TY - JOUR
T1 - Pathogenesis, clinical features, and treatment strategy for rheumatoid arthritis-associated interstitial lung disease
AU - Akiyama, Mitsuhiro
AU - Kaneko, Yuko
N1 - Publisher Copyright:
© 2022 Elsevier B.V.
PY - 2022/5
Y1 - 2022/5
N2 - Rheumatoid arthritis is an autoimmune disease that primarily affects the joints. The emergence of highly effective anti-rheumatic drugs such as biologic agents and janus kinase inhibitors has dramatically improved the management of the disease by preventing irreversible joint destruction and disability. This disease can manifest the serious extra-articular involvements including interstitial lung disease, which has the significant impact on the patients' morbidity and mortality. However, treatment strategy specific for rheumatoid arthritis-associated interstitial lung disease (RA-ILD) has not been yet established. Therefore, understanding the pathogenesis and clinical features of RA-ILD is critical to provide the better management and improve the prognosis of the patients. Accumulation of evidence suggest that it is essentially important to achieve remission or at least low disease activity of arthritis to prevent new emergence, progression, or acute exacerbation of RA-ILD. RA-ILD patients frequently show high titers of autoantibodies including rheumatoid factor and anti-CCP antibody, and the excessive formation of tertiary lymphoid organs is found in the local affected lungs, indicating the adaptive immune response as a key pathogenic inducer. In this regard, non-TNF inhibitors targeting adaptive immune responses such as abatacept and rituximab were reported to be promising for the stabilization and improvement of RA-ILD. Nintedanib, an anti-fibrotic agent, was shown to be effective for reducing the decline of forced vital capacity in RA-ILD. In this review, we summarized the current evidence in the pathogenesis, clinical features, and treatments for RA-ILD and provide future prospects.
AB - Rheumatoid arthritis is an autoimmune disease that primarily affects the joints. The emergence of highly effective anti-rheumatic drugs such as biologic agents and janus kinase inhibitors has dramatically improved the management of the disease by preventing irreversible joint destruction and disability. This disease can manifest the serious extra-articular involvements including interstitial lung disease, which has the significant impact on the patients' morbidity and mortality. However, treatment strategy specific for rheumatoid arthritis-associated interstitial lung disease (RA-ILD) has not been yet established. Therefore, understanding the pathogenesis and clinical features of RA-ILD is critical to provide the better management and improve the prognosis of the patients. Accumulation of evidence suggest that it is essentially important to achieve remission or at least low disease activity of arthritis to prevent new emergence, progression, or acute exacerbation of RA-ILD. RA-ILD patients frequently show high titers of autoantibodies including rheumatoid factor and anti-CCP antibody, and the excessive formation of tertiary lymphoid organs is found in the local affected lungs, indicating the adaptive immune response as a key pathogenic inducer. In this regard, non-TNF inhibitors targeting adaptive immune responses such as abatacept and rituximab were reported to be promising for the stabilization and improvement of RA-ILD. Nintedanib, an anti-fibrotic agent, was shown to be effective for reducing the decline of forced vital capacity in RA-ILD. In this review, we summarized the current evidence in the pathogenesis, clinical features, and treatments for RA-ILD and provide future prospects.
KW - Biologic agents
KW - Interstitial lung disease
KW - Nintedanib
KW - Pathogenesis
KW - Prognosis
KW - Rheumatoid arthritis
UR - http://www.scopus.com/inward/record.url?scp=85124611214&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85124611214&partnerID=8YFLogxK
U2 - 10.1016/j.autrev.2022.103056
DO - 10.1016/j.autrev.2022.103056
M3 - Review article
C2 - 35121155
AN - SCOPUS:85124611214
VL - 21
JO - Autoimmunity Reviews
JF - Autoimmunity Reviews
SN - 1568-9972
IS - 5
M1 - 103056
ER -