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Interstitial lung disease
Original research
Impact of quantitative radiological features of interstitial lung disease on immunomodulatory treatment response in three autoimmune interstitial lung disease cohorts
  1. Scott M Matson1,
  2. Grace Hyun J Kim2,
  3. Stephen M Humphries3,
  4. Michael D Roth4,
  5. Jonathan Goldin5,6,
  6. Donald P Tashkin7,
  7. Mei Leng8,
  8. Bryant R England9,
  9. Joyce S Lee10,
  10. Elizabeth R Volkmann7
  1. 1 Division of Pulmonary, Critical Care and Sleep Medicine, The University of Kansas School of Medicine, Kansas City, Kansas, USA
  2. 2 Department of Radiological Sciences, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
  3. 3 Department of Radiology, National Jewish Health, Denver, Colorado, USA
  4. 4 Department of Medicine and Health Sciences Research, University of California, Los Angeles, Los Angeles, California, USA
  5. 5 Department of Radiologic Sciences, University of California, Los Angeles, Los Angeles, California, USA
  6. 6 UCLA Health, Los Angeles, California, USA
  7. 7 Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Los Angeles, Los Angeles, California, USA
  8. 8 Department of Medicine, Division of Internal Medicine and Health Sciences Research, Los Angeles, California, USA
  9. 9 Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE USA and Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE, USA, Omaha, Nebraska, USA
  10. 10 Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Campus, Aurora, Colorado, USA
  1. Correspondence to Dr Scott M Matson; smatson@kumc.edu

Abstract

Background The defining radiological features of autoimmune interstitial lung disease (ILD) are ground glass opacification (GGO) and fibrosis. The associations between these features and physiological response to immunomodulation remain unclear.

Methods This study leveraged three autoimmune ILD cohorts: two with systemic sclerosis (SSc) and one with rheumatoid arthritis (RA) which were selected for inherent differences in fibrotic extents/patterns. Linear regression models examined associations between baseline quantitative GGO, fibrosis, their ratio and forced vital capacity (FVC)%-predicted changes after 12 months of immunomodulatory therapy.

Results Patients with SSc-ILD (N=262) exhibited a higher GGO-to-fibrosis ratio compared with patients with RA-ILD (N=130) (mean ratio 3.0 vs 0.25). Increased GGO-to-fibrosis was not associated with improved FVC%-predicted in any cohort. Conversely, in patients with SSc-ILD treated with cyclophosphamide (CYC), increased fibrosis (estimate 0.17 (95% CI 0.003, 0.33); p=0.04) and increased GGO (estimate 0.15 (95% CI 0.004, 0.30); p=0.044) were both significantly associated with FVC% improvement. Given the negative direction of the estimate for GGO-to-fibrosis ratio (estimate −0.33 (95% CI −0.61, –0.06); p=0.016), CYC was associated with greater FVC% improvement in patients with a higher degree of fibrosis relative to GGO. No significant correlation was seen in patients with SSc-ILD treated with mycophenolate (N=56) or in patients with RA-ILD treated with immunomodulation (N=130).

Discussion Increased quantitative GGO relative to fibrosis was not significantly associated with improved response to immunomodulation in patients with RA-ILD and SSc-ILD. However, increased quantitative fibrosis and GGO extent were associated with improved response to CYC in SSc-ILD. More research is needed to understand how to use radiological features to guide treatment selection in ILD.

  • Interstitial Fibrosis
  • Rheumatoid lung disease

Data availability statement

Data are available upon reasonable request.

https://doi.org/10.1136/thorax-2024-222367

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Data availability statement

Data are available upon reasonable request.

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Footnotes

  • X @scott_matson

  • Contributors SM and ERV contributed to the study conception and design. SM, GHJK, SMH, MR, JG, DPT, JSL and ERV contributed to acquisition of the data. SM, LN, ML, BE and ERV contributed to the analysis and interpretation of the data. SM and ERV contributed to the initial drafting of the manuscript. All authors contributed to critical revision and final approval of the manuscript. SM is the guarantor of this manuscript and, as such, takes responsibility for the integrity of the data and the accuracy of the data analysis.

  • Funding NIH/NIGMS (P20GM130423): SM, NIH/NHLBI (K23 HL150237): ERV

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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