
Tendon Sheath ◽  
Joint Involvement ◽  
Subclinical Inflammation ◽  
Core Motif ◽  
Dixon Method ◽  
Hind Limbs ◽  
Predicting Factor

Background:In rheumatoid arthritis (RA), anti-citrullinated protein antibodies (ACPAs) are associated with bone loss and pain. Recently, tenosynovitis has been suggested as a predicting factor for arthritis progression in individuals at-risk for RA.Objectives:We aimed to investigate if transfer of human ACPAs into mice could induce tenosynovitis and/or subclinical inflammation.Methods:Monoclonal ACPA (1325:04C03 and 1325:01B09) and control (1362:01E02) antibodies (mAbs) were generated from synovial plasma or memory B cells of RA patients. 2mg of combination of monoclonal ACPAs or control antibody were injected in BALB/c female mice (age 12-16 weeks) (n= 9). Pain-like behavior was monitored by measuring mechanical hypersensitivity using von Frey filaments every 3 days and estimation by up-down Dixon method. Bone morphometrics was analyzed by micro-CT. Using specially designed mobilization casts, dedicated mouse MRI coils, and gadolinium enhanced contrast medium, the hind limbs of these mice were scanned in a 9.4 T scanner and resulting T1-weighted images were evaluated for signs of soft tissue joint inflammation. The MRI images were scored for the presence of joint involvement and tendon inflammatory changes by 3 readers in a blinded manner.Figure 1.NAPA performed on healthy donor mo-DCs incubated with native, PAD2-citrullinated, and PAD4-citrullinated fibrinogen. Alpha, beta, and gamma chains of fibrinogen are shown separately. Each colored line represents a unique peptide. Nested peptides with a common core motif are shown in the same color. Grey bar denotes peptides with identical core motif between samples.Results:ACPAs (1325:04C03 and 1325:01B09) induced pain-like behavior (lasting for at least 4 weeks) and reduction of the trabecular and cortical bone thickness in the hind limbs as compared to control monoclonal antibodies (p<0.05). While no macroscopic or MRI signs of synovial inflammation were detected, MRI subclinical inflammation of the tendon sheaths was present in mice injected with ACPAs, but not in those injected with control mAb. Semi-quantitative scoring of the inflammatory tendon changes showed significant higher values in mice injected with ACPA (median of 1, range 0 to 2) than those injected with control mAb (median of 0, range 0 to 1).Conclusion:We show that ACPA induces pain-like behavior, bone loss and tendon sheath inflammation in mice, a model that mimics the preclinical state of ACPA positive RA.References:[1]Harre, U. et al. J Clin Invest (2012)[2]Krishnamurthy, A. et al. Ann Rheum Dis (2016, 2019), JI 2019[3]Wigerblad, G. et al. Ann Rheum Dis (2016, 2019)[4]KleyerA, Seminars in Arthritis and Rheumatism (2016)Disclosure of Interests:Akilan Krishnamurthy: None declared, Yogan Kisten: None declared, Alexandra Circiumaru: None declared, Koji Sakurabas: None declared, Patrik Jarvolli: None declared, Juan Jimenez Jimenez Andrade: None declared, Peter Damberg: None declared, Heidi Wähämaa: None declared, Vivianne Malmström Grant/research support from: VM has had research grants from Janssen Pharmaceutica, Lars Klareskog: None declared, Camilla Svensson: None declared, Bence Réthi: None declared, Anca Catrina: None declared

scholarly journals Global Deletion of 11β-HSD1 Prevents Muscle Wasting Associated with Glucocorticoid Therapy in Polyarthritis

2021 ◽  
Vol 22 (15) ◽  
pp. 7828
Author(s):  
Justine M. Webster ◽  
Michael S. Sagmeister ◽  
Chloe G. Fenton ◽  
Alex P. Seabright ◽  
Yu-Chiang Lai ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Skeletal Muscle ◽  
Chronic Inflammation ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Ex Vivo ◽  
Glucocorticoid Therapy ◽  
Knock Out ◽  
Fiber Size ◽  
Anti Inflammatory

Glucocorticoids provide indispensable anti-inflammatory therapies. However, metabolic adverse effects including muscle wasting restrict their use. The enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) modulates peripheral glucocorticoid responses through pre-receptor metabolism. This study investigates how 11β-HSD1 influences skeletal muscle responses to glucocorticoid therapy for chronic inflammation. We assessed human skeletal muscle biopsies from patients with rheumatoid arthritis and osteoarthritis for 11β-HSD1 activity ex vivo. Using the TNF-α-transgenic mouse model (TNF-tg) of chronic inflammation, we examined the effects of corticosterone treatment and 11β-HSD1 global knock-out (11βKO) on skeletal muscle, measuring anti-inflammatory gene expression, muscle weights, fiber size distribution, and catabolic pathways. Muscle 11β-HSD1 activity was elevated in patients with rheumatoid arthritis and correlated with inflammation markers. In murine skeletal muscle, glucocorticoid administration suppressed IL6 expression in TNF-tg mice but not in TNF-tg11βKO mice. TNF-tg mice exhibited reductions in muscle weight and fiber size with glucocorticoid therapy. In contrast, TNF-tg11βKO mice were protected against glucocorticoid-induced muscle atrophy. Glucocorticoid-mediated activation of catabolic mediators (FoxO1, Trim63) was also diminished in TNF-tg11βKO compared to TNF-tg mice. In summary, 11β-HSD1 knock-out prevents muscle atrophy associated with glucocorticoid therapy in a model of chronic inflammation. Targeting 11β-HSD1 may offer a strategy to refine the safety of glucocorticoids.

scholarly journals Anti-Rheumatic Effect of Antisense Oligonucleotide Cytos-11 Targeting TNF-α Expression

2021 ◽  
Vol 22 (3) ◽  
pp. 1022
Author(s):  
Tatyana P. Makalish ◽  
Ilya O. Golovkin ◽  
Volodymyr V. Oberemok ◽  
Kateryna V. Laikova ◽  
Zenure Z. Temirova ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Gene Expression ◽  
Rat Model ◽  
Peripheral Blood ◽  
Antisense Oligonucleotide ◽  
Joint Inflammation ◽  
Blood Concentrations ◽  
Tnf Α ◽  
Effective Drugs ◽  
First Time

The urgency of the search for inexpensive and effective drugs with localized action for the treatment of rheumatoid arthritis continues unabated. In this study, for the first time we investigated the Cytos-11 antisense oligonucleotide suppression of TNF-α gene expression in a rat model of rheumatoid arthritis induced by complete Freund’s adjuvant. Cytos-11 has been shown to effectively reduce peripheral blood concentrations of TNF-α, reduce joint inflammation, and reduce pannus development. The results achieved following treatment with the antisense oligonucleotide Cytos-11 were similar to those of adalimumab (Humira®); they also compared favorably with those results, which provides evidence of the promise of drugs based on antisense technologies in the treatment of this disease.

scholarly journals Osteoblastic PLEKHO1 contributes to joint inflammation in rheumatoid arthritis

EBioMedicine ◽  
2019 ◽  
Vol 41 ◽  
pp. 538-555 ◽  
Author(s):  
Xiaojuan He ◽  
Jin Liu ◽  
Chao Liang ◽  
Shaikh Atik Badshah ◽  
Kang Zheng ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Joint Inflammation

Elevated Serum Glucose-6-Phosphate Isomerase Correlates with Histological Disease Activity and Clinical Improvement After Initiation of Therapy in Patients with Rheumatoid Arthritis

2010 ◽  
Vol 37 (12) ◽  
pp. 2452-2461 ◽  
Author(s):  
LIE DAI ◽  
LANG-JING ZHU ◽  
DONG-HUI ZHENG ◽  
YING-QIAN MO ◽  
XIU-NING WEI ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Disease Activity ◽  
Demographic Data ◽  
Elevated Serum ◽  
Serum Marker ◽  
Serum Glucose ◽  
Healthy Controls ◽  
Synovitis Score ◽  
Initiation Of Therapy ◽  
Activity Indices

Objective.To determine serum glucose-6-phosphate isomerase (GPI) concentrations in patients with rheumatoid arthritis (RA), and to test whether they correlate with objective measures of disease activity.Methods.Sera from 116 patients with RA, 69 patients with non-RA rheumatic diseases, and 101 healthy controls were analyzed. Levels of soluble serum GPI were measured by ELISA. Histological disease activity was determined with the synovitis score in synovial needle biopsies from 58 of the 116 patients with RA. Thirty-one of the 58 synovium samples were stained for CD68, CD3, CD20, CD38, CD79a, and CD34 by immunohistochemistry. Demographic data were collected, as well as serological and clinical variables that indicate RA disease activity, for Spearman correlation analysis.Results.Serum GPI level correlated positively with the synovitis score (r = 0.278, p = 0.034). Significantly higher soluble GPI levels were detected in the RA sera compared with sera from healthy controls and the non-RA disease controls (2.25 ± 2.82 vs 0.03 ± 0.05 and 0.19 ± 0.57 μg/ml, respectively; p < 0.0001). The rate of serum GPI positivity was significantly higher in the RA patients than in the non-RA disease controls (64.7% vs 10.1%; p < 0.0001). Spearman analysis showed no significant correlation between serum GPI level and Disease Activity Score in 28 joints at baseline. After initiation of antirheumatic treatments, GPI levels decreased significantly (2.81 ± 3.12 vs 1.44 ± 2.09 μg/ml; p = 0.016), paralleling improvement of the disease activity indices.Conclusion.Elevated serum GPI may be involved in the synovitis of RA and may prove useful as a serum marker for disease activity of RA.

scholarly journals AB0043 EFFECT OF ANTI-INFLAMMATORY MEDICATION ON INTERACTION OF SYNOVIAL FIBROBLASTS WITH MACROPHAGES IN RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1054.1-1054
Author(s):  
M. Schmeller ◽  
M. Diller ◽  
R. Hasseli ◽  
A. Knothe ◽  
S. Rehart ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mononuclear Cells ◽  
Joint Inflammation ◽  
Synovial Fibroblasts ◽  
Therapeutic Effects ◽  
Synergistic Activity ◽  
M1 Macrophages ◽  
Healthy Donors ◽  
Proinflammatory Activity ◽  
Anti Inflammatory

Background:One of the key mechanisms in the pathogenesis of rheumatoid arthritis (RA) is the interaction of macrophages and synovial fibroblasts during joint inflammation. Increased synergistic proinflammatory activity of both cell types leads to the release of high levels of proinflammatory cytokines, especially of interleukin-6 (IL-6), and of matrix degrading enzymes. If this mechanism is uncontrolled, progressive destruction of articular cartilage and bone will take place.In active disease, immediate anti-inflammatory treatment with glucocorticoids is usually replaced by disease-modifying anti-rheumatic drugs (DMARDS), especially by methotrexate (MTX) and biologics such as TNF-α- or IL-6-inhibitors. This led to great improvements in prognosis and outcome for RA patients. However, about 40% of patients experience no remission or suffer from side effects of medication. To optimize established substances and to develop new treatment strategies, it is necessary to understand the mechanisms underlying the limited therapeutic effects.Objectives:Evaluation of the effect of prednisolone, MTX, adalimumab, tocilizumab on IL-6 secretion by RA synovial fibroblasts (RASF) and macrophages.Methods:RA synovium was used for RASF isolation. Peripheral blood mononuclear cells (PBMCs) were isolated from blood of healthy donors and RA patients by using Ficoll© medium followed by density gradient centrifugation. Mononuclear cells were seeded on six well plates (6x10^6/well) and incubated for one week. Then they were stimulated with Interferon-у (20 ng/ml) and LPS (50 ng/ml) for 48h to initiate differentiation into proinflammatory M1 macrophages. The M1 macrophages were co-cultured with RASF (100.000/well) and different treatments added (prednisolone: 10, 25, 50, 75, 100 nM, 1 µM; adalimumab: 100, 500 µg/ml; tocilizumab: 1, 5 µg/ml; MTX: 0,5, 1, 5, 10, 100 nM, 1µM). After 24h culture supernatants were collected and IL-6- and TNFα-ELISAs were performed.Results:IL-6 concentrations of untreated controls were comparable, regardless whether M1 macrophages from healthy donors or RA-patients were used for co-culture. Prednisolone reduced co-culture-induced IL-6 up to 56% (p<0.001) in co-culture of RASF and M1 macrophages of healthy donors and up to 60% (p<0.001) in co-culture of RASF and RA M1 macrophages. Adalimumab reduced IL-6 up to 28% (p<0.05) in M1 of healthy donors and up to 45% (p<0.01) in RA M1 macrophage co-cultures. A minor reduction by 10-20% of IL-6 was observed with tocilizumab and no significant effect could be achieved after treatment with MTX.Conclusion:Prednisolone and adalimumab clearly decrease but do not eliminate proinflammatory synergistic activity of RASF and M1 macrophages. These results confirm the clinical observation, that there is a large number of RA-patients that independent of anti-inflammatory treatment still suffer from low-level joint inflammation.The synergistic proinflammatory activity of M1 macrophages and RASF seems to be a complex and multifactorial mechanism that is difficult to eliminate by a single treatment substance. Since it is one of the key mechanisms in RA pathogenesis, there is a critical need to investigate how therapy effects could be optimized. This study confirmed RASFs as one of the leading effector cells of increased synergistic proinflammatory activity, thus underlining their promising role as a treatment target in rheumatoid arthritis.Disclosure of Interests:None declared

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