To investigate passive smoking throughout the life course and the risk of rheumatoid arthritis (RA), while accounting for personal smoking.

To explore susceptibility loci associated with uveitis in Behcet’s disease (BD).

We congratulate the authors for the excellent review, not only restricted to recently approved therapies, on the treatment of systemic sclerosis-associated interstitial lung disease (SSc-ILD) (1). However, it is our opinion that some aspects that currently affect our medical practice merit further commentary.

We used a clinically oriented phenotype-first approach to identify patients with VEXAS syndrome from a single-center cohort of Italian patients with vasculitis.

We appreciate the insights and concerns shared by Dr. Jain et al. regarding the use of rituximab (RTX) and cyclophosphamide (CYC) for the treatment of granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA), as outlined in the American College of Rheumatology/Vasculitis Foundation (ACR/VF) guideline for the treatment of ANCA-associated vasculitis (AAV) [1]. These concerns are timely

Patients with established rheumatoid arthritis (RA) demonstrate altered immune responses to Epstein-Barr virus (EBV), but the presence and role(s) of EBV have not been fully explored in the preclinical period. We hypothesized that EBV infection, as evidenced by an altered anti-EBV antibody response, could either play an important role in driving the development or be a result of expanded RA-related

We thank Dr. Kao et al for their comments on our article and appreciate the opportunity to address these potential concerns about bias and confounding. In doing so, we will highlight the strengths of our study design that allow us to be confident in our findings on the association between lifestyle behaviors and SLE risk (1).

We read with great interest the article of Choi et al investigating whether a combination of individual factors related to lifestyle is associated with the lower risk of incident SLE.[1] However, it is pity that residual confounders have not been adjusted.

To provide guidance to rheumatology providers on the use of coronavirus disease 2019 (COVID-19) vaccines for patients with rheumatic and musculoskeletal diseases (RMDs).

To develop and validate new Juvenile Arthritis Disease Activity Score 10 (JADAS10) and clinical JADAS10 (cJADAS10) cutoffs to separate the states of inactive disease (ID), minimal disease activity (MiDA), moderate disease activity (MoDA), and high disease activity (HDA) in children with oligoarthritis and with rheumatoid factor–negative polyarthritis, based on subjective disease assessment by the treating

Elevated interleukin 10 (IL10) in SLE patients has B-cell promoting effects, contributing to autoantibody production and tissue damage. We aimed to characterize upregulated IL10+ B-cell subsets and dysregulated IL10 expression in SLE B cells for new therapeutic options.

Protein tyrosine kinases (PTKs) regulate osteoarthritis (OA) progression by activating a series of signal transduction pathways. However, the roles of protein tyrosine phosphatases (PTPs) in OA remain obscure.

To evaluate changes in bone turnover and bone mineral density (BMD) in subjects with rheumatoid arthritis (RA) on glucocorticoid (GC) after discontinuing denosumab for 12 months.

Rheumatologic and musculoskeletal diseases (RMDs) are important causes of morbidity and mortality worldwide. The World Health Organization (WHO) considers musculoskeletal conditions to be the leading cause of disability worldwide, and the greatest independent contributors to chronic pain. Population-based surveys from low- and middle-income countries (LMICs) have demonstrated similar rates of RMDs

Rheumatoid arthritis (RA) patients have almost twice the risk of heart failure (HF) of patients without RA, even when adjusting for presence of ischemic heart disease. Moreover, RA patients remain at two-fold higher risk of mortality from HF compared to non-RA patients. These observations suggest that RA specific inflammatory pathways are significant contributors to this increased risk of HF. We summarize

We used data from the SENSCIS trial to assess the effects of nintedanib versus placebo in subgroups of patients with SSc-ILD based on characteristics associated with progression of SSc-ILD in previous studies.

Managing patients with rheumatic disease during the COVID-19 pandemic has posed a unique challenge. Immunosuppressed patients are at an increased risk for developing severe COVID-19 and may not derive full protection from the vaccine (1-5). Thus, it is paramount we develop strategies whereby rheumatic disease patients can be protected from the pandemic virus and its variants.

Patients with rheumatic and musculoskeletal diseases (RMDs) on immunosuppressants are considered a vulnerable group in COVID-19 pandemic and vaccination is the mainstay for the prevention of this infection (1). To date, recommendations and data for COVID-19 vaccination in adolescent patients with RMDs are lacking (2). International societies and post-authorization safety reports of the novel mRNA COVID-19

Dominantly-inherited PSTPIP1 mutations cause a spectrum of autoinflammatory manifestations epitomized by Pyogenic Arthritis, Pyoderma gangrenosum, and Acne (PAPA) syndrome. The connections between PSTPIP1 and PAPA are poorly understood, although evidence suggests pyrin-inflammasome activation. Interleukin (IL)-18 is an inflammasome-activated cytokine associated with susceptibility to Macrophage Activation

The objectives of the study were to (1) determine the sensitivity of EULAR/ACR criteria to properly classify myositis-specific autoantibody (MSA) positive myositis patients, (2) describe the phenotype and muscle involvement over time in different MSA-positive patients, and (3) compare MSAs with the EULAR/ACR subgroups to predict clinical phenotypes.

To determine the role of gasdermin E (GSDME)-mediated pyroptosis in the pathogenesis and progression of rheumatoid arthritis (RA), and explore the potential therapeutic targets for RA.

We read with great interest the article of Penso et al investigating whether IL17-inhibitors (IL17i) initiation is related to the greater risk of inflammatory bowel disease (IBD) in patients with psoriasis (PsO), psoriatic arthritis (PsA) and ankylosing spondylitis (AS) [1]. However, some points need to be discussed.

Vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome was recently identified by genotype-driven approach. This syndrome is characterised by the presence of somatic mutations affecting methionine-41 (p.Met41) in UBA1 gene. All the identified patients were adult males who had recurrent fevers, cytopenias, dysplastic bone marrow with vacuoles in myeloid and erythroid precursors, neutrophilic

We appreciate the comments from Dr. Cheng-Ruei Yang et al. about our recent article that investigated whether IL17-inhibitors (IL17i) initiation is associated with a higher risk of inflammatory bowel disease (IBD) in patients with psoriasis (PsO), psoriatic arthritis and ankylosing spondylitis (PsA/AS).(1) We demonstrated that treatment with IL17i was not associated with a higher risk of IBD in patients

To evaluate premenopausal women with long-standing RA and to explore the relationship between parameters of systemic and localized bone involvement.

Recent transcriptome analyses revealed that 15-fold expanded HLA-DR+CD90+ synovial fibroblasts (SFs) are potential key mediators of inflammation in rheumatoid arthritis (RA). The reasons for the expansion of HLA-DR+CD90+ SFs are unclear, but genetic signatures indicated a central role of IFNɣ in the generation of this fibroblast subset.

A 90-year-old male presented with an ulcer of the hard palate (panel A) and unilateral orbital swelling following 3 months of nasal crusting. Laboratory investigation revealed WBC 6.6 K/mm3 (normal differential with 1.7% eosinophils), hemoglobin 9.8 g/dL, normal platelets, ESR 98 mm/Hr (normal <15 mm/Hr), CRP 3.7 mg/dL (normal <0.5mg/dL), negative ANCA, negative MPO and PR3 antibodies, elevated IgG

In a recent correspondence, Drs Baer and Hammitt [1] suggested that the terminology of “Sjögren’s syndrome” be changed to “Sjögren’s disease”. The main argument in favor of calling it a disease is that this condition is now very well characterized and identified within the group of connective tissue diseases, with autoimmune pathogenesis. In a very insightful article [2], Dr J. G. Scadding commented

Innate immune responses play key roles in the initiation and perpetuation of a variety of systemic autoimmune diseases, including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).(1) While effective biologics and small molecules targeting innate and adaptive immune responses in these diseases are currently available, there are still significant gaps in the development of therapies that

We thank Dr. Cottin for supporting our call to adopt the term ‘disease’ in lieu of ‘syndrome’ when referring to the distinct systemic disease described by Henrik Sjögren in a comprehensive 150-page monograph published in 1933.

Use a highly potent and selective small molecule inhibitor of interleukin-1 associated kinase (IRAK) 4, PF-06650833, to demonstrate its role in autoimmune pathophysiology in vitro, in vivo and in the clinic.

The objective of this study was to investigate the effect of biological treatments for psoriasis on the incidence of psoriatic arthritis.

To test the hypothesis that an altered gut microbiota (dysbiosis) plays a role in obesity-associated osteoarthritis (OA).

To investigate whether thermogenesis and the hypothalamus may be involved in the physiopathology of experimental arthritis (EA).

To identify predictors of rheumatic immune-related adverse events (rheum-irAEs) after immune checkpoint inhibitor (ICI) treatment for cancer.

We previously demonstrated that tofacitinib was effective in treating skin-predominant refractory dermatomyositis (DM) at 12 weeks in a prospective open label clinical trial, Study of Tofacitinib In Refractory dermatomyositis (STIR) (1). Here, we report the long-term extension results of up to 96 weeks to investigate the treatment durability of tofacitinib in refractory DM. Inclusion criteria and outcome

Multiple recent lines of evidence suggest that, at least in some patients, RA-associated autoimmunity and inflammation may originate in the lung (1, 2). However, what exactly is/are the initiating event(s), and the sequence of subsequent events, is not fully defined.

Mechanisms leading to anti-citrullinated protein antibody (ACPA) generation in rheumatoid arthritis (RA) are hypothesized to originate in the lung. The objective of this study was to understand associations between neutrophil extracellular trap (NET) formation in the lung and local ACPA generation in subjects At-Risk for RA.

We read the report by Mecoli et al on the relationship between cancer and anti-Th/To antibodies (AThAs) in patients with systemic sclerosis (SSc) (1). It is interesting that the presence of AThAs was reported to confer a protective effect against cancer development in those patients. However, cancer development in AThA-positive patients was significantly suppressed only within the first 3 years after

We thank Dr. Evangelatos for his interest in the guideline and his efforts to provide further clarity to this clinical scenario. During the guideline process, the voting panel thoroughly discussed many of these aspects of hypogammaglobulinemia during rituximab treatment that Dr. Evangelatos has adeptly described.

Among the established risk factors associated with developing rheumatoid arthritis (RA), smoking remains one of the leading environmental exposures associated with disease onset. One meta-analysis of ten studies found that the risk of developing RA increased by 26% among those who smoked 1-10 pack-years, and nearly doubled among those with more than 20 pack-years, compared to never smokers[1]. Studies

We read with great interest the recently published American College of Rheumatology guideline for the treatment of patients with rheumatoid arthritis (RA) (1). Among the various issues covered is the hypogammaglobulinemia that occasionally occurs in rituximab-treated RA patients. Hypogammaglobulinemia has been reported in about 17-43% of these patients (2). Risk factors for its occurrence are ill-defined

Mepolizumab proved efficacious for eosinophilic granulomatosis with polyangiitis (EGPA, former Churg-Strauss) at the dosage of 300mg/4 weeks in the randomized controlled MIRRA trial. Few successful real-life experiences with the dosage approved for severe eosinophilic asthma (100mg/4 weeks) were recently reported. We retrospectively assessed the effectiveness and safety of mepolizumab 100 and 300mg/4

To evaluate seroreactivity and disease flares after COVID-19 vaccination in a multi-ethnic/racial cohort of patients with systemic lupus erythematosus (SLE).

B cells can become activated in germinal center (GC) reactions in secondary lymphoid tissue and ectopic GCs in synovium in RA that may be TNF and lymphotoxin (LT) dependent. Here we characterized the peripheral B cell compartment longitudinally during anti-TNF therapy in RA.

To evaluate disease flare and post-vaccination reactions (reactogenicity) in patients with rheumatic and musculoskeletal diseases (RMD) following two-dose SARS-CoV-2 mRNA vaccination.

To provide guidance to rheumatology providers on the use of coronavirus disease 2019 (COVID-19) vaccines for patients with rheumatic and musculoskeletal diseases (RMDs).

To provide clinical guidance to rheumatology providers who treat children with pediatric rheumatic disease (PRD) in the context of the coronavirus disease 2019 (COVID-19) pandemic.

To provide evidence-based recommendations and expert guidance for the management of giant cell arteritis (GCA) and Takayasu arteritis (TAK) as exemplars of large vessel vasculitis.

To provide evidence-based recommendations and expert guidance for the management of antineutrophil cytoplasmic antibody–associated vasculitis (AAV), including granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA).

To provide evidence-based recommendations and expert guidance for the management of systemic polyarteritis nodosa (PAN).

In the article by Chatham et al in the May 2021 issue of Arthritis & Rheumatology (Long-Term Safety and Efficacy of Anifrolumab in Adults With Systemic Lupus Erythematosus: Results of a Phase II Open-Label Extension Study [pages 816–825]), the term “serious adverse events of special interest” or “serious AEs of special interest” was inadvertently used in place of the term “adverse events of special

A 40-year-old previously healthy woman presented to the Rheumatology department with suspected arthritis because of bilateral lower limb pain, swelling, and difficulty walking for the last six months. Physical examination revealed multiple subcutaneous hematomas, gingival hyperplasia, bilateral knee effusion, lower extremities muscle weakness, and right hip joint movement limitation. The laboratory

While the association between individual factors related to lifestyle and the risk of SLE has been previously evaluated, it is unclear how the combination of these factors might affect the risk of incident SLE. We prospectively evaluated whether a combination of healthy lifestyle factors is associated with lower risk of incident SLE and its subtypes (dsDNA positive and negative).

Systemic sclerosis (SSc; scleroderma) has the highest individual mortality of all rheumatic diseases and interstitial lung disease (ILD) is among the leading causes of SSc-related death. Two drugs are now approved by the Food & Drug Administration (FDA) and indicated for slowing the rate of decline in pulmonary function in patients with SSc-ILD: nintedanib (a tyrosine kinase inhibitor) and tocilizumab

To define the prevalence and clinical phenotype of anti-cortactin autoantibodies in adult and juvenile myositis.

It is unclear why activated platelets and platelet-derived microparticles (µPs) accumulate in the blood of patients with systemic sclerosis (SSc). Here we investigated whether defective phagocytosis might contribute.

Early selection steps preventing autoreactive naïve B cell production are often impaired in patients with autoimmune diseases, but central and peripheral B cell tolerance checkpoints have not been assessed in patients with systemic sclerosis (SSc).

To develop a Standardized Steroid dosing Regimen (SSR) by physicians treating childhood-onset systemic lupus erythematosus (cSLE) complicated by lupus nephritis (LN), using consensus formation methodology.

Idiopathic inflammatory myopathies (IIM) are a heterogeneous group of complex autoimmune conditions characterized by inflammation in skeletal muscle and extra-muscular compartments and interferon system activation. Here we aimed to examine the contribution of genetic variation to disease susceptibility and to identify novel avenues for research in IIM.