Rheumatoid arthritis-associated interstitial lung disease: Pathogenesis, risk stratification, and management

Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is one of the most clinically significant extra-articular manifestations of rheumatoid arthritis and an important cause of morbidity and premature mortality. Its clinical spectrum ranges from asymptomatic radiographic abnormalities to rapidly progressive fibrosing lung disease with respiratory failure. Current evidence indicates that RA-ILD is biologically heterogeneous and arises from the interplay of mucosal autoimmunity, genetic susceptibility, epithelial injury, dysregulated innate and adaptive immune responses, and aberrant tissue repair. This heterogeneity has important implications for diagnosis, prognosis, and treatment selection. High-resolution computed tomography remains central to disease detection and radiologic phenotyping, while pulmonary function testing, serologic profiling, circulating biomarkers, and multidisciplinary discussion improve risk stratification and longitudinal assessment. Management should integrate the relative contribution of inflammation and fibrosis with current conditional guideline recommendations, and may include short-term glucocorticoids, conventional immunosuppressants, biologic or targeted synthetic disease-modifying antirheumatic drugs, antifibrotic therapy for documented progressive pulmonary fibrosis, and evaluation for pulmonary hypertension-associated ILD in advanced disease. However, clinical decision-making remains limited by the scarcity of randomized RA-ILD-specific trials, the lack of standardized definitions of disease progression, and uncertainty regarding optimal treatment sequencing. This review summarizes current understanding of the pathogenesis, risk factors, diagnostic evaluation, treatment strategies, and prognostic determinants of RA-ILD, with emphasis on phenotype-oriented management and practical issues relevant to respiratory and multidisciplinary care.