Galectin-3 level in idiopathic pulmonary fibrosis patients and its relationship with response to antifibrotic treatment

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dc.contributor.authorEmre, Sibel
dc.contributor.authorFazlioglu, Nevin
dc.contributor.authorEmre, Ersan
dc.contributor.authorMutlu, Levent Cem
dc.contributor.authorYilmaz, Ahsen
dc.date.accessioned2025-04-06T12:23:52Z
dc.date.available2025-04-06T12:23:52Z
dc.date.issued2025
dc.departmentTekirdağ Namık Kemal Üniversitesi
dc.description.abstractObject: Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease with characterized by progressive fibrosis. Galectin-3(Gal-3) is a B-galactoside binding lectin plays a central role in inflammation and fibrosis. In our study, we aimed to define levels of serum galectin-3 protein in IPF patients by comparing them with healthy subjects. We also aimed to show that galectin-3 concentrations can be used as a diagnostic and prognostic biomarker in the serum of IPF patients and that the use of galectin-3 inhibitors in combination with antifibrotic treatments may be useful in the therapeutic management of fibrosis. Methods: 44 patients with IPF and 35 control patients who were followed up in our outpatient clinic between 2016 and 2022 were evaluated, anamnesis, spirometric measurements and galectin-3 results were recorded. Patients were grouped according to their antifibrotic treatment. Results: The mean galectin-3 level in the patient group was 8.4 ng/ml and in the control group was 8.2 ng/ml. Serum levels were 8.9 ng/ml in pirfenidone users and 8.2 ng/ml in nintedanib users. Gal-3 was found to be higher in patients taking pirfenidone compared to nintedanib, but there was no statistically significant difference (p > 0.05). Conclusion: Galectin-3 levels were found to be slightly higher in IPF patients compared to healthy subjects. In addition, gal-3 levels decreased as the follow-up period increased in IPF patients in our study. Considering that the patients were receiving pirfenidone or nintedanib treatment during the follow-up period, it may be possible that galectin-3 levels decreased as exposure to these drugs increased. Further studies are needed to clarify these mechanisms.
dc.identifier.doi10.1016/j.rmed.2025.108028
dc.identifier.issn0954-6111
dc.identifier.issn1532-3064
dc.identifier.pmid40049461
dc.identifier.scopus2-s2.0-86000569625
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1016/j.rmed.2025.108028
dc.identifier.urihttps://hdl.handle.net/20.500.11776/17222
dc.identifier.volume240
dc.identifier.wosWOS:001446601200001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherW B Saunders Co Ltd
dc.relation.ispartofRespiratory Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250406
dc.subjectIdiopathic pulmonary fibrosis
dc.subjectGalectin-3
dc.subjectBiomarker
dc.titleGalectin-3 level in idiopathic pulmonary fibrosis patients and its relationship with response to antifibrotic treatment
dc.typeArticle

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