Interstitial lung diseases (ILD) can be observed in 10–30 % of patients with rheumatoid arthritis (RA) [1,2]. Compared to ILD associated with other systemic autoimmune rheumatic diseases (SARDs), RA-ILD is characterized by a high frequency of fibrosing ILD subtypes, with usual interstitial pneumonia (UIP) being the most frequent, followed by other subtypes such as fibrotic non-specific interstitial pneumonia (NSIP) [3]. RA-ILD is a severe manifestation and ILD progression has been reported in about half of the patients [4,5]. Once clinically significant, it is associated with an increased mortality, estimated to be 2- to 10-fold higher than in RA without ILD [6], [7], [8], [9], [10].

Antifibrotic therapies include nintedanib and pirfenidone, which were initially approved by the US Food and Drug Agency (FDA) to slow the progression of idiopathic pulmonary fibrosis (IPF) [11,12]. Recently, each drug has been tested in several randomized controlled trials (RCT) for other causes of ILD, including SARDs such as RA-ILD [13], [14], [15]. In the INBUILD trial, nintedanib was associated with a significantly lower annual rate of decline of the forced vital capacity (FVC) among patients with progressive fibrosing ILD (PF-ILD), regardless of the underlying etiology, leading to US FDA approval in this population [13]. Sub-analyses of the 89 patients with RA-ILD in the INBUILD trial showed similar efficacy compared to other causes of PF-ILD [16]. Pirfenidone has been tested in RA-ILD in TRAIL1, a placebo-controlled trial dedicated to RA-ILD [14]. Although the primary outcome (a composite endpoint including a decline in percent predicted FVC [FVCpp] of 10 % or more or death at one year) was not met, the use of pirfenidone was associated with a clinically significant slower rate of FVCpp decline in patients with RA-ILD compared with placebo. Post-hoc analyses found that the effect of pirfenidone on the decline in FVC was more pronounced in patients with an UIP pattern [14].

Despite their positive impact on slowing ILD progression, nintedanib and pirfenidone are both associated with adverse events (AEs) that can limit their use. In the above-mentioned clinical trials, gastrointestinal (GI) AEs were frequently reported, including diarrhea (67 % for nintedanib), nausea (29 % for nintedanib and 53 % for pirfenidone), decreased appetite and weight loss, and rash for pirfenidone [13,14]. Elevated liver enzymes were also observed in 11 % of the patients treated with nintedanib [13]. In the clinical trials, these AEs led to drug discontinuation (20 % for nintedanib and 24 % for pirfenidone) or drug dose reduction (33 % for nintedanib) [13,14]. While information provided by clinical trials is important, real-world studies are also of interest since they are more representative of the population seen in clinical practice and potentially have longer follow-up. Outside of RCTs, literature about the real-world effectiveness and safety of nintedanib and pirfenidone has mostly been described in IPF patients [17], [18], [19], [20], [21]. Studies investigating other causes of ILD have included a limited number of patients with RA-ILD and mostly treated with nintedanib [22], [23], [24], [25]. Therefore, our objective was to investigate the effectiveness and tolerability of antifibrotics in a real-world cohort of patients with RA-ILD.