Identification, monitoring, and management of rheumatoid arthritis–associated interstitial lung disease

Interstitial lung disease (ILD) is a frequent complication of rheumatoid arthritis (RA) that is associated with a significant increase in mortality. Several risk factors for the development of ILD in patients with RA have been identified, but ILD can still develop in the absence of these risk factors. Screening tools for RA‐ILD are required to facilitate early detection of RA‐ILD. Close monitoring of patients with RA‐ILD for progression is crucial to enable timely implementation of treatment strategies to improve outcomes. Patients with RA are commonly treated with immunomodulatory therapies, although their efficacy in slowing the progression of RA‐ILD remains the subject of debate. Clinical trials have shown that antifibrotic therapies slow decline in lung function in patients with progressive fibrosing ILDs, including patients with RA‐ILD. The management of patients with RA‐ILD should be based on multidisciplinary evaluation of the severity and progression of their ILD and the activity of their articular disease. Close collaboration between rheumatologists and pulmonologists is essential to optimize patient care

Rheumatoid arthritis and idiopathic pulmonary fibrosis: a bidirectional Mendelian randomisation study

BackgroundA usual interstitial pneumonia (UIP) pattern of lung injury is a key feature of idiopathic pulmonary fibrosis (IPF) and is also observed in up to 40% of individuals with rheumatoid arthritis (RA)-associated interstitial lung disease (RA-ILD). The RA-UIP phenotype could result from either a causal relationship of RA on UIP or vice versa, or from a simple co-occurrence of RA and IPF due to shared demographic, genetic or environmental risk factors.MethodsWe used two-sample bidirectional Mendelian randomisation (MR) to test the hypothesis of a causal effect of RA on UIP and of UIP on RA, using variants from genome-wide association studies (GWAS) of RA (separately for seropositive (18 019 cases and 991 604 controls) and seronegative (8515 cases and 1 015 471 controls) RA) and of IPF (4125 cases and 20 464 controls) as genetic instruments. Sensitivity analyses were conducted to assess the robustness of the results to violations of the MR assumptions.FindingsIPF showed a significant causal effect on seropositive RA, with developing IPF increasing the risk of seropositive RA (OR=1.06, 95% CI: 1.04 to 1.08, p</p