Data_Sheet_1_Inflammatory profile of incident cases of late-onset compared with young-onset rheumatoid arthritis: A nested cohort study.docx

ObjectivesTo describe the characteristics of patients between late-onset rheumatoid arthritis (LORA) with young-onset (YORA), and analyze their association with cumulative inflammatory burden.MethodsWe performed a nested cohort study in a prospective cohort comprising 110 patients with rheumatoid arthritis (RA) and 110 age- and sex-matched controls. The main variable was cumulative inflammatory activity according to the 28-joint Disease Activity Score with erythrocyte sedimentation rate (DAS28-ESR). High activity was defined as DAS28 ≥ 3.2 and low activity as DAS28 ResultsA total of 22/110 patients (20%) met the criteria for LORA (≥ 60 years). Patients with LORA more frequently had comorbid conditions than patients with YORA and controls. Compared with YORA patients, more LORA patients had cumulative high inflammatory activity from onset [13 (59%) vs. 28 (31%); p = 0.018] and high values for CRP (p = 0.039) and IL-6 (p = 0.045). Cumulative high inflammatory activity in patients with RA was associated with LORA [OR (95% CI) 4.69 (1.49–10.71); p = 0.008], smoking [OR (95% CI) 2.07 (1.13–3.78); p = 0.017], anti–citrullinated peptide antibody [OR (95% CI) 3.24 (1.15–9.13); p = 0.025], average Health Assessment Questionnaire (HAQ) score [OR (95% CI) 2.09 (1.03–14.23); p = 0.034], and physical activity [OR (95% CI) 0.99 (0.99–0.99); p = 0.010]. The second model revealed similar associations with inflammatory activity in patients with LORA.ConclusionControl of inflammation after diagnosis is poorer and comorbidity more frequent in patients with LORA than in YORA patients and healthy controls.</p

Genotype frequencies of the <i>FCGR2A</i> polymorphism rs1801274 in anti-CCP positive RA patients according to the clinical response at week 12.

<p>^aFisher's exact test; ANTI-CCP: anti-citrullinated protein antibodies; OR: Odds ratio using allele G as reference.</p><p>Genotype frequencies of the <i>FCGR2A</i> polymorphism rs1801274 in anti-CCP positive RA patients according to the clinical response at week 12.</p

Genotype frequencies of the <i>FCGR2A</i> polymorphism rs1801274 according to the clinical response at week 12.

<p>^aFisher's exact test; OR: Odds ratio using allele G as reference.</p><p>Genotype frequencies of the <i>FCGR2A</i> polymorphism rs1801274 according to the clinical response at week 12.</p

Epidemiological and Clinical Features of the Patient Study Cohort.

<p>Except where indicated otherwise, values are the mean ±SD. RF: rheumatoid factor; Anti-CCP: anti-citrullinated protein antibodies; DMARDs: disease-modifying antirheumatic drugs; ΔDAS28; delta DAS28 (DAS28 baseline—DAS28 endpoint); EULAR: European League Against Rheumatism response, where Good and Moderate EULAR responders were merged into a single Responder category.</p><p>Epidemiological and Clinical Features of the Patient Study Cohort.</p

Additional file 1 of Seven-chain adaptive immune receptor repertoire analysis in rheumatoid arthritis reveals novel features associated with disease and clinically relevant phenotypes

Additional file 1: Table S1. Main clinical and epidemiological characteristics of the study population. All RA patients, RA patients at baseline, RA patients after 12 weeks of TNFi therapy and control individuals are separately characterized. Abbreviations: N, sample size; NA, not applicable; M, mean; RA, rheumatoid arthritis

Additional file 1: of Urine metabolome profiling of immune-mediated inflammatory diseases

Supplementary note (Members of the Immune-Mediated Inflammatory Disease (IMID) Consortium), Supplementary methods, Supplementary Tables (Table S1: Sample quality control; Table S2: Urine metabolite panel; Table S3: List of metabolic associations when comparing phenotypically closer IMID diseases; Table S4: List of metabolites with replicated associations to disease activity in Crohn’s disease (CD) patients) and Supplementary Figures (Figure S1: Distribution of disease activity indices in the extreme low and high activity patient subgroups; Figure S2: Distribution of epidemiological and sample collection variables across the IMID and control groups; Figure S3: Distribution of trigonelline concentration according to daily coffee/tea consumption; Figure S4: Distribution of trigonelline concentration on each IMID cohort stratified by coffee/tea consumption; Figure S5: ROC curves of the diagnostic partial least squares discriminant analysis classification models and metabolite loadings of the CD and UC models). (PDF 2486 kb

Established CVD risk variants associated with CVD risk in the six autoimmune diseases.

<p>Established CVD risk variants associated with CVD risk in the six autoimmune diseases.</p

Established autoimmune susceptibility variants also associated with CVD risk.

<p>Established autoimmune susceptibility variants also associated with CVD risk.</p

Genetic variants showing heterogeneous genetic effects on CVD risk across autoimmune diseases.

<p>For each associated SNP (<b>A:</b> rs17465637. <b>B:</b> rs11924705. <b>C:</b> rs2895811. <b>D:</b> rs6789378) the Odds Ratio (OR, black dots) and 95% confidence intervals (horizontal lines) are shown for each of the 6 autoimmune diseases and the combined autoimmune cohort (AID). The SNPs showing a significant association with CVD risk in an autoimmune disease are highlighted in red. For each of the three genotypes of each SNP (risk allele homozygous, heterozygous, non-risk allele homozygous), the incidence of CVD is described in the accompanying table.</p

Functional characterization of the genetic clusters associated with CVD risk across autoimmune diseases.

<p>Functional characterization of the genetic clusters associated with CVD risk across autoimmune diseases.</p