Objective To evaluate rheumatoid arthritis (RA) disease activity and risk of RA‐associated interstitial lung disease (RA‐ILD). Methods We investigated disease activity and risk of RA‐ILD using the Brigham RA Sequential Study (BRASS, 2003–2016). All patients were diagnosed as having RA according to accepted criteria. Disease Activity Scores in 28 joints (DAS28) and covariate data were measured prospectively at annual study visits. Diagnosis of RA‐ILD was determined by review of images from clinically indicated chest computed tomography scans. We analyzed patients without RA‐ILD at baseline. We used Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for RA‐ILD, using annually updated DAS28 data, with adjustment for known RA‐ILD risk factors (age, sex, smoking status, RA duration, and serologic status). We performed alternative analyses that did not censor at the time of missing DAS28 data and included adjustment for use of methotrexate, use of glucocorticoids, presence of bone erosions, and presence of rheumatoid nodules. Results Among 1,419 participants, the mean ± SD age was 55.8 ± 14.2 years, and 68.6% were seropositive for either cyclic citrullinated peptide or rheumatoid factor. We identified 85 incident cases of RA‐ILD during a mean ± SD follow‐up duration of 8.9 ± 4.2 years per patient. The moderate/high disease activity group had a multivariable HR of 2.22 (95% CI 1.28–3.82) for RA‐ILD compared to the remission/low disease activity group. Risk of RA‐ILD increased across disease activity categories: multivariable HR 1.00 (reference) for remission, 1.41 (95% CI 0.61–3.28) for low disease activity, 2.08 (95% CI 1.06–4.05) for moderate disease activity, and 3.48 (95% CI 1.64–7.38) for high disease activity (P for trend = 0.001). For each unit increase in the DAS28, the risk of RA‐ILD increased by 35% (95% CI 14–60%). Results were similar in analyses that included follow‐up for missing DAS28 data and with adjustment for use of methotrexate, use of glucocorticoids, presence of bone erosions, or presence of rheumatoid nodules. Conclusion Active articular RA was associated with an increased risk of developing RA‐ILD. These results suggest that decreasing systemic inflammation may alter the natural history of RA‐ILD development.

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Background COVID-19 can induce a hyperinflammatory state, which might lead to poor clinical outcomes. We aimed to assess whether patients with a systemic rheumatic disease might be at increased risk for hyperinflammation and respiratory failure from COVID-19. Methods We did a retrospective, comparative cohort study of patients aged 18 years or older admitted to hospital with PCR-confirmed COVID-19 at Mass General Brigham (Boston, USA). We identified patients by a search of electronic health records and matched patients with a systemic rheumatic disease 1:5 to comparators. We compared individual laboratory results by case status and extracted laboratory results and COVID-19 outcomes for each participant. We calculated the COVID-19-associated hyperinflammation score (cHIS), a composite of six domains (a score of ≥2 indicating hyperinflammation) and used logistic regression to estimate odds ratios (ORs) for COVID-19 outcomes by hyperinflammation and case status. Findings We identified 57 patients with a systemic rheumatic disease and 232 matched comparators who were admitted to hospital with COVID-19 between Jan 30 and July 7, 2020; 38 (67%) patients with a rheumatic disease were female compared with 158 (68%) matched comparators. Patients with a systemic rheumatic disease had higher peak median neutrophil-to-lymphocyte ratio (9·6 [IQR 6·4–22·2] vs 7·8 [4·5–16·5]; p=0·021), lactate dehydrogenase concentration (421 U/L [297–528] vs 345 U/L [254–479]; p=0·044), creatinine concentration (1·2 mg/dL [0·9–2·0] vs 1·0 mg/dL [0·8–1·4], p=0·014), and blood urea nitrogen concentration (31 mg/dL [15–61] vs 23 mg/dL [13–37]; p=0·033) than comparators, but median C-reactive protein concentration (149·4 mg/L [76·4–275·3] vs 116·3 mg/L [58·8–225·9]; p=0·11) was not significantly different. Patients with a systemic rheumatic disease had higher peak median cHIS than comparators (3 [1–5] vs 2 [1–4]; p=0·013). All patients with a peak cHIS of 2 or more had higher odds of admission to intensive care (OR 3·45 [95% CI 1·98–5·99]), mechanical ventilation (66·20 [8·98–487·80]), and in-hospital mortality (16·37 [4·75–56·38]) than patients with a peak cHIS of less than 2. In adjusted analyses, patients with a rheumatic disease had higher odds of admission to intensive care (2·08 [1·09–3·96]) and mechanical ventilation (2·60 [1·32–5·12]) than comparators, but not in-hospital mortality (1.78 [0·79–4·02]). Among patients who were discharged from hospital, risk of rehospitalisation (1·08 [0·37–3·16]) and mortality within 60 days (1·20 [0·58–2·47]) was similar in patients and comparators. Interpretation Patients with a systemic rheumatic disease who were admitted to hospital for COVID-19 had increased risk for hyperinflammation, kidney injury, admission to intensive care, and mechanic...

Purpose: Lifestyle may be important in the development of rheumatoid arthritis (RA). Therefore, changing behaviors may delay or even prevent RA onset. We reviewed the evidence basis for the associations of lifestyle factors with RA risk and consider future directions for possible interventions to reduce RA risk. Methods: We reviewed the literature for cross-sectional studies, case-control studies, cohort studies, and clinical trials investigating potentially modifiable lifestyle factors and RA risk or surrogate outcomes on the path towards development, such as RA-related autoimmunity or inflammatory arthritis. We summarized the evidence related to cigarette smoking, excess weight, dietary intake, physical activity, and dental health for RA risk. Findings: Cigarette smoking has the strongest evidence base as a modifiable lifestyle behavior that increases seropositive RA risk. Smoking may increase seropositive RA risk through geneenvironment interactions, increasing inflammation and citrullination locally in pulmonary/oral mucosa or systemically, and thereby inducing RA-related autoimmunity. Prolonged smoking cessation may reduce seropositive RA risk. Evidence suggests that excess weight may increase RA risk, though this effect may differ by sex, serologic status, and age at RA onset. The effect of dietary intake may also impact RA risk: overall healthier patterns, high fish/omega-3 polyunsaturated fatty acids, and moderate alcohol intake may reduce RA risk, while caffeine and sugar-sweetened soda may increase RA risk. The impact of physical activity is less clear but high levels may reduce RA risk. Periodontal disease may induce citrullination and RA-related autoimmunity, but the effect of dental hygiene behaviors on RA risk is unclear. Although the effect size estimates for these lifestyle factors on RA risk are generally modest, there may be relatively large public health benefits for targeted interventions given the high prevalence of these unhealthy behaviors. With the exception of smoking cessation, the impact of behavior change of these