Blood eosinophilia: possible biomarker of response to Nintedanib in Idiopathic Pulmonary Fibrosis.

<bold>Background:</bold> There is a need in Idiopathic Pulmonary Fibrosis (IPF) of therapeutic and prognostic markers. <bold>Aims and Objectives:</bold> our aim was to demonstrate a possible role of eosinophils in the fibrogenic process and as markers of response to antifibrotic therapy. <bold>Methods:</bold> we enrolled 38 patients with IPF (followed at the respiratory department of the University of Ferrara) on antifibrotic treatment: Nintedanib (IPF-Nint), Pirfenidone (IPF-Pirf) and without treatment (IPF). We monitored blood eosinophil counts (BECs) at baseline (T0, time of diagnosis) and after 12 months (T12) of antifibrotic treatment. <bold>Results:</bold> no difference between groups were observed in baseline BEC values. IPF patients on Nintedanib exhibit a higher BECs at T12 (0.54 ± 0.13 x10<sup>3</sup>/mcrl, p< 0,0001), compared to patients on Pirfenidone (0.13 ± 0.10 x10<sup>3</sup>/mcrl) or those not receiving antifibrotic treatment (0.02 ± 0.01 x10<sup>3</sup>/mcrl) (Figure1). The blood eosinophilia in the Nintedanib group statistically correlated with the functional stability of FVC and DLCO (percentage) after one year of antifibrotic therapy. Furthermore, in the Nintedanib group no acute exacerbation of IPF occurred, unlike patients on Pirfenidone and those without therapy. <bold>Conclusions:</bold> BEC is a potential biomarkers of response to antifibrotic therapy (Nintedanib) in IPF. This finding could be related to an effect of the Nintedanib on the endothelial cells. <fig><object-id>erj;66/suppl_69/PA1825/F1</object-id><object-id>F1</object-id><object-id>F1</object-id><graphic></graphic></fig>

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Published
2025-09-27
DOI
https://doi.org/10.1183/13993003.congress-2025.pa1825
Primary Topic
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
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article
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article

Blood eosinophilia: possible biomarker of response to Nintedanib in Idiopathic Pulmonary Fibrosis.

Miriana d’Alessandro, Lucia Vietri, Alberto Papi, A. Bosio et al.
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
article

Blood eosinophilia: possible biomarker of response to Nintedanib in Idiopathic Pulmonary Fibrosis.

Miriana d’Alessandro, Lucia Vietri, Alberto Papi, A. Bosio, Mariano Reginato, Olga Dell'Adami De Tarczal
article en

Abstract

<bold>Background:</bold> There is a need in Idiopathic Pulmonary Fibrosis (IPF) of therapeutic and prognostic markers. <bold>Aims and Objectives:</bold> our aim was to demonstrate a possible role of eosinophils in the fibrogenic process and as markers of response to antifibrotic therapy. <bold>Methods:</bold> we enrolled 38 patients with IPF (followed at the respiratory department of the University of Ferrara) on antifibrotic treatment: Nintedanib (IPF-Nint), Pirfenidone (IPF-Pirf) and without treatment (IPF). We monitored blood eosinophil counts (BECs) at baseline (T0, time of diagnosis) and after 12 months (T12) of antifibrotic treatment. <bold>Results:</bold> no difference between groups were observed in baseline BEC values. IPF patients on Nintedanib exhibit a higher BECs at T12 (0.54 ± 0.13 x10<sup>3</sup>/mcrl, p< 0,0001), compared to patients on Pirfenidone (0.13 ± 0.10 x10<sup>3</sup>/mcrl) or those not receiving antifibrotic treatment (0.02 ± 0.01 x10<sup>3</sup>/mcrl) (Figure1). The blood eosinophilia in the Nintedanib group statistically correlated with the functional stability of FVC and DLCO (percentage) after one year of antifibrotic therapy. Furthermore, in the Nintedanib group no acute exacerbation of IPF occurred, unlike patients on Pirfenidone and those without therapy. <bold>Conclusions:</bold> BEC is a potential biomarkers of response to antifibrotic therapy (Nintedanib) in IPF. This finding could be related to an effect of the Nintedanib on the endothelial cells. <fig><object-id>erj;66/suppl_69/PA1825/F1</object-id><object-id>F1</object-id><object-id>F1</object-id><graphic></graphic></fig>

University of Siena (IT), University of Ferrara (IT)
Openalex Percentile: Top 48%
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
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