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Related Experiment Video

Updated: Jul 14, 2025

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

Phenotyping by persistent inflammation in systemic sclerosis associated interstitial lung disease: a EUSTAR database

Sabina Guler^1,2, Adela-Cristina Sarbu³, Odile Stalder⁴

¹Department of Pulmonary Medicine, Inselspital University Hospital Bern, Bern, Switzerland Sabina.Guler@insel.ch.

|October 5, 2023

Summary

Systemic sclerosis with persistent inflammation significantly increases mortality risk in SSc-ILD patients. Early immunosuppressive treatment stabilizes lung function in the inflammatory phenotype of systemic sclerosis.

Keywords:

Interstitial Fibrosis Rheumatoid lung disease Systemic disease and lungs

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Published on: July 7, 2017

Area of Science:

Rheumatology
Pulmonology
Immunology

Background:

Systemic sclerosis (SSc) is a complex autoimmune disease.
Interstitial lung disease (SSc-ILD) is a common and serious complication of SSc.
Inflammation plays a critical role in SSc pathogenesis and progression.

Purpose of the Study:

To evaluate the prognostic value of phenotyping SSc and SSc-ILD patients based on inflammation levels.
To characterize disease trajectories in SSc and SSc-ILD stratified by inflammatory status and immunosuppressive treatment.

Main Methods:

Utilized data from the European Scleroderma Trials and Research (EUSTAR) cohort.
Classified patients into persistent inflammatory, intermediate, and non-inflammatory phenotypes based on C-reactive protein (CRP) levels.
Employed Cox regression for mortality risk analysis and mixed-effects models for FVC and DLCO trajectory analysis.

Main Results:

Patients with SSc-ILD and a persistent inflammatory phenotype faced a 6.7-fold higher 5-year mortality risk compared to non-inflammatory phenotypes.
In the inflammatory phenotype, forced vital capacity (FVC) declined without treatment but stabilized with immunosuppressive therapy.
FVC declined in the non-inflammatory phenotype, with a more pronounced decline observed in patients receiving immunosuppressive treatment.

Conclusions:

Phenotyping by persistent inflammation offers significant prognostic insights in SSc and SSc-ILD, independent of other clinical factors.
Early immunosuppressive treatment is recommended for SSc-ILD patients exhibiting persistent inflammation.
Inflammation-based phenotyping can guide treatment decisions and improve outcomes in SSc-ILD.