Joint bone spine · 2025
Quantitative HRCT as a surrogate outcome measure for nintedanib treatment in systemic sclerosis-interstitial lung disease and idiopathic pulmonary fibrosis.
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Di Battista Marco, Romei Chiara, Tavanti Laura, Uggenti Vincenzo, Mitolo Sara, Airò Edoardo, Pistelli Francesco, Chimera Davide, Carrozzi Laura, Neri Emanuele, De Liperi Annalisa, Della Rossa Alessandra, Mosca Marta
Аннотация
OBJECTIVE: We assessed the effect of nintedanib (NIN) in terms of quantitative HRCT changes in both idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated progressive interstitial lung disease (SSc-ILD), evaluating the relationships between imaging variations and clinical-functional outcomes.
METHODS: We prospectively enrolled SSc-ILD and IPF patients treated with NIN and retrospectively selected the same number of subjects from a historical untreated cohort comparable for disease, age, gender and follow-up period. HRCT scans were processed with CALIPER software, obtaining the percentage of normal parenchyma, ILD and vascular-related structures (VRS).
RESULTS: Quantitative HRCT changes of 36 NIN treated patients (12 SSc-ILD and 24 IPF) were compared with 36 untreated subjects with pulmonary fibrosis. After a mean follow-up period of 22 months, NIN therapy was associated with a percentage stabilization of normal parenchyma (from 81.3±11.8% to 78.6±15.6%; P=not significant) and ILD (from 14.5±10.4% to 16.7±14.2%; P=not significant) both in SSc-ILD and IPF, avoiding the loss of normal parenchyma (from 87.4±7.3% to 78.8±16.7%; P<0.001) and ILD worsening (from 9.0±5.9% to 16.5±14.8%; P<0.001) observed in the untreated cohort. VRS was significantly increased regardless of antifibrotic therapy (P<0.001). NIN treated patients who experienced a clinically meaningful worsening at pulmonary function tests or at the reported dyspnoea, presented a significant loss of normal parenchyma in parallel with a greater increase in ILD (P<0.05 for all).
CONCLUSION: NIN appears effective in reducing the radiological decline of pulmonary fibrosis. Quantitative HRCT is proposed as a surrogate outcome measure for clinical practice and future trials.
METHODS: We prospectively enrolled SSc-ILD and IPF patients treated with NIN and retrospectively selected the same number of subjects from a historical untreated cohort comparable for disease, age, gender and follow-up period. HRCT scans were processed with CALIPER software, obtaining the percentage of normal parenchyma, ILD and vascular-related structures (VRS).
RESULTS: Quantitative HRCT changes of 36 NIN treated patients (12 SSc-ILD and 24 IPF) were compared with 36 untreated subjects with pulmonary fibrosis. After a mean follow-up period of 22 months, NIN therapy was associated with a percentage stabilization of normal parenchyma (from 81.3±11.8% to 78.6±15.6%; P=not significant) and ILD (from 14.5±10.4% to 16.7±14.2%; P=not significant) both in SSc-ILD and IPF, avoiding the loss of normal parenchyma (from 87.4±7.3% to 78.8±16.7%; P<0.001) and ILD worsening (from 9.0±5.9% to 16.5±14.8%; P<0.001) observed in the untreated cohort. VRS was significantly increased regardless of antifibrotic therapy (P<0.001). NIN treated patients who experienced a clinically meaningful worsening at pulmonary function tests or at the reported dyspnoea, presented a significant loss of normal parenchyma in parallel with a greater increase in ILD (P<0.05 for all).
CONCLUSION: NIN appears effective in reducing the radiological decline of pulmonary fibrosis. Quantitative HRCT is proposed as a surrogate outcome measure for clinical practice and future trials.