Symptoms Of Inflammatory Arthritis Research Articles

Occupational impacts of early inflammatory arthritis: results from the National Early Inflammatory Arthritis Audit.

Inflammatory arthritis causes significant work disability. Studies regarding this frequently fail to report important contextual information such as employment type. Our objective was to explore work participation, by gender and occupation type, in early inflammatory arthritis. Data are from the National Early Inflammatory Arthritis Audit for 2018-2020. At diagnosis, clinicians collected information on demographics, inflammatory arthritis disease activity, and working status. Participants completed patient-reported outcomes at baseline, 3 months and 12 months, including occupation and Work Productivity and Activity Impairment (WPAI). Descriptive analyses of work participation and WPAI scores by occupational class at all time points were performed. Regression models were used to examine associations between WPAI score and occupation. In all, 12 473 people received a diagnosis of inflammatory arthritis and reported employment status, among whom 5999 (47%) were in paid work for at least 20 hours/week. At diagnosis, the working cohort had statistically significant lower measures of disease activity (P < 0.001). Occupational data were available for 3694 individuals. At diagnosis, 2793 completed a WPAI; 200 (7.2%) had stopped work and 344 (12.3%) changed jobs because of inflammatory arthritis symptoms. There was a high burden of absenteeism (30%) and presenteeism (40%). Compared with managerial or professional workers, the burden of work disability was greater among those in routine (manual) occupations. During follow-up, 9.4% of WPAI completers stopped work and 14.6% changed roles. Work drop-out occurred almost entirely among people doing routine jobs. It is easier to retain work in certain employment sectors. Participation in routine jobs is more affected, which may widen health inequalities.

The comparative performance of three screening questionnaires for psoriatic arthritis in a primary care surveillance study.

The objective of this study was to compare the performance of three PsA screening questionnaires in a primary care psoriasis surveillance study. Participants with psoriasis, and not known to have PsA, were identified from general practice databases and invited to attend a secondary care centre for a clinical assessment. The three patient-completed screening questionnaires (PEST, CONTEST and CONTESTjt) were administered, along with other patient-reported measures, and a clinical examination of skin and joints was performed. Participants who demonstrated signs of inflammatory arthritis suggestive of PsA were referred, via their GP, for a further assessment in a secondary care rheumatology clinic. A total of 791 participants attended the screening visit, and 165 participants were judged to have signs and symptoms of inflammatory arthritis, of which 150 were referred for assessment. Of these, 126 were seen and 48 were diagnosed with PsA. The results for each questionnaire were as follows: PEST: sensitivity 0.625 (95% CI 0.482, 0.749), specificity 0.757 (0.724, 0.787); CONTEST: sensitivity 0.604 (0.461, 0.731), specificity 0.768 (0.736, 0.798); and CONTESTjt: sensitivity 0.542 (0.401, 0.676), specificity 0.834 (0.805, 0.859). CONTESTjt demonstrated marginally superior specificity to PEST, though the area under the ROC curve was similar for all three instruments. Minimal differences between the three screening questionnaires were found in this study, and no preferred questionnaire is indicated by these results. The choice of which instrument to choose will depend on other factors, such as simplicity and low patient burden.

Assessment of patients with painful joints

Joint pain makes up a significant proportion of presentations to general practice. Causes range from minor mechanical issues to serious conditions such as septic arthritis. Clues from the history such as onset, progression, and extra-articular symptoms aid diagnosis. Many cases of joint pain are appropriately investigated and managed in general practice, but some presentations require referral to secondary care, such as those with signs or symptoms of inflammatory arthritis. It is crucial that red flags for serious or life-threatening causes of joint pain are identified and acted upon urgently.

P129 DNA methylation of the tumour necrosis factor gene as a biomarker of diagnosis in early rheumatoid arthritis patients

Abstract Background/Aims Rheumatoid arthritis (RA) is an autoimmune inflammatory condition that affects the synovial joints. RA exists on a disease continuum where immunological changes occur before the onset of clinical symptoms. Changes in DNA methylation status of genes are thought to be early triggers of the progression from health to disease. Tumour necrosis factor (TNF) is a pro-inflammatory cytokine that contributes to RA. Recently it has been shown that the loss of DNA methylation in the promoter region of the TNF gene is related to early RA. This study aims to establish the predictive value of the levels of DNA methylation of the TNF gene as a biomarker for diagnosis of RA. Methods Blood samples from a retrospective cohort of patients with symptoms of inflammatory arthritis between 2010 and 2019 at the Leeds Early Arthritis Clinic were selected. Data obtained include clinical symptoms of disease progression over 2 years to establish a diagnosis. DNA methylation levels of the TNF gene were measured by quantitative polymerase chain reaction (qPCR) and analysed using binary logistic regression with forward (LR) variable selection for added value as a diagnostic biomarker. Results For the 284 patients with a mean age of 53.8, 202 (71.7%) were female and 82 (28.9%) were male. From N = 284, 190 (66.9%) were diagnosed with RA and 94 (33.1%) with another conditions. The predictive accuracy of the regression model was increased by 3.5% from 85.8% to 89.3% when TNF DNA-methylation levels was added to demographic and clinical variables. The AUC of the model with TNF was 0.940 compared to 0.911 without TNF DNA-methylation levels. The sensitivity and specificity of the prediction with DNA methylation data were 94.6% and 77.9% respectively. This TNF model has a positive predictive value of 90.2% and a negative predictive value of 87.0%. Conclusion DNA methylation of the TNF gene is an important biomarker for RA diagnosis. This study showed that including levels of TNF DNA-methylation improves the accuracy of diagnosing RA. Disclosure M.C. Liu: None. H. Ng: None. F. Ponchel: None.

P069 Stress matters: inflammatory arthritis patients' perspective of impact of stress

Abstract Background/Aims The objective of this survey was to gather patients’ perspectives on how stress triggered their inflammatory arthritis as well as exacerbates flares in their disease. Methods NRAS wanted to reach people living with RA and other forms of inflammatory arthritis via a national survey to gauge how they recognise and manage stress, and whether health professionals considered stress as a factor in their active disease. The survey was designed to capture demographics, impact of stress on patients’ disease as well as work status and restrictions on lifestyle. The national online survey was distributed via all NRAS social media platforms as well as email. Results 1265 responses from across the UK were gathered. The majority of respondents were female (87.0%) and over the age of 55 years old (70.5%). Approximately 45% had a disease duration of more than 10 years, 30% between 4 and 10 years, and 23% less than 3 years. When asked on a scale of 1 (not at all) to 5 (completely) how much stress had impacted the onset of their arthritis symptoms, 56% responded either ‘completely’ or ‘greatly’. Only 9% reported that stress did not have an impact on the onset of their symptoms. When asked if they felt a stressful event in the 12 months prior to their diagnosis had triggered their inflammatory arthritis 28% said yes and 48% responded maybe. Some of the top reported causes of stress prior to diagnosis were: death of a close family member, menopause, work difficulties and family commitments. The majority of respondents (67%) said that health professionals did not ask them about stress during the diagnosis process, with only 11% saying this was discussed. Participants were asked how much they agreed with the statement that they are often asked about their mental health in routine appointments - 75% disagreed or strongly disagreed. Conclusion With the majority of respondents identifying that stress and stressful events exacerbate their symptoms of inflammatory arthritis, more should be done to measure and offer support for managing stress. While many had found their own ways of coping with stress more needs to be done to make support more easily accessible. Further research would be beneficial in identifying if managing stress within this patient population could significantly reduce inflammatory arthritis symptoms, reducing the distress and pain caused by flares and also reduce the impact on the health service of clinical intervention. Disclosure C. Jacklin: Grants/research support; InMedix funded with hands off grant this survey work. E. Caton: None. S. Matthews: None.

Incidence of Autoimmune Arthritis Disease Flare Following SARS-CoV-2 Vaccination and its Association with Concurrent NSAID Use

Background: This study aims to analyze the association between COVID-19 vaccination and an inflammatory arthritis reaction in autoimmune arthritis patients. Methods: A survey was completed by participants with inflammatory arthritis between August 17 and 18, 2021. Survey participants (n = 1348) responded to questions about their diagnosis, the length of their diagnosis, current medication, brand of vaccine received, incidence of inflammatory arthritis symptoms after COVID-19 vaccination, and how long the symptoms persisted. Participants were also asked to report any other notable side effects experienced after vaccination. Results: Participants reported a diagnosis of rheumatoid arthritis (83.9%), psoriatic arthritis (6.5%), ankylosing spondylitis (2.5%), fibromyalgia (1.1%), lupus (0.5%), or other inflammatory arthritides (5.5%). Most participants reported having their condition for 5–10 years (25.3%), with only 4.6% having been diagnosed within the last year. Current use of disease-modifying antirheumatic drugs (DMARDs) was reported by 36.8% of participants, while 15% and 7.7% reported taking a biologic drug/infusion or non-steroidal anti-inflammatory drugs (NSAIDs), respectively, and 22.8% indicated that they were taking no medication. Types of COVID-19 vaccine reported were Pfizer-BioNTech (51.9%), Oxford AstraZeneca (24.2%), Moderna (19.2%), Janssen/Johnson &amp; Johnson (3.2%), and Sinopharm (1.5%). Following vaccination, 21% of participants reported experiencing inflammatory arthritis symptoms, with 14% indicating a possible mild flare (“perhaps a little”). These symptoms were reported to be ongoing by 40.7% of participants. Statistical analysis revealed that vaccine brand and diagnosis had no significant effect on the incidence of self-reported post-vaccination inflammatory arthritis symptoms. Participants currently taking NSAIDs were significantly more likely to report a vaccine-induced inflammatory arthritis reaction; however, it remains unclear if this was due to concurrent NSAID use or because of the likely increased disease activity in participants taking NSAIDs. Conclusion: In support of other published studies, our data indicate a low incidence of COVID-19 vaccine-induced inflammatory arthritis reaction in autoimmune arthritis patients. Patients currently taking NSAIDs may have an increased risk of experiencing inflammatory arthritis symptoms following their COVID-19 vaccination.

Cadmium Body Burden and Inflammatory Arthritis: A Pilot Study in Patients from Lower Silesia, Poland.

The purpose of this study was to determine the relationship between cadmium exposure and the likelihood of developing or exacerbating symptoms of inflammatory arthritis (IA). The study included 51 IA patients and 46 control subjects. Demographic and lifestyle data were collected. Haematological and biochemical parameters and blood cadmium levels (Cd-B) were determined. Cd-B correlated positively with age, smoking, living in a high-traffic area, and serum levels of inflammatory markers and negatively with mean corpuscular haemoglobin concentration (MCHC). The binary logistic regression model implied that high Cd-B (≥0.65 μg/L) is linked with an increased risk of IA in the studied population (odds ratio: 4.4). High levels of DNA oxidative damage marker (8-hydroxy-2’-deoxyguanosine) (≥7.66 ng/mL) and cyclooxygenase-2 (≥22.9 ng/mL) and frequent consumption of offal was also associated with increased risk of IA. High Cd-B was related to increased risk of disease symptoms onset in the group of IA patients, decreased the level of interleukin 10, and positively correlated with the disease activity. Increased Cd-B is associated with intensified inflammatory processes and decreased haemoglobin levels; in IA patients with decreased anti-inflammatory interleukin 10. These changes partly explain why cadmium exposure and a high cadmium body burden may raise the risk of IA and of disease symptoms exacerbation.

Patients with checkpoint inhibitor-induced inflammatory arthritis do not become seropositive for anti-cyclic citrullinated peptide when followed over time.

Patients with checkpoint inhibitor-induced inflammatory arthritis do not become seropositive for anti-cyclic citrullinated peptide when followed over time.

Rheumatoid Arthritis Pathogenesis, Prediction, and Prevention: An Emerging Paradigm Shift.

Rheumatoid arthritis (RA) is currently diagnosed and treated when an individual presents with signs and symptoms of inflammatory arthritis (IA) as well as other features, such as autoantibodies and/or imaging findings, that provide sufficient confidence that the individual has RA-like IA (e.g., meeting established classification criteria) that warrants therapeutic intervention. However, it is now known that there is a stage of seropositive RA during which circulating biomarkers and other factors (e.g., joint symptoms) can be used to predict if and when an individual who does not currently have IA may develop future clinically apparent IA and classifiable RA. Indeed, the discovery of the "pre-RA" stage of seropositive disease has led to the development of several clinical trials in which individuals are studied to identify ways to delay or prevent the onset of clinically apparent IA/RA. This review focuses on several issues pertinent to understanding the prevention of RA. These include discussion of the pathogenesis of pre-RA development, prediction of the likelihood and timing of future classifiable RA, and a review of completed and ongoing clinical trials in RA prevention. Furthermore, this review discusses challenges and opportunities to be addressed to effect a paradigm shift in RA, where in the near future, proactive risk assessment focused on prevention of RA will become a public health strategy in much the same manner as cardiovascular disease is managed today.

Appropriating and asserting power on inflammatory arthritis teams: A social network perspective.

BackgroundTherapeutic interventions for people with inflammatory arthritis (IA) increasingly involve multidisciplinary teams and strive to foster patient‐centred care and shared decision making. Participation in health‐care decisions requires patients to assert themselves and negotiate power in encounters with clinicians; however, clinical contexts often afford less authority for patients than clinicians. This disadvantage may inhibit patients' involvement in their own health care.ObjectiveTo identify communication attributes, IA patients use to influence and negotiate their treatment with members of their health‐care network.MethodA qualitative social network approach was used to analyse data from a larger study that investigated IA patients' overall experiences of multidisciplinary care. Fourteen patients with IA attended individual semi‐structured interviews. Researchers used thematic analysis to identify patterns of assertiveness and influence in the data.ResultsParticipants experienced loss of identity, control and agency in addition to the physical symptoms of IA. However, they had a sense of personal responsibility for managing their health care. Perceptions of health‐care team support enhanced patients' influence in treatment negotiations. Notably, there appeared to be an underlying tension between being empowered or disempowered.Discussion and conclusionsThe findings have significant implications for treatment decision communication approaches to IA care. A social network perspective may provide a pathway for clinicians to better understand the complexities of communication with their patients. This approach may reduce unequal power dynamics that occur within clinician/patient interactions and afford people with IA agency, control and affirmation of identity within their health‐care network.

Examining the cross-sectional and longitudinal effects of anxiety sensitivity on indicators of disease severity among patients with inflammatory arthritis

Few studies have investigated anxiety sensitivity (AS) in the context of inflammatory arthritis (IA), despite evidence of a relationship between AS and pain. This study examined cross-sectional and longitudinal relationships between AS and indicators of IA severity in 148 participants with IA. AS and its factors (social, physical, cognitive) were self-reported. Arthritis severity was physician-assessed (disease activity scales) and self-reported (physical function; pain and fatigue). Cross-sectional correlations assessed the association between AS and arthritis severity outcomes. Longitudinal multivariable mixed-effect regressions assessed the association of AS total and AS factors at each visit with disease severity outcomes. All AS factors were significantly and positively correlated (at the same visit) with function, pain, and fatigue. AS total significantly predicted pain, fatigue, and function. Cognitive AS significantly predicted fatigue, and physical AS significantly predicted pain and fatigue. Social AS significantly predicted pain, fatigue, function and weighted joint count (articular burden). AS is associated with several indicators of disease severity among those with IA; unique findings emerged across factors with the broadest disease impact by social AS. The AS factors, especially social AS, may contribute to the development and severity of IA symptoms, which may have implications for interventions.

Clinical presentation of immune checkpoint inhibitor-induced inflammatory arthritis differs by immunotherapy regimen

IntroductionImmune checkpoint inhibitors (ICIs) are a class of cancer immunotherapy, increasingly utilized to treat malignancies. Inflammatory arthritis (IA) is a potential consequence of ICI use, but there is limited information to guide evaluation and management of this immune-related adverse event (irAE). This study aimed to characterize clinical phenotypes, IA treatment and response in the largest cohort of patients with ICI-induced IA reported to date. MethodsPatients with rheumatologist-confirmed IA occurring during or after ICI treatment with no prior history of autoimmune disease were included. Data were analyzed by ICI treatment regimen; treatments included combination CTLA-4/PD-1 inhibition, anti-PD-1 or anti-PD-L1 monotherapy. Relationship to the development of other irAEs, management of IA, and outcomes of IA management were evaluated. ResultsOf 30 patients identified, those treated with combination ICI therapy were more likely to present with knee arthritis, to have higher levels of C-reactive protein, to have already had another irAE, and to have a reactive arthritis-like phenotype. In contrast, patients treated with ICI monotherapy were more likely to have initial small joint involvement and to have IA as their only irAE. Ten patients required additional immunosuppression beyond corticosteroids, with TNF-inhibitors and/or methotrexate. Tumor progression while on non-corticosteroid immunosuppression was not seen in those with initial tumor response to ICIs. ConclusionThese data suggest that distinct IA phenotypes may emerge with exposure to different ICI regimens. The majority of patients referred to rheumatology required systemic immunosuppression to manage their IA symptoms. Tumor progression was not seen in patients requiring TNF-inhibitors.

IK acts as an immunoregulator of inflammatory arthritis by suppressing TH17 cell differentiation and macrophage activation

Pathogenic T helper cells (TH) and macrophages have been implicated in the development of rheumatoid arthritis (RA), which can lead to severe synovial inflammation and bone destruction. A range of therapies have been widely used for RA, including specific monoclonal antibodies and chemical inhibitors against inflammatory cytokines produced by these cells. However, these have not been sufficient to meet the medical need. Here, we show that in transgenic mice expressing truncated IK (tIK) cytokine, inflammatory arthritis symptoms were ameliorated as the result of suppression of the differentiation of TH1 and TH17 cells and of macrophage activation. During inflammatory responses, tIK cytokine systemically regulated macrophage functions and TH17 cell differentiation through inactivation of the MAPK and NF-κB pathways. Interestingly, the level of tIK cytokine was higher in synovial fluid of RA patients compared with that in osteoarthritis (OA) patients. Our observations suggest that tIK cytokine can counterbalance the induction of inflammatory cells related to RA and thus could be a new therapeutic agent for the treatment of RA.

AB0259 Anti-Carbamylated Protein (ANTI-CARP) Antibodies Are Present in the Sera of Individuals at Different Stages of the Inflammatory Arthritis Continuum

BackgroundIn inflammatory arthritis (IA) the spectrum varies from individuals “at-risk” to the full rheumatoid arthritis phenotype. ACPA are highly specific for RA and associated with severe progression. Recently, anti-carbamylated protein...

AB0719 Active synovitis at the wrist level detected by doppler ultrasound (us) is the most common finding in patients with inflammatory arthritis, irrespective of their underlying diagnosis – results from a cohort study.

BackgroundThe possibility to identify patterns of joint involvement in different types of inflammatory arthritis without obvious clinical synovitis has a practical approach, giving the possibility to implement simplified protocols for...

THU0535 Significantly Better Patient-Reported Outcomes in Women with Early Inflammatory Arthritis Using Oral Contraceptives Compared to Never Users

BackgroundData on the effects of oral contraceptives (OC) on the course of inflammatory arthritis (IA) are controversial. While some observations suggested a beneficial effect on disease activity, others did not....

Learning about the natural history of rheumatoid arthritis development through prospective study of subjects at high risk of rheumatoid arthritis–related autoimmunity

Multiple studies have demonstrated abnormalities of rheumatoid arthritis (RA)–related autoantibodies and biomarkers of inflammation prior to the presence of the signs and symptoms of inflammatory arthritis (1–18). Many of these studies were performed using retrospectively assembled samples from subjects who fortuitously had biologic specimens available from before their diagnosis of RA. Therefore, our understanding of the precise temporal relationship between biomarker abnormalities and the onset of the signs and symptoms of inflammatory arthritis is limited. However, despite these limitations, overall these studies have had a profound impact on the understanding of the early development of RA. Furthermore, these studies, in conjunction with studies that have established genetic risk factors for RA (such as the shared epitope [19]), support the concept that RA development occurs in several phases, as depicted in Figure 1.

Science Signaling Podcast: 26 April 2011

A growth factor that antagonizes signaling by tumor necrosis factor–α relieves symptoms of inflammatory arthritis.

Antisynthetase Syndrome Presenting as Rheumatoid-Like Polyarthritis

The antisynthetase syndrome is a systemic inflammatory disease associated with anti-tRNA synthetase antibodies and consisting of the clinical features of inflammatory myopathy arthritis, interstitial lung disease (ILD), fever, Raynaud syndrome, and rash. It rarely presents with symmetric arthritis as the initial manifestation of the disease. The aim of the study was to describe the clinical, laboratory, and radiographic characteristics of patients with antisynthetase syndrome who presented with symptoms of inflammatory arthritis, mimicking rheumatoid arthritis (RA) at the time of initial evaluation. Six cases derived from a single university-based rheumatology clinic in Wisconsin are presented. The major clinical, laboratory, radiographic, and histopathologic data are described. All 6 patients demonstrated symmetric synovitis involving the hands. Five patients met the American College of Rheumatology classification criteria for RA. Three patients had nail-fold capillary abnormalities, and 4 patients were observed to have Raynaud phenomenon. Three patients demonstrated a cytoplasmic pattern when testing for antinuclear antibodies by immunofluorescent assay, and all had t-RNA synthetase antibodies. Two patients had positive rheumatoid factors, but none had strongly positive cyclic citrullinated peptide antibodies. None of the patients demonstrated radiographic erosions. All patients had evidence of ILD by imaging or pulmonary function testing. Prognosis was generally favorable, although disease severity and treatment varied considerably. In patients who present with features mimicking but atypical for RA, such as early ILD, nail-fold capillary abnormalities, Raynaud phenomenon, cytoplasmic antinuclear antibody pattern, negative cyclic citrullinated peptide antibody status, and nonerosive arthritis, the antisynthetase syndrome should be considered.

Tumor Necrosis Factor Inhibitor–Associated Dermatomyositis

Dermatomyositis is an autoimmune disease of unknown etiology characterized by inflammation of the skin and muscles. Several medications have been implicated in the development of dermatomyositis; however, the disease has rarely been linked to the use of tumor necrosis factor (TNF) inhibitors. We report 4 cases of dermatomyositis that developed or were exacerbated by exposure to the TNF inhibitors etanercept and adalimumab. Observation Four patients with symptoms of inflammatory arthritis were treated with TNF inhibitors for a duration ranging from 2 months to 2 years. All 4 patients developed symptoms consistent with dermatomyositis, including inflammatory rash and muscle weakness. Their symptoms persisted after discontinuation of the treatment with the TNF inhibitors but responded to treatment with corticosteroids and immunosuppressive medications. Tumor necrosis factor inhibitors have been associated with the onset of a number of autoimmune disorders, most commonly vasculitis and a lupuslike syndrome. Rarely have they been associated with dermatomyositis. The 4 cases reported herein indicate that TNF inhibitor use can be associated with either induction or exacerbation of dermatomyositis.