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Background Cardiovascular disease (CVD) is the most common cause of mortality in rheumatoid arthritis (RA), and Inflammation has a decisive role in its pathogenesis. CXCL9 contributes to multi aspects of inflammatory reactions associated with the pathogenesis of CVD. In the current study, we evaluated the association of plasma CXCL9 and CXCR3 gene expression with Cardiovascular risk factors in RA patients for the first time.Material and methods Thirty newly diagnosed, 30 under-treatment RA patients and 30 healthy subjects were recruited in this study. The plasma concentration of CXCL9 and CXCR3 gene expression were measured using ELISA and Real-Time PCR, respectively. The CVD risk was evaluated using Framingham Risk Score (FRS) and Systematic Coronary Risk Evaluation (SCORE).Results The plasma levels of CXCL9 were significantly higher in the newly diagnosed and under-treatment RA patients compared to the control group (P P P P P = 0.0005, r = 0.436; P = 0.0002, r = 0.463, respectively). The FRS was remarkably higher in newly diagnosed and under-treatment patients (P = 0.014 and P = 0.035, respectively). The CXCR3 gene expression significantly correlated with age, systolic blood pressure, FRS, and SCORE (P = 0.020, r = 0.298; P = 0.006, r = 0.346; P = 0.006, r = 0.349; P = 0.007, r = 0.341, respectively). The CXCL9 plasma concentration had a significant negative correlation with plasma HDL and LDL levels (P = 0.033, r=-0.275; P = 0.021, r=-0.296, respectively).Conclusion CXCL9 and CXCR3 correlates with different variables of CVD in RA.

Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID-19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID-19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll-like receptor-7 (TLR-7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS-CoV-2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS-CoV-2 by disrupting cytokine function and triggering neutrophil hyper-reactivity. Finally, the pathologic effects of these AABs will be further described in COVID-19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS-C), acute respiratory distress syndrome (ARDS), and recently described post-acute sequelae of COVID-19 (PASC) or long-COVID.

Background Microscopic polyangiitis (MPA) is an antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) that affects predominantly small- sized vessels. A causal relationship between viral infections and vasculitis has been postulated. Aim of the work To present the concomitant association of coronavirus disease 2019 (COVID-19) infection with MPA in an elderly Iranian male. Case presentation A 67 year old Iranian man with the history of COVID-19 infection and a positive polymerized chain reaction (PCR) test four weeks before admission to the neurology department with acute onset pain, numbness and progressive weakness in both hands grip, sudden left foot drop and paresthesia. Erythrocyte sedimentation rate (ESR) was 95 mm/hr, ferritin 912 ng/ml and C-reactive protein (CRP) positive, proteinuria 1.1 g/24 h and markedly elevated perinuclear (P-ANCA): 526 IU/ml. Diagnosis of MPA was held presenting with mononeuritis multiplex, glomerulonephritis followed by diffuse alveolar hemorrhage and infiltration of lymphocytes in muscle fibers and vessels wall in sural nerve biopsy. He was successfully treated by methylprednisolone (1 g/day for 3 days) followed by 1 mg/kg with gradual tapering along with cyclophosphamide (CYC) (2 mg/kg). Intravenous immunoglobulin (IVIG, 2 g/kg in four divided doses) started for the management of inflammatory mononeuritis multiplex with gradual improvement. During hospitalization, plasmapheresis was performed due to alveolar hemorrhage for 5 day. The patient returned home on day 32 and followed-up in the rheumatology clinic with improvement of muscle power and handgrip strength. Conclusion Vasculitis is potentially one of COVID-19′s presenting symptoms and prompt diagnosis and treatment is crucial in improving outcome of patients.

Systemic sclerosis (scleroderma/SSc) is a rare, connective autoimmune multisystem disease with wide-reaching consequences. SSc is recognized by the presence of serum autoantibodies and fibroproliferative changes in the microvasculature which, in turn, results in too much accumulation of collagen fibres in the skin and internal organs. Gastrointestinal (GI) involvement is highly prevalent among SSc patients (seen in over 90% of cases). Altered GI function and subsequent nutritional disorders are common outcomes of SSc, affecting the quality of life (QoL) and possibly carrying an associated rate of morbidity and mortality. Disease-related malnourishment is also considered to have a detrimental effect on clinical outcomes. There is little information on dietary advice for SSc patients, and as GI complaints are risk factors for bad nutritional status, perceptive assessment seems to be necessary. As the SSc pathogenesis is yet to be explored, recent investigations have aimed to evaluate the effect of diet in terms of triggering or altering the course of the disease. The present review aimed to discuss current knowledge relating to the effect of nutrition on SSc pathogenesis.

This study was designed to describe COVID-19 infection in rheumatic patients and to investigate possible risk factors for hospital admission and death related to COVID-19 infection considering the type of rheumatic disease and medications used to treat it. In this observational cross-sectional study, patients under follow-up in Kermanshah rheumatology units were investigated in a 6-month period between February 18 and August 22, 2020. Confirmed COVID-19 cases were collected. The following data were obtained: age, sex, rheumatic disease diagnosis, rheumatic disease medication (glucocorticoids, csDMARDs, ts/bDMARDs). Rheumatic patients were divided into two groups of hospitalized and non-hospitalized. The data from the two groups were compared. In total, 221 patients were enrolled in this study. Of these, 38 patients (17.19%) were hospitalized, and 9 patients (4.07%) died. No significant difference was observed between hospitalized and non-hospitalized patients except for vasculitis and prior use of Janus kinase inhibitors (Tofacitinib). A greater rate of hospitalized patients had vasculitis (6 (15.79%) vs. 1 (0.55%), p < 0.0001 ). A greater rate of them were on Tofacitinib therapy (2 (1.09%) vs. 0, p value = 0.03). A greater rate of patients who died used Tofacitinib (2 (22.22%) vs. 0, p value = 0.001) and Mycophenolate Mofetil (4 (44.44%) vs. 23 (10.85%), p value = 0.014). Hospitalization and mortality rates in rheumatic patients are comparable to the general population. A higher risk for hospitalization was observed only in vasculitis patients and users of Tofacitinib, and a higher risk for mortality was seen only in users of Mycophenolate Mofetil and Tofacitinib, though this finding should be interpreted with caution due to the small size of these subgroups. In conclusion, most rheumatic patients do not seem to be at higher risk for severe COVID-19.

Rheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation characterized by joint damage and even extra-articular involvement. In this study, the gene expression levels of MALAT1, H19 and their possible downstream microRNAs, miR-199a-5p, miR-1-3p, and the predicted targets of these miRNAs, HSPA5 and MMD, were examined.Twenty-five newly diagnosed RA patients and 25 healthy individuals were included. For six months, patients were treated with conventional disease-modifying antirheumatic drugs (DMARDs) and Methylprednisolone (mPRED). Blood samples were obtained from healthy controls and patients (before and after treatment). After RNA extraction, the RT-qPCR technique was used to evaluate the expression level of the studied genes.Data showed that the expression level of MALAT1, H19, miR-199a-5p, and miR-1-3p was significantly higher in the newly diagnosed patients with RA than the healthy subjects, but the increase in the expression level of HSPA5 and MMD genes in the new cases was not significant compared to healthy controls. After treatment, except for the expression level of lncRNAs, the expression level of miRNAs, HSPA5, and MMD significantly increased. Based on ROC curve analysis of MALAT1, H19, miR-199a-5p and miR-1-3p have a high ability to identify patients from healthy individuals (AUC = 0.986, AUC = 0.995, AUC = 0.855, AUC = 0.675, respectively).MALAT1 and H19 may be candidates as potential biomarkers for the discrimination between RA patients and controls. DMARDs plus mPRED therapy do not have a desirable effect on reducing inflammatory responses and ER stress.

Background: Coronavirus disease-2019 (COVID-19) is a novel infectious disease, which presents with various clinical manifestations. There is growing evidence of an association between COVID-19 infection and autoimmune diseases. The aim of this case report was to demonstrate the association of COVID-19 infection and the development of systemic lupus erythematosus (SLE). Case presentation: A 38 year old Iranian woman presented with progressive icterus, pleuritic chest pain, palpitation, dyspnea, photosensitivity and arthralgia 18-days after COVID-19 symptoms proved by a positive polymerized chain reaction (PCR). The chest and abdomen computerized tomography (CT) scan showed pericardial and pleural effusion and enlarged liver and abdominal lymph nodes. Antinuclear antibody (ANA), anti-double stranded deoxyribonucleic acid (anti-ds DNA) antibody and perinuclear anti-neutrophil cytoplasmic antibody (P-ANCA) were positive. She was diagnosed as SLE and was successfully treated with prednisolone 30 mg daily, hydroxychloroquine 200 mg daily and azathioprine 150 mg daily and she remarkably improved. Repeated anti-ds DNA antibody was positive. Due to nausea and abdominal discomfort, azathioprine was discontinued and replaced with mycophenolate mofetil 1500 mg daily. In the article, similar cases were presented;the mean interval between COVID symptoms and SLE presentations was 24.86 days. Pulmonary and renal involvements were the most common presentations of SLE triggered by COVID-19. The most frequently reported autoantibody was ANA Conclusion: It is necessary to be aware of the development of lupus disease in COVID-19 infected patients, because prompt diagnosis and treatment is very important to improve their outcome. © 2021 THE AUTHORS

Introduction Takayasu arteritis (TA) is a large vessel vasculitis characterized by the involvement of the aorta and its branches. In the present study, the nailfold videocapillaroscopy (NVC) findings of the TA patients were evaluated and compared to healthy individuals. Additionally, the association of NVC abnormalities with disease activity and subclavian artery involvement was also investigated. Method In the present study, NVC changes of 15 TA patients and 15 age- and sex-matched healthy controls were compared. The frequency of hypertension, dyslipidemia, and smoking status was not different between the case and control group. Capillary density, avascular area, tortuosity, micro-hemorrhages, and ramification were investigated. Among capillaries' diameters; capillary length and width, arterial and venous limbs diameters were also compared between two groups. Results The capillary length and venous limb diameter were lower in TA patients compared to control cases (P-value: 0.026 and 0.049, respectively). Moreover, TA patients have more tortuous capillaries (P-value: 0.035). Among TA patients; capillary length, width, arterial and venous limbs diameter was lower in hands with subclavian involvement (P-value: 0.014, 0.034, 0.009 and 0.022, respectively). Furthermore, the arterial and venous limbs diameter were lower in TA patients with active disease compared to patients with inactive disease (P-value: 0.018 and 0.049, respectively). Conclusion In the present study, we have shown that the hands with subclavian artery involvement have short, thin and tortuous capillaries which could be secondary to hypoperfusion. To the best of our knowledge, this is the first report describing NVC changes in TA.

Rheumatoid arthritis (RA) is a systemic autoimmune disease that primarily affects small joints. The impaired chemokine and cytokine responses are essential pathological mechanisms for the RA clinical presentation. Given the role of chemokines and inflammatory reactions in RA pathogenesis, we evaluate the association between the plasma concentration of CCL20 with the clinical and laboratory parameters in newly diagnosed RA patients.Forty-five newly diagnosed RA patients and forty-five healthy subjects were enrolled in this study. The plasma levels of CCL20, rheumatoid factor, and anti-citrullinated peptide antibodies were measured using the enzyme-linked immunosorbent assay (ELISA) technique.The plasma levels of CCL20 were increased significantly in RA patients compared to the healthy controls (p 0.0001). There was a positive correlation between CCL20 and RF, anti-CCP, ESR, and DAS-28 (p 0.0001, r = 0.669; p 0.015, r = 0.358; p 0.0001, r = 0.586; p 0.0001, r = 0.769).The increased plasma levels of CCL20 in newly diagnosed RA patients may contribute to RA pathogenesis, and it is in association with clinical and laboratory parameters. Key Points • CCL20 has a contribution to the early phase of RA.