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Objective: The aim of the study was to analyse associations between anti-inflammatory treatment before a first acute myocardial infarction (AMI) and survival up to 365 days post-AMI in patients with and without rheumatoid arthritis (RA).

Method: Data for 199 071 patients with a first AMI during 2006–2017, including 3725 RA patients, and for anti-inflammatory medical treatment during the 6 months before a first AMI, were drawn from Swedish registries. Drugs were categorized as corticosteroids, non-steroidal anti-inflammatory drugs, conventional synthetic (cs) disease-modifying anti-rheumatic drugs (DMARDs), tumour necrosis factor inhibitors (anti-TNFs), or other biological DMARDs. Multivariable logistic regression analysis was used to assess mortality associations up to 30 days and multivariable Cox proportional hazard models to assess associations from 31 to 365 days.

Results: No treatment was associated with survival within 30 days after the AMI. From 31 to 365 days post-AMI, corticosteroid treatment was associated with increased mortality [in RA: hazard ratio (HR) 1.43, 95% confidence interval (CI) 1.27–1.62; without RA: HR 1.37, 95% CI 1.33–1.41]. csDMARDs were associated with increased survival in RA patients (HR 0.86, 95% CI 0.78–0.96), as were anti-TNF treatments (HR 0.72, 95% CI 0.56–0.94). Among non-RA patients, csDMARDs were associated with increased mortality (HR 1.14, 95% CI 1.04–1.24).

Conclusion: Anti-inflammatory treatment was not associated with mortality within 30 days after a first AMI. From 31 to 365 days post-AMI, corticosteroid treatment was associated with increased mortality risk for all patients, and csDMARDs and anti-TNFs were associated with increased survival for RA patients.

Rheumatoid Arthritis associated Interstitial Lung Disease (RA-ILD) is an extraarticular manifestation of rheumatoid arthritis (RA) associated with increased morbidity and mortality. Several risk factors for RA-ILD have been identified, one is the promotor variant of mucin 5 B gene (MUC5B). Juge et al., Wheeler et al. and Koduri et al. have developed risk scores for identifying patients with RA at risk of RA-ILD. We aimed to externally validate the three risk scores and further investigate the frequency of MUC5B promotor variant and its association with subclinical lung changes in patients with RA in northern Sweden. Our cohort consisted of 54 patients with RA. The risk score variables were evaluated in binary logistic regression and validated using area under the receiver operating characteristics curve (AUC ROC). The genetic material was purified and genotyped for MUC5B. The Juge et al. risk score performed an AUC ROC of 0.71 (95% CI 0.57;0.86), the Wheeler et al. risk score an AUC ROC of 0.75 (95% CI 0.59;0.90) and Koduri et al. risk score an AUC ROC of 0.70 ((95% CI 0.55;0.85) in our cohort. The differences in AUC were not statistically significant. The MUC5B promotor variant frequency was 26% (n = 14). In our cohort, MUC5B was not significantly associated with subclinical lung changes. The three externally validated risk scores for RA-ILD performed well in this cohort and could be used clinically. In patients with RA in northern Sweden, MUC5B was not found to be independently associated with subclinical RA-ILD.

Objectives: Through this meta-analysis, we aim to provide an overview and statistical synthesis of the prevalence of MetS and its components in psoriatic arthritis (PsA) compared to the general populations, patients with cutaneous psoriasis (PsO), and patients with other inflammatory arthropathies.

Method: A search was conducted in Ovid Medline, Web of Science, and Scopus up to February 2024. Original articles investigating the prevalence of MetS in PsA in adults compared to one or more comparison populations were included. Bias risk was assessed by means of a funnel plot. The data was analyzed by means of a random effects model and presented in forest plots.

Results: Of 1526 articles in the original search, 20 relevant were identified. Meta-analyses showed an increased prevalence of MetS in PsA compared to the general population, rheumatoid arthritis (RA), and ankylosing spondylitis (AS) (LogOR 0.93, 0.63, and 1.04, respectively). Meta-analysis showed no difference in the prevalence of MetS in PsA compared to PsO (LogOR 0.15, I2 0.63). Meta-analysis of the prevalence of the different components of MetS in PsA compared to RA showed an increased prevalence of central obesity, hypertriglyceridemia, impaired glucose tolerance, and diabetes mellitus.

Conclusions: PsA was associated with an increased risk of MetS compared to the risk in the general population, in RA and in AS, respectively. This emphasizes the importance of screening for and taking necessary measures to prevent MetS in patients with PsA. (Table presented.)

OBJECTIVES: To investigate the relationship between biomarkers known to be involved in both chronic inflammation and subclinical atherosclerosis, as measured by carotid intima media thickness (cIMT), in patients with RA compared to controls.

METHODS: Between 2000 and 2004, all patients under 60 years of age with newly diagnosed RA in the northern region of Sweden were invited to participate in this study. Measurements of cIMT were undertaken at inclusion (T0), after five years of follow-up (T5) and after eleven years of follow-up (T11). Patients were clinically assessed and blood was drawn for analysis of biomarkers.

RESULTS: In patients with RA (n=54), linear regression models showed that cIMT at T11 was associated with levels of GDF-15 at T5 and T11, but not with baseline levels. GDF-15 was strongly associated with age. At T11, mean level of GDF-15 was elevated compared to controls. Levels of adiponectin, MCP-1, cathepsin S, endoglin and IL-6 were higher in patients with RA compared to controls, but showed no association with cIMT. In multivariable linear regression models with cIMT at T11 as dependent variable, change in GDF-15 from T0 to T11 was associated to an increase in cIMT at T11. Adjusting for systolic blood pressure and age respectively rendered this association statistically non-significant,

CONCLUSIONS: Among these patients with RA GDF-15 was associated to cIMT after 11 years of follow-up. GDF-15 should be a biomarker of interest in future research, to further understand its role in the accelerated atherogenesis in patients with RA.

Objective: Interstitial lung disease (ILD) is an important cause of mortality in patients with rheumatoid arthritis (RA). Early RA-ILD detection is essential to improve prognosis. Here, we investigated eight serological biomarkers that may contribute to RA-ILD detection.

Method: Fifty-five patients from the Early Rheumatoid Arthritis Program were evaluated for ILD with high-resolution computed tomography (HRCT) and pulmonary function tests (PFTs) using the SCAPIS protocol. Blood samples were obtained for biomarker analysis, and patients’ clinical records were reviewed. We defined ILD using five different models based on the measurements used to confirm ILD: Model A = HRCT; B = PFTs; C = A plus B; D = C plus symptoms; and E = D plus inhalations.

Results: Among 55 patients, two had an ILD diagnosis before the study, but over one-third fulfilled the ILD criteria. Cancer antigen 15-3 (CA15-3) and matrix metalloproteinase-7 (MMP-7) differentiated between RA with and without ILD (all p < 0.05). Surfactant protein D (SP-D) showed similar trends, as did macrophage inflammatory protein-1β (MIP-1β) and chitinase 3-like protein-1 (YKL-40). Based on Pearson’s correlation coefficients, MIP-1β and YKL-40 were significantly correlated with DAS28 (MIP-1β: 0.3; YKL-40: 0.4), ESR (MIP-1β: 0.3; YKL-40: 0.4), and CRP (only MIP-1β: 0.4) (all p < 0.05). CA15-3 was correlated with rheumatoid factor and anti-citrullinated peptide antibodies (Pearson’s correlation 0.3; both p = 0.03).

Conclusions: CA15-3 was the most significant biomarker for ILD detection in RA patients with stable low disease activity, closely followed by MMP-7. SP-D, MIP-1β, and YKL-40 may also contribute to RA-ILD diagnosis.

Studies investigating the immunogenicity of additional COVID-19 vaccine doses in immunosuppressed patients with inflammatory rheumatic diseases (IRD) are still limited. The objective was to explore the antibody response including response to omicron virus subvariants (sBA.1 and sBS.2) after third and fourth COVID-19 vaccine doses in Swedish IRD patients treated with immunomodulating drugs compared to controls. Antibody levels to spike wild-type antigens (full-length protein and S1) and the omicron variants sBA.1 and sBA.2 (full-length proteins) were measured. A positive response was defined as having antibody levels over cut-off or ≥fourfold increase in post-vaccination levels for both antigens. Patients with arthritis, vasculitis, and other autoimmune diseases (n = 414), and controls (n = 61) receiving biologic/targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs) with or without conventional synthetic DMARDs participated. Of these, blood samples were available for 370 patients and 52 controls after three doses, and 65 patients and 15 controls after four doses. Treatment groups after three vaccine doses were rituximab (n = 133), abatacept (n = 22), IL6r inhibitors (n = 71), JAnus Kinase inhibitors (JAK-inhibitors) (n = 56), tumor necrosis factor inhibitor (TNF-inhibitors) (n = 61), IL12/23/17 inhibitors (n = 27), and controls (n = 52). The percentage of responders after three and four vaccine doses was lower in rituximab-treated patients (59% and 57%) compared to controls (100%) (P < 0.001). After three doses, the percentage of responders in all other groups was 100%, including response to omicron sBA.1 and sBA.2. In rituximab-treated patients, higher baseline immunoglobulin G (IgG) and longer time-period between rituximab and vaccination predicted better response. In this Swedish nationwide study including IRD patients three and four COVID-19 vaccine doses were immunogenic in patients treated with IL6r inhibitors, TNF-inhibitors, JAK-inhibitors, and IL12/23/17-inhibitors but not in rituximab. As >50% of rituximab patients responded to vaccines including omicron subvariants, these patients should be prioritized for additional vaccine doses.

Background: It is established that the risk of cardiovascular disease (CVD) is increased in patients with Rheumatoid Arthritis (RA). Heart rate variability (HRV) is a method for evaluating the activity in the cardiac autonomic nervous system. Our aim was to assess the longitudinal development of HRV in patients with RA and compare with healthy controls. Furthermore, we wanted to investigate associations between HRV, inflammatory disease activity and cardiovascular complications in patients with RA over time.

Method: HRV was assessed with frequency-domain analysis at baseline and after five years in 50 patients with early RA, all being younger than 60 years. HRV indices were age-adjusted based on the estimated age-dependency in 100 age and sex matched healthy controls. Additionally, clinical data including serological markers, disease activity, and blood pressure were collected from the patients. Eleven years after inclusion CVD was assessed.

Results: At baseline, patients with RA presented with lower HRV compared to controls during deep breathing (6 breaths/min), paced normal breathing (12 breaths/min) and after passive tilt to the upright position. No significant change in HRV was observed at the five-year follow-up. A significant negative correlation was found between HRV parameters and systolic blood pressure (SBP) at baseline. A significant positive correlation was found between heart rate and inflammatory markers at baseline but not after five years. Nine patients had developed CVD after 11 years, but no significant association was found with baseline HRV data.

Conclusion: This study showed that patients with RA have autonomic imbalance both at an early stage of the disease and after five years, despite anti-rheumatic medication, but no correlation between HRV and inflammation markers were observed. Reduced HRV was also significantly negatively correlated with increased SBP. Hypertension is a common finding in patients with RA. Thus, significant decline of HRV could be a useful early marker for development of hypertension in patients with RA.

Objectives: Normal age-related decline and temporary restrictions in mobility complicate the understanding of spinal mobility deterioration over time in patients with ankylosing spondylitis (AS). In this study, we aimed to determine whether spinal mobility deterioration occurred linearly in patients with AS. We also aimed to compare patterns of change with corresponding age-related normal values and analyze variations in temporary fluctuations in mobility measurements over time.

Methods: We included 111 men and 30 women (median age 20.9 years at symptom onset), who were followed for median 34 years since symptom onset. This resulted in 9 697 spinal mobility measurements for analysis. Individual linear regression models for development of lateral spinal flexion (LSF), 10 cm Schober test (ST10), chest expansion (CE), and cervical rotation (CR) were analyzed and compared with normal age-related decline over time.

Results: The median values for the constants of all measurements were significantly lower than the norm data. However, LSF, ST10, and CE followed a yearly linear decline comparable to the norm data, whereas CR declined about twice as fast as expected from the norm data (beta median [25th-75th percentile]: -0.62° [-1.16°, -0.22°] and -0.35° [-0.35°, -0.35°]), respectively. Temporary fluctuations in LSF and CE were significantly higher during the early phase of the disease, with decreasing residuals over time.

Conclusion: Based on median constants of our data, mobility restrictions related to AS seem to mainly occur during the first years of disease, indicating a narrow window of opportunity for prevention.

Objective: Rheumatoid cachexia (RC) is prevalent among patients with established rheumatoid arthritis (RA). Although changes in muscle mass and fat mass have been reported in early RA, these findings have not been classified according to existing RC definitions. This study aimed to describe the prevalence of RC and associated variables in patients with early RA.

Method: This cross-sectional study included 87 patients. Body composition was evaluated with dual-energy X-ray absorptiometry after a median disease duration of 15 months. RC was defined as a fat-free mass index < 10th percentile and fat mass index > 25th percentile. We also assessed the erythrocyte sedimentation rate (ESR), C-reactive protein, Disease Activity Score in 28 joints, aerobic capacity, physical activity, traditional cardiovascular disease risk factors, functional disability, and sociodemographic data. Associations between RC and the independent variables were determined with logistic regression analyses.

Results: The prevalence of RC was 24%. RC was significantly associated [odds ratio (95% confidence interval)] with aerobic capacity [0.28 (0.09–0.89), p = 0.030], low-intensity physical activity [0.77 (0.60–0.99), p = 0.048], body mass index [0.78 (0.70–0.92), p = 0.002], waist circumference [0.96 (0.92–0.99), p = 0.023], body weight [0.94 (0.90–0.98), p = 0.004], and ESR at the time of diagnosis [1.02 (1.00–1.05), p = 0.033]. All of these associations remained significant after adjusting for age and gender.

Conclusion: RC was highly prevalent in early RA. Patient outcome may be improved by detecting this condition early and applying treatments for improving inflammation, aerobic capacity, physical activity, and body composition.