Rheumatoid Arthritis Interstitial Lung Disease: Treating the Trajectory, Not the Pattern

Abstract

Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) requires more than a radiological diagnosis. A usual interstitial pneumonia pattern describes pulmonary architecture, but does not by itself establish whether disease is progressing, which component is modifiable, or how safely treatment can be deferred. This narrative review revisits the disease-behaviour approach and distinguishes susceptibility to ILD, prognosis after ILD develops, and prediction of treatment benefit. It integrates contemporary classification and guidance with evidence from immunomodulatory cohorts, INBUILD, TRAIL1 and FIBRONEER-ILD. We propose a reserve-aware interpretation of trajectory: structural burden and the pace of deterioration should be considered alongside remaining physiological reserve, competing hazards and the likely cost of waiting. This is a clinical reasoning framework, not a validated score. Progressive pulmonary fibrosis provides a useful operational definition, but should neither be mistaken for proof of an exclusively fibrotic mechanism nor become a prerequisite for treating already consequential lung disease. Molecular advances, including MUC5B, telomere length and protein signatures, illustrate the distance between biological plausibility and treatment selection. Antifibrotic evidence supports slowing functional loss; newer survival analyses require careful separation of overall pulmonary fibrosis populations from RA-specific inference. The therapeutic objective is therefore not to treat an imaging label or normalise an isolated measurement, but to preserve useful lung function while controlling systemic disease and limiting treatment-related harm.