Conventional DMARDs therapy decreases disease activity and inflammation in newly diagnosed patients with rheumatoid arthritis by increasing FoxP3, Sema-3A, and Nrp-1 gene expression.

BACKGROUND: Semaphorins are axonal guidance molecules involved in neural development and contribute to the regulation of various phases of the immune response. This study aimed to investigate the plasma levels of the pro-inflammatory cytokine interleukin-6 (IL-6) and the regulatory T (Treg) cell-related cytokine interleukin-10 (IL-10), as well as the gene expression levels of forkhead box P3 (FoxP3), Semaphorin-3A (Sema-3A), Neuropilin-1 (Nrp-1), Semaphorin-4A (Sema-4A), and Plexin-D1 (Plxn-D1), in the peripheral blood of newly diagnosed rheumatoid arthritis (RA) patients treated with conventional disease-modifying antirheumatic drugs (DMARDs) for 6 months compared with healthy controls. METHODS: Peripheral blood samples were obtained from 40 newly diagnosed RA patients (before and after treatment) and 40 age- and sex-matched healthy subjects. The plasma concentrations of IL-6 and IL-10 were quantified via enzyme-linked immunosorbent assay (ELISA), and the mRNA expression levels of FoxP3, Sema-3A, Nrp-1, Sema-4A, and Plxn-D1 were assessed via quantitative real-time PCR. RESULTS: Compared with those in the controls, the plasma IL-6 levels in the RA patients (both pre- and post-treatment) were significantly greater (P < 0.001). Compared with the pre-treatment levels, the plasma IL-6 levels decreased significantly after DMARD therapy (P < 0.05). Moreover, plasma IL-10 levels were significantly greater in post-treatment RA patients than in controls (P < 0.05). The gene expression of FoxP3, Sema-3A, and Nrp-1 was significantly lower in pre-treated RA patients than in controls (P < 0.001). Compared with that in pre-treatment RA patients, the gene expression of FoxP3, Sema-3A, and Nrp-1 in DMARDs-treated RA patients was strongly increased (P < 0.05, P < 0.01, and P < 0.01, respectively). There was a positive correlation between Sema-3A gene expression and the gene expression of FoxP3 (r = 0.292, P < 0.01) and Nrp-1 (r = 0.569, P < 0.0001). CONCLUSION: Conventional DMARDs therapy effectively reduces disease activity and inflammation in newly diagnosed RA patients by increasing FoxP3, Sema-3A, and Nrp-1 gene expression.

miR-6089 may prevent the inflammatory events leading to cardiovascular disorders in RA patients.

Background: Cardiovascular disease (CVD) is the most important comorbid condition in rheumatoid arthritis (RA) patients. Dysregulated expression of non-coding RNA families has a critical role in RA-associated inflammatory events, including cardiovascular manifestations. The long non-coding RNA (lncRNA)- HIX003209 has a role in RA associated inflammation. In the current study, we investigated the association of HIX003209 and its downstream microRNA, miR-6089, with various cardiovascular and inflammatory biomarkers in RA patients. Material and methods: 60 RA patients, including 30 newly diagnosed and 30 on-treatment patients were recruited in this study, and 30 healthy people were selected as a control group. The gene expression of HIX003209, miR-6089, and CXCR3 were measured using Real-time PCR. The CVD risk was measured using Systematic Coronary Risk Evaluation (SCORE) and Framingham Risk Score (FRS). Results: The gene expression of LncRNA-HIX003209 was elevated significantly in newly-diagnosed compared to under-treatment and control groups (p < 0.05). The miR-6089 gene expression was elevated significantly in under-treatment RA patients group compared to control group (p < 0.001). There was a significant positive correlation between LncRNA-HIX003209 with CXCR3 gene expression (p < 0.01, r = 0.341). There was a significantly negative correlation between the gene expression of miR-6089 with DAS-28 (p < 0.05, r = -0.309), NT-proBNP plasma level (p = 0.039, r = -0.268), and CXCL9 plasma level (p < 0.001, r = -0.421). Conclusion: Regarding its anti-inflammatory effects, miR-6089 may play an important role in preventing the pathological events of cardiovascular disorders in RA patients, through its inhibitory effects on inflammatory chemokines, such as CXCL9, and NT-ProBNP. Higher expression of LncRNA-HIX003209 may disrupt the anti-inflammatory effect of miR-6089 in RA patients.

The development of anticyclic citrullinated peptide (anti-CCP) antibody following severe COVID-19.

OBJECTIVES: The dysregulated immune response is one of the cardinal features of severe coronavirus disease 2019 (COVID-19). This study was conducted to clarify the occurrence of autoantibodies (AABs) associated with systemic autoimmune rheumatic diseases (SARDs) in hospitalized patients with a moderate, severe, and critical form of COVID-19. METHODS: The serum samples obtained from 176 hospitalized COVID-19 patients were investigated in this study, including patients with moderate (N = 90), severe (N = 50), and critical (N = 36) forms of COVID-19. Also, the serum samples collected from healthy subjects before the COVID-19 pandemic were used as controls (N = 176). The antinuclear antibodies (ANAs), antidouble-stranded DNA (anti-dsDNA), cytoplasmic-anti neutrophil cytoplasmic antibody (c-ANCA), perinuclear ANCA (p-ANCA), antiphospholipid antibodies (aPLs), and anticyclic citrullinated peptide (anti-CCP) occurrence was evaluated using a solid-phase enzyme-linked immunosorbent assay (ELISA). RESULTS: The results showed that the occurrence of ANAs, anti-dsDNA, anti-CCP, c-ANCA, and p-ANCA was significantly higher in the COVID-19 patients compared to serum obtained from healthy subjects (p < .0001, p < .0001, p < .0001, p < .05, and p < .001, respectively). The positive number of anti-CCP tests increased significantly in severe COVID-19 compared to the moderate group (p < .01). CONCLUSION: Our study further supports the development of autoantibodies related to systemic autoimmune rheumatologic diseases. To the best of our knowledge, this is the first study with a large sample size that reported the occurrence of anti-CCP in a severe form of COVID-19.

CXCL9 and NT-proBNP, a notable link between inflammatory mediator and cardiovascular disease biomarker in rheumatoid arthritis.

INTRODUCTION: Cardiovascular disease (CVD) is the most critical extra-articular manifestation of rheumatoid arthritis, and inflammatory molecules contribute to its pathogenesis. Recently, CXCL9 has been considered an inflammatory chemokine associated with the pathogenesis of CVD. Here, we evaluated the association of plasma CXCL9 with well-established cardiac biomarkers, including HS-CRP (High sensitivity C-reactive protein) and NT-ProBNP (N-terminal pro-B-type natriuretic peptide), in newly diagnosed and under-treatment RA patients. METHODS: Thirty newly diagnosed patients, 30 under-treatment RA patients, and 30 healthy subjects were recruited. The plasma concentration of CXCL9 and NT-ProBNP was measured using the ELISA method. The HS-CRP levels was measured in plasma samples using latex-enhanced immunoturbidimetric test. RESULTS: We found increased plasma levels of CXCL9, HS-CRP, and NT-proBNP in RA patients compared to healthy subjects, besides that the concentration of CXCL9, HS-CRP, and NT-ProBNP showed elevated levels in newly diagnosed RA patients compared to under-treatment group. The mean plasma concentration of CXCL9, NT-proBNP, and HS-CRP were statistically different among healthy subjects, newly diagnosed, and under-treatment RA patients (p < 0.001, p = 0.016, and p < 0.001, respectively). We also found a significant positive correlation between CXCL9 and DAS-28 (p = 0.0005, r = 0.436) in the patients' group (new-case + under-treatment). There was a significantly positive correlation between CXCL9 and NT-proBNP in newly diagnosed and under-treatment patients (p = 0.020, r = 0.424; p < 0.0001, r = 0.853, respectively). In the patient's group (new-case + under-treatment), there was a significantly positive correlation between CXCL9 with NT-proBNP (p < 0.001, r = 0.703) and CXCL9 with HS-CRP (p = 0.015, r = 0.313). CONCLUSION: CXCL9 correlates significantly with well-established cardiovascular biomarkers, including HS-CRP and NT-ProBNP in RA patients. Key Points • CXCL9 is an inflammatory marker in RA. • CXCL9 has correlated with DAS-28. • There is a strong correlation between CXCL9 with NT-proBNP and HS-CRP.

Overexpression of Synoviolin and miR-125a-5p, miR-19b-3p in peripheral blood of rheumatoid arthritis patients after treatment with conventional DMARDs and methylprednisolone.

PURPOSE: SYVN1 is an endoplasmic reticulum (ER)-resident E3 ubiquitin ligase that has an essential function along with SEL1L in rheumatoid arthritis (RA) pathogenesis. This study aimed to investigate the changes in the expression of peripheral blood ncRNAs and SYVN1-SEL1L affected by DMARDs treatment. METHODS: Twenty-five newly diagnosed RA patients were randomly assigned to receive conventional DMARDs (csDMARDs) and methylprednisolone for six months. The peripheral blood gene expression of SYVN1 and SEL1L and possible regulatory axes, NEAT1, miR-125a-5p, and miR-19b-3p, were evaluated before and after qRT-PCR. We also compared differences between the patients and healthy controls (HCs), and statistical analyses were performed to determine the correlation between ncRNAs with SYVN1-SEL1L and the clinical parameters of RA. RESULTS: Expression of NEAT1 (P = 0.0001), miR-19b-3p (P = 0.007), miR-125a-5p (P = 0.005), and SYVN1 (P = 0.036) was significantly increased in newly diagnosed patients compared to HCs; also, miR-125a-5p, miR-19b-3p, and SYVN1 were significantly overexpressed after treatment (P = 0.001, P = 0.001, and P = 0.005, respectively). NEAT1 was positively correlated with SYVN1, and miR-125a-5p had a negative correlation with anti-cyclic citrullinated peptides. The ROC curve analysis showed the potential role of selected ncRNAs in RA pathogenesis. CONCLUSION: The results indicate the ineffectiveness of the csDMARDs in reducing SYVN1 expression. The difference in expression of ncRNAs might be useful markers for monitoring disease activity and determining therapeutic responses in RA patients. Key Points • The expression of NEAT1 is significantly upregulated in RA patients compared to HC subjects. • miR-19b-3p, miR-125a-5p, and SYVN1 are significantly upregulated in RA patients compared to HC subjects. • The expression of miR-19b-3p and miR-125a-5p is significantly increased in RA patients after treatment with DMARDs and methylprednisolone. • NEAT1 is positively correlated with SYVN1.

The effect of a six-week Aqua Pilates and Aqua Stretch intervention on pain, function, and quality of life in patients affected by ankylosing spondylitis: A rater-blind randomized controlled trial.

BACKGROUND: There has been a dearth of research into the benefits of water-based workouts for ankylosing spondylitis (AS) patients. OBJECTIVE: This study aimed to compare the effect of Aqua Stretch and Aqua Pilates in improving quality of life (QOL), function, and pain in AS patients. METHODS: This study was conducted on 40 patients, who were randomly assigned to the Aqua Pilates, Aqua Stretch, and control groups. The experimental groups attended interventions for six-week. QOL, pain intensity, function, and fatigue were measured before and after treatments. RESULTS: Except for the chest expanding, all variables in the Aqua Stretch group changed significantly after six weeks (p< 0.05). QOL (p= 0.002), 6MWT (p= 0.016), and Schober flexion (p= 0.011) showed changes, while BASDAI (p= 0.0001), VAS (p= 0.0001), fatigue (p= 0.0001), and Schober extension (p= 0.028) showed significant decreases. Except for chest expansion and Schober extension, which did not alter significantly after six-week of Aqua Pilates (p> 0.05), all other variables did. There was an increasing trend in 6MWT and Schober flexion (p= 0.021) and a decreasing trend in BASDAI (p= 0.002), VAS (p= 0.0001) and fatigue (p= 0.002). Except for QOL (p= 0.016), no statistically significant differences were found between the groups. CONCLUSION: All variables had a significant change after six-week Aqua Stretch, except for the chest expanding. Chest expanding and Schober extension were the variables which had no significant change after six-week Aqua Pilates. With the exception of QOL, no statistically significant differences were found between the groups. Aqua Stretch had the greatest effect on the VAS, as measured by the minimum clinically relevant differences (MCID). Moreover, in Aqua Stretch alone, there was a notable impact on fatigue, QOL, and the BASDAI.

Increased gene expression of CCR6 and RORγt in peripheral blood cells of rheumatoid arthritis patients and their correlation with anti-cyclic citrullinated peptide and disease activity.

OBJECTIVES: The significance of T helper 17 (Th17) cells in the pathogenesis of rheumatoid arthritis (RA) has recently been demonstrated in many studies. Retinoic acid receptor-related orphan receptor γt (RORγt) is a transcription factor that is specifically involved in the generation of Th17 cells. Besides, the chemokine receptor CCR6, the receptor for CCL20, is characteristically expressed by these cells. Considering the pivotal roles of Th17 cells in RA pathogenesis, in this study, we assessed the gene expression of CCR6 and RORγt in the peripheral blood leukocytes of new case RA patients. Also, we evaluated their association with anticyclic citrullinated peptide (anti-CCP) antibodies and disease activity. METHODS: Forty-five new case RA patients and 45 healthy persons have been recruited in this investigation. The gene expression of CCR6 and RORγt was evaluated by quantitative real-time PCR (qRT-PCR), and anti-CCP antibodies plasma levels were measured using the enzyme-linked immunosorbent assay (ELISA) technique. Disease activity was measured according to the disease activity score-28 (DAS-28) formula. RESULTS: The gene expression of CCR6 and RORγt increased remarkably in new case RA patients compared to healthy controls (p < .05 and p < .01, respectively). Moreover, there was a positive correlation between RORγt gene expression and parameters, including gene expression of CCR6 (p = .001, r = .461), plasma levels of CCL20 (p = .0009, r = .477), ESR (p = .004, r = .419), DAS-28 (p = .006, r = .402), anti-CCP (p = .019, r = .346), and RF (p = .001, r = .451). Also, CCR6 gene expression was positively associated with the DAS-28 (p = .037, r = .310), plasma levels of anti-CCP (p = .037, r = .312), and ESR (p = .029, r = .327). CONCLUSION: Increased gene expression of CCR6 and RORγt in peripheral blood leukocytes of new case RA patients may contribute to the exacerbation and pathogenesis of RA.

Improvement in the clinical manifestations of interstitial lung disease following treatment with placental mesenchymal stromal cell extracellular vesicles in a patient with systemic sclerosis: A case report.

Background: Interstitial lung disease (ILD) is a severe systemic sclerosis (SSc) complication with no current approved or golden standard treatment. This report aims to investigate the effectiveness of treatment with placental mesenchymal stromal cell (MSC) extracellular vesicles (EVs) in a patient with ILD due to SSc. Case presentation: The patient was a 55-year-old woman with a ten years history of SSc complicated by severe ILD. Over time, her lung disease progressed to interstitial fibrosis despite being treated with mycophenolate mofetil and monthly pulses of cyclophosphamide. Thus, she was treated with eight doses of placenta MSC-EVs. Four weeks after the third dose (Day 31 after the first dose), she reported marked improvement in her clinical symptoms, such as dyspnea and cough. Also, chest computed tomography (CT) scans demonstrated a significant reduction in ground glass consolidations and fibrotic changes. The patient was subsequently followed for twelve months, with findings showing significant improvement in exercise tolerance and reduced supplemental oxygen need. Conclusion: In this single case, placental MSC-EVs were seen to provide a potentially efficient treatment for SSc-related ILD; however, further investigation and clinical trials are necessary.

CXCL9 and its Receptor CXCR3, an Important Link Between Inflammation and Cardiovascular Risks in RA Patients.

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. Thirty newly diagnosed, 30 on-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). The plasma levels of CXCL9 were significantly higher in the newly diagnosed and on-treatment RA patients compared to the control group (P < 0.0001 and P < 0.001, respectively). Also, The CXCR3 gene expression was strongly elevated in newly diagnosed and on-treatment patients (P < 0.001 and P < 0.01, respectively). The CXCL9 and CXCR3 were significantly associated with RA disease activity (P = 0.0005, r = 0.436; P = 0.0002, r = 0.463, respectively). The FRS was remarkably higher in newly diagnosed and on-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). CXCL9 and CXCR3 correlates with different variables of CVD in RA.

Partners in crime: Autoantibodies complicit in COVID-19 pathogenesis.

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.

The effect of Aqua Stretching exercises and Pilates on pain, function and spine posture in patients with ankylosing spondylitis: a randomized controlled trial.

BACKGROUND: Aqua Pilates and Aqua Stretch exercises are different and new methods for the rehabilitation of musculoskeletal disorders. This study aimed to compare the effectiveness of Aqua Stretch and Aqua Pilates interventions in the treatment of pain, function, and posture of the spine in ankylosing spondylitis (AS) patients. METHODS: Forty patients participated in this study who were randomly allocated into Aqua Stretch, aqua Pilates, and control. The experimental groups received four 60-min training sessions each week for six weeks. However, the control group had only its routine drug treatment (NSAIDs & Anti TNF). Pain with Visual Analog Scale (VAS), function with Bath Ankylosing Spondylitis Functional Index (BASFI) and 40-m walking test (MWT), quality of life with ankylosing spondylitis quality of life (ASQoL), and posture of the spine with the Spinal Mouse were evaluated. Evaluations were performed before and after the interventions. Repeated measure ANOVA was employed to determine the main and interaction effects. RESULTS: Aqua Stretch and Aqua Pilates had a significant effect on pain (Aqua-Pilates: P = 0.0001; Aqua-Stretch: P = 0.0001), BASFI (Aqua-Pilates: P = 0.01; Aqua-Stretch: P = 0.02), 40-MWT (Aqua-Pilates: P = 0.006; Aqua-Stretch: P = 0.0001) and ASQoL (Aqua-Pilates: P = 0.01; Aqua-Stretch: P = 0.001), spinal range of motion (ROM) (Aqua-Pilates: P = 0.0001; Aqua-Stretch: P = 0.0001) at a similar ratio. However, the control group did not present any improvement in these factors (P > 0.05). Moreover, the minimal clinically important difference (MCID) revealed that the Aqua Stretch group performed better than the Aqua Pilates group in terms of VAS, ASQOL, and 40-MWT factors. CONCLUSIONS: Aqua Stretch and Aqua Pilates had statistically the same effect on improving pain, function, quality of life, and spinal ROM, while MCID results revealed that the Aqua Stretch group performed better than the Aqua Pilates in terms of VAS-ASQOL-40-MWT. Trial registration It is notable that local ethics committee approval was obtained (IR.KUMS.REC.1399.1137), and the study was registered in Iranian Registry of Clinical Trials (IRCT; IRCT20190426043377N3; registered on 22/05/2021, https://fa.irct.ir/user/trial/56058/view ) and patient recruitments were started on 06/07/2021.

Efficacy of DMARDs and methylprednisolone treatment on the gene expression levels of HSPA5, MMD, and non-coding RNAs MALAT1, H19, miR-199a-5p, and miR-1-3p, in patients with rheumatoid arthritis.

BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.

Increased plasma levels of CCL20 in peripheral blood of rheumatoid arthritis patients and its association with clinical and laboratory parameters.

INTRODUCTION: 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. MATERIAL AND METHODS: 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. RESULT: 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). CONCLUSION: 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.

Frequency, characteristics and outcome of corona virus disease 2019 (COVID-19) infection in Iranian patients with rheumatic diseases.

Aim of the work: To investigate the frequency, clinical characteristics and outcome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in rheumatic diseases patients. Patients and methods: One thousand patients with rheumatic diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), psoriatic arthritis (PsA), axial spondyloarthritis (SpA), systemic sclerosis (SSc), Sjögren's syndrome (SS), Behçets disease (BD), vasculitis, idiopathic inflammatory myositis (IIM), relapsing polychondritis, sarcoidosis and antiphospholipid syndrome (APS) were studied. The following data were collected: age, sex, disease diagnosis, rheumatic disease medication. Rheumatic diseases patients were divided into two groups of infected and non-infected patients with COVID-19 and collected data were compared. Results: The 1000 patients mean age was 43.4 ± 13 years and 84.1% were females. The main diagnosis was RA (37.1%), followed by SLE (23.8%), SpA (13.4%), SSc (12.4%), vasculitis, BD and rhupus in 2.4%, 2.3% and 2.2% respectively, SS and SSc in 0.7% each. Most patients were taking glucocorticoids (78.4%). A large majority of patients were taking at least one of the cDMARDs. 16.1% were taking biologic therapy. 221 rheumatic diseases patients with COVID-19 were identified. Of these, 38 patients (17.2%) were hospitalized and 9 patients (4.1%) died. No significant difference was observed for compared variables in patients with and without COVID-19 except for prednisolone >20 mg/d (0.64% vs 2.26%; p = 0.048). Conclusion: Most rheumatic diseases do not seem to be a risk factor for developing COVID-19 infection and despite immunosuppressive therapies, there is no poorer outcome. Only, patients using prednisolone >20 mg/d are at higher risk of developing COVID-19 infection.

Systemic lupus erythematosus after coronavirus disease-2019 (COVID-19) infection: Case-based review.

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.

Microscopic polyangiitis associated with coronavirus disease-2019 (COVID-19) infection in an elderly male.

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 workTo 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.