# Rheumatoid Arthritis‐Associated Interstitial Pneumonia Refractory to Initial Therapy: Successful Control Through Combined Anti‐Inflammatory, Antifibrotic and JAK‐STAT‐Targeted Treatment

## TL;DR

A patient with severe rheumatoid arthritis-related lung disease improved significantly after combining anti-inflammatory, antifibrotic, and JAK-targeted treatments.

## Contribution

This case demonstrates the effectiveness of a multi-target treatment strategy, including JAK inhibition, in refractory rheumatoid arthritis-associated interstitial pneumonia.

## Key findings

- Combining corticosteroids, tacrolimus, nintedanib, and baricitinib led to marked clinical and radiological improvement.
- JAK inhibition may offer therapeutic benefit in RA-ILD cases resistant to conventional treatments.
- TGF-β is suggested as a key mediator in the fibrotic process, supporting the use of multi-target strategies.

## Abstract

Connective tissue disease (CTD)–associated interstitial lung disease (ILD) accounts for a significant proportion of ILD cases, with rheumatoid arthritis (RA) being one of the most common underlying disorders. Although immunosuppressive therapy plays a central role in CTD‐ILD, its efficacy is limited in fibrotic ILDs, particularly those with a usual interstitial pneumonia (UIP) pattern. We report a case of RA‐associated ILD in an elderly woman who experienced acute disease progression despite ongoing treatment. A multimodal approach combining corticosteroids, tacrolimus, antifibrotic therapy (nintedanib) and the Janus kinase (JAK) inhibitor baricitinib led to marked clinical, radiological and biomarker improvement. This case underscores the potential benefit of a multi‐target strategy addressing both inflammation and fibrosis and suggests a possible role for JAK inhibition in refractory RA‐ILD.

We describe an elderly woman with RA‐ILD who showed insufficient response to corticosteroids, tacrolimus and nintedanib, but achieved marked improvement with the addition of the Janus kinase (JAK) inhibitor baricitinib. We also discuss potential molecular mechanisms underlying this therapeutic response, particularly the role of Transforming Growth Factor‐β (TGF‐β) as a pivotal mediator in the fibrotic process.