Effectiveness of biological disease-modifying antirheumatic drugs in progressive pulmonary fibrosis associated with rheumatoid arthritis
Authors' conclusion
In this real-world comparative study, IL-6Ri may have contributed to improved FVC, whereas CTLA4-Ig may have a favourable safety profile.
Study context
- Population
- Patients with rheumatoid arthritis (RA)-associated progressive pulmonary fibrosis (PPF) initiating biological disease-modifying antirheumatic drugs (bDMARDs)of 2484 RA patients initiating bDMARDs
- Participants
- 135 patients
- Exposure
- Tumour necrosis factor inhibitor (TNFi) vs CTLA4-Ig vs IL-6Ri in RA-associated PPF
- TNFin = 35reference
- CTLA4-Ign = 45
- IL-6Rin = 55
- Outcome
- Change in pulmonary function and CT visual scores
- Follow-up
- Week 52
Methodological detailsreal-world data, propensity score-based inverse probability of treatment weighting (PS-IPTW)
- Real-world data
- Propensity score-based inverse probability of treatment weighting (PS-IPTW)
Main finding
As reported in the abstract
Pulmonary function and CT scores
- Pulmonary function and computed tomography (CT) scores remained stable with bDMARDs
Observational data: associations, not effects.
Secondary outcomes
| Outcome | TNFi | IL-6Ri | Cohen's d | P value |
|---|---|---|---|---|
| FVC changeIL-6Ri vs TNFi · FVC improved in IL-6Ri · PS-IPTW-adjusted | + 3.3% | −3.2% | 0.630 | P = 0.011 |
Clinical Disease Activity Index (CDAI) with bDMARDs · week 52
- bDMARDs markedly improved CDAI
CDAI, CT scores and drug retention rates between bDMARD groups
- No significant differences among bDMARD groups
- PS-IPTW-adjusted
Independent predictors of forced vital capacity (FVC) improvement
- IL-6Ri treatment, non-UIP pattern and lower CDAI at week 52 (multivariate logistic regression)
Safety
Adverse events
- Less frequent in CTLA4-Ig
Original publication
Effectiveness of biological disease-modifying antirheumatic drugs in progressive pulmonary fibrosis associated with rheumatoid arthritis. Rheumatology (Oxford). Published 20 August 2026. doi:10. 1093/ rheumatology/ keag421
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