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ID PMID Title PublicationDate abstract
33498379 Body Mass Index and Disease Activity in Chronic Inflammatory Rheumatic Diseases: Results o 2021 Jan 20 OBJECTIVE: Since obesity has been associated with a higher inflammatory burden and worse response to therapy in patients with chronic inflammatory rheumatic diseases (CIRD), we aimed to confirm the potential association between body mass index (BMI) and disease activity in a large series of patients with CIRDs included in the Spanish CARdiovascular in rheuMAtology (CARMA) registry. METHODS: Baseline data analysis of patients included from the CARMA project, a 10-year prospective study of patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) attending outpatient rheumatology clinics from 67 Spanish hospitals. Obesity was defined when BMI (kg/m(2)) was >30 according to the WHO criteria. Scores used to evaluate disease activity were Disease Activity Score of 28 joints (DAS28) in RA, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) in AS, and modified DAS for PsA. RESULTS: Data from 2234 patients (775 RA, 738 AS, and 721 PsA) were assessed. The mean ± SD BMI at the baseline visit were: 26.9 ± 4.8 in RA, 27.4 ± 4.4 in AS, and 28.2 ± 4.7 in PsA. A positive association between BMI and disease activity in patients with RA (β = 0.029; 95%CI (0.01- 0.05); p = 0.007) and PsA (β = 0.036; 95%CI (0.015-0.058); p = 0.001) but not in those with AS (β = 0.001; 95%CI (-0.03-0.03); p = 0.926) was found. Disease activity was associated with female sex and rheumatoid factor in RA and with Psoriasis Area Severity Index and enthesitis in PsA. CONCLUSIONS: BMI is associated with disease activity in RA and PsA, but not in AS. Given that obesity is a potentially modifiable factor, adequate control of body weight can improve the outcome of patients with CIRD and, therefore, weight control should be included in the management strategy of these patients.
33431459 Primary Sjögren's syndrome manifesting as sclerotic metabolic bone disease. 2021 Jan 11 Primary Sjögren's syndrome (pSS) is a chronic slowly progressive autoimmune disease characterised by lymphocytic infiltration of salivary and lacrimal glands with varying degree of systemic involvement. Renal involvement, a recognised extraglandular manifestation of pSS, is commonly related to tubular dysfunction and generally manifests as distal renal tubular acidosis (RTA), proximal RTA, tubular proteinuria and nephrogenic diabetes insipidus. Untreated long-standing RTA is known to cause metabolic bone disease. Here, we present the report of a patient with sclerotic metabolic bone disease related to pSS with combined distal and proximal RTA and negative workup for other causes of sclerotic bone disease. A significant clinical and biochemical improvement, including recovery of proximal tubular dysfunction, was noted with alkali therapy. This case suggests the need to consider pSS in the diagnostic algorithm of a patient presenting with sclerotic bone disease.
33648375 Denervation as a Treatment for Arthritis of the Hands: A Systematic Review of the Current 2021 Mar 1 Joint denervation has been proposed as a less invasive option for surgical management of hand arthritis that preserves joint anatomy while treating pain and decreasing postoperative recovery times. The purpose of this systematic review was to investigate the efficacy and safety of surgical joint denervation for osteoarthritis in the joints of the hand. EMBASE, MEDLINE, and PubMed databases were searched from January 2000 to March 2019. Studies of adult patients with rheumatoid arthritis or osteoarthritis of the hand who underwent joint denervation surgery were included. Two reviewers performed the screening process, data abstraction, and risk of bias assessment (Methodological Index for Non-Randomized Studies). This review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and was registered with PROSPERO (#125811). Ten studies were included, 9 case series and 1 cohort study, with a total of 192 patients. In all studies, joint denervation improved pain and hand function at follow-up (M = 36.8 months, range = 3-90 months). Pooled analysis of 3 studies on the first carpometacarpal joint showed a statistically significant (P < .001) reduction in pain scores from baseline (M = 6.61 ± 2.03) to postoperatively (M = 1.69 ± 1.27). The combined complication rate was 18.8% (n = 36 of 192), with neuropathic pain or unintended sensory loss (8.8%, n = 17 of 192) being the most common. This review suggests that denervation may be an effective and low-morbidity procedure for treating arthritis of the hand. Prospective, comparative studies are required to further understand the outcomes of denervation compared with traditional surgical interventions.
33815378 Adiponectin Enhances B-Cell Proliferation and Differentiation via Activation of Akt1/STAT3 2021 Although B cells have been shown to contribute to the pathogenesis of rheumatoid arthritis (RA), the precise role of B cells in RA needs to be explored further. Our previous studies have revealed that adiponectin (AD) is expressed at high levels in inflamed synovial joint tissues, and its expression is closely correlated with progressive bone erosion in patients with RA. In this study, we investigated the possible role of AD in B cell proliferation and differentiation. We found that AD stimulation could induce B cell proliferation and differentiation in cell culture. Notably, local intraarticular injection of AD promoted B cell expansion in joint tissues and exacerbated arthritis in mice with collagen-induced arthritis (CIA). Mechanistically, AD induced the activation of PI3K/Akt1 and STAT3 and promoted the proliferation and differentiation of B cells. Moreover, STAT3 bound to the promoter of the Blimp-1 gene, upregulated Blimp-1 expression at the transcriptional level, and promoted B cell differentiation. Collectively, we observed that AD exacerbated CIA by enhancing B cell proliferation and differentiation mediated by the PI3K/Akt1/STAT3 axis.
34735867 The glycolysis inhibitor 2-deoxyglucose ameliorates adjuvant-induced arthritis by regulati 2021 Dec Macrophages are highly plastic cells critical for the development of rheumatoid arthritis (RA). Macrophages exhibit a high degree of pro-inflammatory plasticity in RA, accompanied by a metabolic reprogramming from oxidative phosphorylation (OXPHOS) to glycolysis. 2-deoxyglucose (2-DG), a glycolysis inhibitor, has previously been shown to exhibit anti-inflammatory and anti-arthritic properties. However, the specific mechanisms of inflammatory modulation by 2-DG remain unclear. This study used 2-DG to treat rats with adjuvant arthritis (AA) and investigated its specific anti-arthritic mechanisms in the murine-derived macrophage cell line RAW264.7 in vitro. 2-DG reduced the arthritis index as well as alleviated cellular infiltration, synovial hyperplasia, and bone erosion in AA rats. Moreover, 2-DG treatment modulated peritoneal macrophage polarization, increasing levels of the arginase1 (Arg1) and decreasing expression of the inducible nitric oxide synthase (iNOS). 2-DG activated AMP-activated protein kinase (AMPK) via phosphorylation and reduced activation of the nuclear factor κB (NF-κB) in peritoneal macrophages of AA rats. In vitro, we verified that 2-DG promoted macrophage transition from M1 to M2-type by upregulating the expression of p-AMPKα and suppressing NF-κB activation in LPS-stimulated RAW264.7 cells. LPS-induced macrophages exhibited a metabolic shift from glycolysis to OXPHOS following 2-DG treatment, as observed by reduced extracellular acidification rate (ECAR), lactate export, glucose consumption, as well as an elevated oxygen consumption rate (OCR) and intracellular ATP concentration. Importantly, changes in polarization and metabolism in response to 2-DG were dampened after AMPKα knockdown. These findings indicate that the anti-arthritic 2-DG effect is mediated by a modulation of macrophage polarization in an AMPK-dependent manner.
34422427 Coexistence of Rheumatoid Arthritis, Systemic Lupus Erythematosus, Sjogren Syndrome, Antip 2021 A 37-year-old Bangladeshi woman presented with low back and several joints pain and swelling for months together; there was significant morning stiffness for more than two hours. Repeated abortions, dry eye, hair fall, photosensitivity, and oral ulcer were the additional complaints. Clinical examination unveiled asymmetrical peripheral and both sacroiliac joint tenderness, positive modified Schober's test, and limited chest expansion. Schirmer's test was positive. The history of rheumatoid arthritis (RA) and ankylosing spondylitis (AS) among 1st-degree relatives was also significant. Biochemical analysis revealed pancytopenia, raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and mild microscopic proteinuria. The patient was seropositive for rheumatoid factor (RF), antibodies against cyclic citrullinated peptides (anti-CCP), antinuclear antibody (ANA), anti-Sm antibody, anti-Sjögren's-syndrome-related antigen A and B (anti-SSA/SSB), antiphospholipid (aPL-IgG/IgM), and HLA B27; however, serum complement (C3 and C4) levels were normal. Basal cortisol level measured elevated. Besides, X-ray and MRI of lumbosacral spines demonstrated sacroiliitis. There was radiological cardiomegaly, echocardiography unveiled atrial regurgitation, and ascending aorta aneurysm. Based on the abovementioned information, RA, AS, and systemic lupus erythematosus (SLE) have been diagnosed. Moreover, the patient developed Sjogren's syndrome (SS), antiphospholipid lipid syndrome (APS), Cushing syndrome, ascending aorta aneurysm, and atrial regurgitation. Her disease activity score for RA (DAS28), DAS for AS (ASDAS), SLE disease activity index (SLEDAI), and Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) scores were 3.46, 2.36, 23, and 5, respectively. The patient received hydroxychloroquine (200 mg daily), pulsed cyclophosphamide, prednisolone (20 mg in the morning), and naproxen 500 mg (twice daily). To our best knowledge, this is the first report documenting RA, AS, and SLE with secondary SS and APS.
34386704 Gout and AA-Amyloidosis: A Case-Based Review. 2021 Mar BACKGROUND: AA-amyloidosis complicates many chronic infections and inflammatory diseases, including rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis, but its relationship to gout is extremely rare. As it is unknown definitely what the pathophysiological connections between gout and amyloidosis are, treatment issues of the diseases are open for discussion. AIM: To establish a link between gout and AA-amyloidosis, and to improve the quality of treatment in patients suffering from gout and AA-amyloidosis. METHODS: We reviewed the English-language literature sources, searching not only for rare cases of the combination of gout and AA amyloidosis, but also detailed descriptions of the medical treatments for the two pathologies. RESULTS: By July 2020, we had identified 14 cases describing AA amyloidosis in patients with gout. Most of those patients had been suffering tophaceous gout for at least 10 years, and were prescribed various methods of treatment; however, not all patients took colchicine regularly. In some cases, therapy with allopurinol and colchicine was effective against attacks of gouty arthritis, although amyloidogenic inflammation was not controlled sufficiently. However, there were no cases that described in detail the successful treatment of both diseases. Besides those 14 patients described in literature, we examined one more patient with amyloidosis that is secondary to gout, in whom the protein of amyloid A (AA) had affected the kidneys, intestines, and adrenal glands. The patient has been successfully treated with the combination of canakinumab, prednisone, colchicine and allopurinol. CONCLUSION: Clinicians should be aware that patients may have atypical combinations of diseases like gout and amyloidosis. The obtained results help to explain some pathogenic processes associated with AA-amyloidosis. Further research is necessary to confirm the effectiveness of different treatment options such as lifestyle biologic agents or other medicines with anti-inflammatory properties.
32674107 Combination of LMT-28 and Metformin Improves Beneficial Anti-Inflammatory Effect in Collag 2021 OBJECTIVES: The interleukin-6 (IL-6)-mediated signaling pathway plays an essential role in the development of rheumatoid arthritis. LMT-28 suppresses the activation of the IL-6-mediated signaling by direct targeting of gp130. Although LMT-28 and metformin both possess anti-inflammatory activity, the beneficial effect of LMT-28 and metformin combination on a collagen-induced arthritis (CIA) model has not yet been investigated. This study aimed to investigate the anti-inflammatory effect and mechanism of a combination of LMT-28 and metformin in a CIA model. METHODS: In MH7A cells, cell proliferation and the IL-6-mediated signaling pathway following administration of LMT-28 and metformin combination was analyzed through MTT assay and Western blotting. The level of T helper 17 (Th17) cell differentiation from CD4+ T cells was analyzed in mouse splenocytes and human peripheral blood mononuclear cells. Arthritis score, incidence rate, inflammatory cytokine, and T-cell subsets were measured in CIA mice following administration of LMT-28 and metformin combination. RESULTS: Combination treatment with LMT-28 and metformin diminished proliferation of MH7A cells and IL-6-mediated gp130, STAT3, and ERK signaling more than in individual treatments. Furthermore, the differentiation of CD4+ T cells into Th17 cells was attenuated more by combination treatment with LMT-28 and metformin than individual treatments. The combination of LMT-28 and metformin ameliorated the arthritic score better than individual treatments. The combination significantly reduced tumor necrosis factor and IL-6 levels in the sera and had an anti-inflammatory effect on the distribution of Treg/Th17 cells in the lymph nodes. CONCLUSION: Combination treatment with LMT-28 and metformin significantly ameliorates arthritic symptoms in CIA by suppressing Th17 differentiation and IL-6 signaling.
34214886 The PI3Kδ inhibitor parsaclisib ameliorates pathology and reduces autoantibody formation 2021 Sep Dysregulation of phosphoinositide 3-kinase δ (PI3Kδ) signaling pathway has been implicated in the pathogenesis of inflammatory and autoimmune diseases. Parsaclisib (INCB050465) represents a potent and selective PI3Kδ inhibitor, which is being clinically investigated for treatment of autoimmune hemolytic anemia and hematological malignancies. We characterized the potential of parsaclisib to ameliorate autoimmune mechanisms implicated in the pathophysiology of systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS). Spontaneous mouse models of SLE and SS were utilized to elucidate the efficacy of orally administered parsaclisib on autoreactive B-cell-mediated antibody-driven disease. Parsaclisib significantly reduced disease symptoms and pathology in three distinct mouse models of SLE. Parsaclisib effectively preserved renal function as measured by glomerular filtration rate, abrogated histopathological evidence of nephritis, modulated discrete immune cell subsets, and decreased anti-dsDNA antibody level. Furthermore, parsaclisib demonstrated efficacy in two spontaneous mouse models of SS. Oral parsaclisib treatment ameliorated the severity of salivary gland inflammation and reduced circulating levels of autoantibodies. Parsaclisib mediated improvement of salivary gland inflammation coincided with reduced B-cell activating cytokine (BAFF) in saliva. Transcriptomic analysis of kidney and salivary gland tissues revealed a downregulation in inflammatory gene expression consistent with PI3Kδ pathway inhibition. Parsaclisib reduced autoreactive B-cells and autoantibody levels, and significantly improved nephritis and salivary gland inflammation. These data provide the scientific rationale for PI3Kδ inhibition as a therapeutic strategy for treatment of B-cell-mediated antibody-driven autoimmune diseases.
34539657 IL-17 and CCR9(+)α4β7(-) Th17 Cells Promote Salivary Gland Inflammation, Dysfunction, an 2021 Previous studies have evaluated the roles of T and B cells in the pathogenesis of Sjögren's syndrome (SS); however, their relationships with age-dependent and metabolic abnormalities remain unclear. We examined the impacts of changes associated with aging or metabolic abnormalities on populations of T and B cells and SS disease severity. We detected increased populations of IL-17-producing T and B cells, which regulate inflammation, in the salivary glands of NOD/ShiLtJ mice. Inflammation-induced human submandibular gland cell death, determined based on p-MLKL and RIPK3 expression levels, was significantly increased by IL-17 treatment. Among IL-17-expressing cells in the salivary gland, peripheral blood, and spleen, the α4β7 (gut-homing integrin)-negative population was significantly increased in aged NOD/ShiLtJ mice. The α4β7-positive population markedly increased in the intestines of aged NOD/ShiLtJ mice following retinoic acid (RA) treatment. A significant increase in α4β7-negative IL-17-expressing cells in salivary glands may be involved in the onset and progression of SS. These results suggest the potential therapeutic utility of RA in SS treatment.
34281285 Metformin as a Treatment Strategy for Sjögren's Syndrome. 2021 Jul 5 Sjögren's syndrome (SS), a chronic inflammatory disease involving the salivary and lacrimal glands, presents symptoms of sicca as well as systemic manifestations such as fatigue and musculoskeletal pain. Only a few treatments have been successful in management of SS; thus treatment of the disease is challenging. Metformin is the first-line agent for type 2 diabetes and has anti-inflammatory potential. Its immunomodulatory capacity is exerted via activation of 5' adenosine monophosphate-activated protein kinase (AMPK). Metformin inhibits mitochondrial respiratory chain complex I which leads to change in adenosine mono-phosphate (AMP) to adenosine tri-phosphate (ATP) ratio. This results in AMPK activation and causes inhibition of mammalian target of rapamycin (mTOR). mTOR plays an important role in T cell differentiation and mTOR deficient T cells differentiate into regulatory T cells. In this manner, metformin enhances immunoregulatory response in an individual. mTOR is responsible for B cell proliferation and germinal center (GC) differentiation. Thus, reduction of B cell differentiation into antibody-producing plasma cells occurs via downregulation of mTOR. Due to the lack of suggested treatment for SS, metformin has been considered as a treatment strategy and is expected to ameliorate salivary gland function.
33911236 Epithelial-immune cell interplay in primary Sjögren syndrome salivary gland pathogenesis. 2021 Jun In primary Sjögren syndrome (pSS), the function of the salivary glands is often considerably reduced. Multiple innate immune pathways are likely dysregulated in the salivary gland epithelium in pSS, including the nuclear factor-κB pathway, the inflammasome and interferon signalling. The ductal cells of the salivary gland in pSS are characteristically surrounded by a CD4(+) T cell-rich and B cell-rich infiltrate, implying a degree of communication between epithelial cells and immune cells. B cell infiltrates within the ducts can initiate the development of lymphoepithelial lesions, including basal ductal cell hyperplasia. Vice versa, the epithelium provides chronic activation signals to the glandular B cell fraction. This continuous stimulation might ultimately drive the development of mucosa-associated lymphoid tissue lymphoma. This Review discusses changes in the cells of the salivary gland epithelium in pSS (including acinar, ductal and progenitor cells), and the proposed interplay of these cells with environmental stimuli and the immune system. Current therapeutic options are insufficient to address both lymphocytic infiltration and salivary gland dysfunction. Successful rescue of salivary gland function in pSS will probably demand a multimodal therapeutic approach and an appreciation of the complicity of the salivary gland epithelium in the development of pSS.
33936039 Predicted Disease-Specific Immune Infiltration Patterns Decode the Potential Mechanisms of 2021 Primary Sjogren's syndrome (pSS) is a chronic progressive autoimmune disease with clinical phenotypic "Sicca symptoms". In some cases, the diagnosis of pSS is delayed by 6-7 years due to the inefficient differential diagnosis of pSS and non-SS "Sicca". This study aimed to investigate the difference between these two diseases, and in particular, their immunopathogenesis. Based on their gene expression profiles, we systematically defined for the first time the predicted disease-specific immune infiltration pattern of patients with pSS differentiated from normal donors and patients with non-SS "Sicca". We found that it was characterized by the aberrant abundance and interaction of tissue-infiltrated immune cells, such as a notable shift in the subpopulation of six immune cells and the perturbed abundance of nine subpopulations, such as CD4+ memory, CD8+ T-cells and gamma delta T-cells. In addition, we identified essential genes, particularly long non-coding RNAs (lncRNAs), as the potential mechanisms linked to this predicted pattern reprogramming. Fourteen lncRNAs were identified as the potential regulators associated with the pSS-specific immune infiltration pattern in a synergistic manner, among which the CTA-250D10.23 lncRNA was highly relevant to chemokine signaling pathways. In conclusion, aberrant predicted disease-specific immune infiltration patterns and relevant genes revealed the immunopathogenesis of pSS and provided some clues for the immunotherapy by targeting specific immune cells and genes.
34067842 Treatment with an Anti-CX3CL1 Antibody Suppresses M1 Macrophage Infiltration in Interstiti 2021 May 17 CX3C Motif Chemokine Ligand 1 (CX3CL1; fractalkine) has been implicated in the pathogenesis of rheumatoid arthritis (RA) and its inhibition was found to attenuate arthritis in mice as well as in a clinical trial. Therefore, we investigated the effects of an anti-CX3CL1 monoclonal antibody (mAb) on immune-mediated interstitial lung disease (ILD) in SKG mice, which exhibit similar pathological and clinical features to human RA-ILD. CX3CL1 and CX3C chemokine receptor 1 (CX3CR1), the receptor for CX3CL1, were both expressed in the fibroblastic foci of lung tissue and the number of bronchoalveolar fluid (BALF) cells was elevated in ILD in SKG mice. No significant changes were observed in lung fibrosis or the number of BALF cells by the treatment with anti-CX3CL1 mAb. However, significantly greater reductions were observed in the number of M1 macrophages than in M2 macrophages in the BALF of treated mice. Furthermore, CX3CR1 expression levels were significantly higher in M1 macrophages than in M2 macrophages. These results suggest the stronger inhibitory effects of the anti-CX3CL1 mAb treatment against the alveolar infiltration of M1 macrophages than M2 macrophages in ILD in SKG mice. Thus, the CX3CL1-CX3CR1 axis may be involved in the infiltration of inflammatory M1 macrophages in RA-ILD.
33216641 The use of anti-TNF-alpha therapies for patients with systemic lupus erythematosus. Where 2021 May INTRODUCTION: Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease characterized by multiple pathologies in which sustained inflammatory activity leads to progressive tissue destruction and organ damage. One of the main proinflammatory cytokines playing a key role in autoimmune diseases such as rheumatoid arthritis (RA) or SLE, is tumor necrosis factor (TNF) alpha. AREAS COVERED: The introduction of TNF-alpha inhibitors revolutionized the treatment of RA and other conditions including psoriatic arthritis and ankylosing spodylitis. We review here the efficacy and safety of TNF-alpha blockers in SLE focussing on why it has not been more widely used since TNF-alpha was reported to be increased in SLE patients and to correlate with disease activity. EXPERT OPINION: We summarize the reported SLE cases that have received TNF-alpha blockers and the main results to date. We reflect on whether there is a case to reconsider the use of TNF-alpha blockade in SLE.
34445367 Hyperbilirubinemia Maintained by Chronic Supplementation of Unconjugated Bilirubin Improve 2021 Aug 12 Rheumatoid arthritis (RA) is a chronic multisystem disease, therapy of which remains a challenge for basic research. The present work examined the effect of unconjugated bilirubin (UCB) administration in adjuvant-induced arthritis (AIA)-an experimental model, in which oxidative stress (OS), inflammation and inadequate immune response are often similar to RA. Male Lewis rats were randomized into groups: CO-control, AIA-untreated adjuvant-induced arthritis, AIA-BIL-adjuvant-induced arthritis administrated UCB, CO-BIL-control with administrated UCB. UCB was administered intraperitoneally 200 mg/kg of body weight daily from 14th day of the experiment, when clinical signs of the disease are fully manifested, to 28th day, the end of the experiment. AIA was induced by a single intradermal immunization at the base of the tail with suspension of Mycobacterium butyricum in incomplete Freund's adjuvant. Clinical, hematologic, biochemical and histologic examinations were performed. UCB administration to animals with AIA lead to a significant decrease in hind paws volume, plasma levels of C-reactive protein (CRP) and ceruloplasmin, drop of leukocytes, lymphocytes, erythrocytes, hemoglobin and an increase in platelet count. UCB administration caused significantly lowered oxidative damage to DNA in arthritic animals, whereas in healthy controls it induced considerable oxidative damage to DNA. UCB administration also induced atrophy of the spleen and thymus in AIA and CO animals comparing to untreated animals. Histological signs of joint damage assessed by neutrophils infiltration and deposition of fibrin were significantly reduced by UCB administration. The effects of exogenously administered UCB to the animals with adjuvant-induced arthritis might be identified as therapeutic, in contrast to the effects of UCB administration in healthy animals rather classified as toxic.
34596719 COVID-19 from a rheumatology perspective: bibliometric and altmetric analysis. 2021 Dec The Coronavirus disease 2019 (COVID-19) outbreak turned out the greatest pandemic for decades. It challenged enormously the global health system, forcing it to adjust to the new realities. We aimed to analyze articles covering COVID-19 papers in the rheumatological field and outline emerging topics raising within this frame. We applied the bibliometric database Scopus for our literature search and conducted it on the 5th of June using the following keywords: "rheumatic" OR "rheumatology" OR "rheumatoid arthritis" OR "systemic lupus erythematosus" OR "myositis" OR "systemic sclerosis" OR "vasculitis" OR "arthritis" OR "ankylosing spondylitis" AND "COVID-19". We analyzed all selected articles according to various aspects: type of document, authorship, journal, citations score, rheumatology field, country of origin, language, and keywords. With the help of the software tool VOSviewer version 1.6.15, we have built the visualizing network of authors and keywords co-occurrence. The measurement of the social impact of articles was made using Altmetric data. This study included 1430 retrieved articles with open access mostly. The top five journals in this field were Annals of the Rheumatic Diseases (n = 65), Rheumatology International (n = 51), Clinical Rheumatology (n = 50), Lancet Rheumatology (n = 50), and Frontiers In Immunology (n = 33). Most studies originate from countries with a high incidence of COVID-19 among the general population (the USA-387; Italy-268; UK-184; France-114; Germany-110; India-98 and Spain-96, China-94, Canada-73 Turkey-66). Original Articles (42.1%) were the most common articles' type, following by Letters (24.4%), Reviews (21.7%), Notes (6%), Editorials (4.8%), Erratum (1%). According to the citations scores, articles dedicated to the clinical course of COVID-19 in patients with rheumatic diseases were of the highest importance for the scientific rheumatologic community. Rheumatoid arthritis (n = 527), systemic lupus erythematosus (n = 393), vasculitis (n = 267), myositis (n = 71), systemic sclerosis (n = 68), and psoriatic arthritis (n = 68) were the most widely discussed rheumatic diseases in the view of COVID-19. The analysis of Altmetric and citations scores revealed a moderate correlation between them. This article provides a comprehensive bibliometric and altmetric analysis of COVID-19 related articles in the rheumatology field and summarizes data about features of rheumatology service in the time of the pandemic.
33993118 Canadian Rheumatology Association Meeting Virtual Congress February 24 - 26, 2021. 2021 Jul The 75th Annual Meeting of The Canadian Rheumatology Association was held virtually on February 24-26, 2021. The program consisted of presentations covering original research, symposia, awards, and lectures. Highlights of the meeting include the following 2021 Award Winners: Distinguished Rheumatologist, Rachel Shupak; Distinguished Investigator, Sasha Bernatsky; Distinguished Teacher-Educator, Elaine Yacyshyn; Emerging Investigator, Zahi Touma; Ian Watson Award for the Best Abstract on SLE Research by a Trainee, Raffaella Carlomagno; Phil Rosen Award for the Best Abstract on Clinical or Epidemiology Research by a Trainee, Kimberley Yuen; Best Abstract by a Rheumatology Resident, Ariane Barbacki; Best Abstract on Basic Science Research by a Trainee, Andrew Kwan; Best Abstract by a Post-Graduate Research Trainee, Luiza Grazziotin; Best Abstract on Quality Care Initiatives in Rheumatology, Nadia Luca; Best Abstract by a Medical Student, Daniel Levin; Best Abstract by an Undergraduate Student, Anson Lee; Best Abstract by a Rheumatology Post-Graduate Research Trainee, Jennifer Lee; Best Abstract on Research by Young Faculty, Lihi Eder; Best Abstract on Spondyloarthritis Research, Sandeep Dhillon; Practice Reflection Award, Gold, Stephanie Gottheil; CRA Master Awards, Ciarán M. Duffy, Mary-Ann Fitzcharles, James M. Henderson. Lectures and other events included: Keynote Lecture by Danielle Martin: Delivering on What Matters: Lessons from Canada's Response to the COVID-19 Pandemic; State of the Art Lecture by Michael Libman: Vaccination and Travel: Should I or Shouldn't I?; Dunlop-Dottridge Lecture by Dan Kastner: Rheumatic Disease and the Human Condition; and the Great Debate: Be it Resolved that Telemedicine Allows Rheumatologists to Provide Excellent Care to Patients with Autoimmune Rheumatic Diseases. Arguing for: Alexandra Saltman and Tommy Gerschman, and against: Brent Ohata and Jocelyne Murdoch. Topics including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjögren syndrome, psoriatic arthritis, spondyloarthritis, vasculitis, osteoarthritis, fibromyalgia, and their respective diagnoses, treatments, and outcomes are reflected in the abstracts, which we are pleased to publish in this issue of The Journal.
34575614 Metabolomic Biomarker Candidates for Skeletal Muscle Loss in the Collagen-Induced Arthriti 2021 Aug 26 There is no consensus for diagnosis or treatment of RA muscle loss. We aimed to investigate metabolites in arthritic mice urine as biomarkers of muscle loss. DBA1/J mice comprised collagen-induced arthritis (CIA) and control (CO) groups. Urine samples were collected at 0, 18, 35, 45, 55, and 65 days of disease and subjected to nuclear magnetic resonance spectroscopy. Metabolites were identified using Chenomx and Birmingham Metabolite libraries. The statistical model used principal component analysis, partial least-squares discriminant analysis, and partial least-squares regression analysis. Linear regression and Fisher's exact test via the MetaboAnalyst website were performed (VIP-score). Nearly 100 identified metabolites had CIA vs. CO and disease time-dependent differences (p < 0.05). Twenty-eight metabolites were muscle-associated: carnosine (VIPs 2.8 × 10(2)) and succinyl acetone (VIPs 1.0 × 10) showed high importance in CIA vs. CO models at day 65; CIA pair analysis showed histidine (VIPs 1.2 × 10(2)) days 55 vs. 65, histamine (VIPs 1.1 × 10(2)) days 55 vs. 65, and L-methionine (VIPs 1.1 × 10(2)) days 0 vs. 18. Carnosine was fatigue- (0.039) related, creatine was food intake- (-0.177) and body weight- (-0.039) related, and both metabolites were clinical score- (0.093; 0.050) and paw edema- (0.125; 0.026) related. Therefore, muscle metabolic alterations were detected in arthritic mice urine, enabling further validation in RA patient's urine, targeting prognosis, diagnosis, and monitoring of RA-mediated muscle loss.
34824724 Peri-operative Morbidity Associated with Bilateral Hip Arthroplasty for Inflammatory Arthr 2021 Oct AIM: This study aims to assess the risks and peri-operative morbidity associated with a single-stage sequential bilateral hip arthroplasty (SBHA) when performed in patients with arthritis secondary to inflammatory arthropathy. METHODS: Data of patients who underwent SBHA between 2012 and 2018 for inflammatory arthritis were extracted from a database, for peri-operative complications and functional improvement. SBHA for other causes was excluded. RESULTS: Data of 84 consecutive patients with a mean age of 34.5 years were analyzed. The mean follow-up was 2.4 years. 66% had ankylosing spondylitis, while 14% had rheumatoid arthritis. 50% of the patients had bilateral fusion of the hips, and 34% had flexion deformity > 30°.None of the patients had peri-operative cardiac or pulmonary complications. 2.4% had per-operative hypotension (MAP < 50 mmHg) and 1.2% had desaturation (SpO(2) < 90%). The mean drop in hematocrit was 9.3%. While 31% did not require blood transfusion, 35% required more than 1 unit of blood. Patients with pre-operative PCV of > 36% had a significantly lower risk of being transfused > 1 unit of blood (p = 0.02). ICU admission was 6%-mostly for post-operative monitoring. While one patient had a local hematoma that needed a wash-out, there were no infections, dislocations, or mortality in these patients. The modified Harris hip score improved from a mean of 26.5-85. The mean hip flexion improved post-operatively from 32° to 92°. CONCLUSIONS: SBHA for inflammatory arthritis can be performed with minimum complications in a multidisciplinary setting. Pre-operatively, PCV of > 36 is advised to reduce transfusion rates.