ABSTRACT
Introduction: Interstitial lung disease (ILD) is a common, devastating pulmonary complication. An increased number of reports suggesting that biological disease modifying antirheumatic drugs (DMARDs) induced or exacerbated ILDs in rheumatoid arthritis (RA) patients has garnered increased attention.
Areas covered: This article discusses ILDs induced by or exacerbated during biological therapy in RA patients. The article summarizes the efficacy and safety of a variety of licensed and off-label biologics clinically used for rheumatic diseases, focusing on the onset or exacerbation of RA-associated ILDs (RA-ILDs) in RA patients treated with biologics targeting tumor necrosis factor, CD20, interleukin 1 (IL-1) and IL-6 receptors. Additionally, the pathogenesis of RA-ILDs is discussed.
Expert opinion: To some extent, the possibility of biologic-induced RA-ILDs increases the difficulty in choosing an optimal regimen for RA treatment with biological agents, as the relationship between biological therapy safety and the induction or exacerbation of RA-ILDs has not been established. A framework to assess baseline disease severity, particularly standardizing the evaluation of the pulmonary condition stage in RA patients and monitoring the outcome during the biological therapy treatment, is highly needed and may substantially help guide treatment decisions and predict the treatment benefits.
Article highlights
Pulmonary complications, particularly interstitial lung diseases (ILDs), cause mortality in patients with rheumatoid arthritis (RA) and systemic sclerosis (SSc).
The introduction of biologics for treating autoimmune diseases poses promised outcomes; however, they may also induce or accelerate ILDs in rheumatic patients.
The risks associated with biologics-based immunosuppressive therapy and developing or exacerbating RA-associated ILDs (RA-ILDs) currently remain uncertain.
Accumulating clinical evidence suggests a necessity to evaluate the pulmonary condition of patients treated with a regimen of biologics.
A better understanding of the mechanisms underpinning the pathogenesis of RA-ILDs, as well as roles of biological therapies in rheumatic diseases, may improve the efficacy and safety of biologics in clinical settings.
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Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.