Abstract

Background RA-associated interstitial lung disease (RA-ILD) is an extra-articular manifestation of RA and is one of the leading causes of death in patients (pts) with RA.1 Previous studies have indicated that clinical factors such as age, sex, smoking and autoantibody positivity are strongly associated with RA-ILD.2 There is also evidence of active RA being related to increased risk for clinically apparent ILD.3 However, there are limited data on how pts with RA-ILD are managed for their joint conditions and joint outcomes. Objectives To evaluate RA treatment patterns in pts with subclinical and clinical RA-ILD compared with pts with RA without ILD, and to assess joint disease activity at baseline and change in disease activity by treatment in all cohorts. Methods Data from adult pts with RA enrolled in a longitudinal sequential RA registry were analysed. Pts in the registry were evaluated annually by a rheumatologist for disease activity and treatment, and semi-annually on multiple clinical patient-reported outcomes (PROs) and resource utilisation parameters. Pts with chest computed tomography (CT) scans performed to evaluate clinical indications for ILD and with blood samples were included in this analysis. Pts with chest CT scans that were indeterminate for ILD were excluded from the study. Pts were then divided into two mutually exclusive groups: non-ILD RA pts and RA-ILD pts. RA-ILD pts were further divided into subclinical and clinically evident ILD. Date of chest CT scan was considered the index date. The two cohorts were compared using descriptive statistics to summarise baseline differences in demographics, disease activity measures, serostatus and treatments. Kruskal–Wallis test for continuous variables and chi-square test for categorical variables were performed, with two-sided significance level of 0.05. Multivariable linear regression was used to evaluate change from baseline to 12 months in joint disease activity for pts with available data at baseline and follow-up. Results 75 pts with chest CT scans were included in the analysis. Of these, 38.7% (n=29) were non-ILD RA and 61.3% (n=46) had some manifestation of RA-ILD. Of the RA-ILD cohort, 63.0% (n=29) and 37.0% (n=17) were classified as subclinical and clinically evident RA-ILD, respectively. At the time of chest CT scan, RA-ILD (vs non-ILD RA) pts were older with longer disease duration, a greater proportion were male and had higher anti-citrullinated protein antibody and RF titres (Table 1). In terms of RA treatments, a significantly greater proportion of RA-ILD (vs non-ILD RA) pts were on corticosteroids (CS; 47.8% vs 20.7%) and a significantly greater proportion of clinically evident RA-ILD (vs non-ILD RA) were on non-TNF inhibitor (TNFi) biologics. RA-ILD (vs non-ILD RA) pts had numerically higher joint disease activity and modified HAQ score at baseline (Table 1). However, the change in joint disease activity and PROs in RA-ILD pts was numerically greater vs non-ILD RA pts. In a multivariable analysis, RA-ILD status did not impact change in joint disease activity, but baseline joint disease activity was significantly associated with reduction in joint disease activity at 12 months (Table 2). Conclusion RA-ILD pts compared with non-ILD RA pts in clinical practice are more likely to be managed with CS therapy and non-TNFi bDMARDs. The improvement in joint disease activity was similar between RA-ILD and non-ILD RA pts. The analysis was limited by small sample size; further studies with larger pt numbers are required to confirm the findings.

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