İdiyopatik pulmoner fibrozis hastalarında galektin-3 düzeyi ve antifibrotik tedaviye yanıt ile ilişkisi
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Tarih
2022
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Tekirdağ Namık Kemal Üniversitesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
İdiyopatik pulmoner fibrozis (İPF) nedeni bilinmeyen, prognozu kötü, progresif fibrozisle karakterize, kronik bir akciğer hastalığıdır. Sağ kalımın tanı konulduktan sonra 3-5 yıl civarı olduğu bilinen bu hastalıkta erken tanı önemliyken tanıda kullanılabilecek biyobelirteç olmadığından tanı genelde geç konulmaktadır. Galektin-3 çeşitli hücrelerde eksprese edilen, inflamasyon ve fibroziste merkezi bir rol oynayan B-galaktozid bağlayıcı bir lektindir. Çalışmamızda serum galektin-3 proteinin idiyopatik pulmoner fibrozis hastalarında kullandıkları antifibrotik tedaviye göre gruplandırarak seviyelerini sağlıklı deneklerle karşılaştırarak tanımlamayı amaçladık. Ayrıca galektin-3 konsantrasyonlarının İPF hastalarının serumunda tanısal ve prognostik biyobelirteç olarak kullanılabilirliği ve galektin-3 inhibitörlerinin tedavide antifibrotik tedavilerle kombine olarak kullanılmasının fibrozisin terapatik yönetiminde faydalı olabileceğini göstermeyi amaçladık. Çalışmamızda polikliniğimizde 2016-2022 yılları arasında İPF tanısı ile takip edilen 44 hasta ve 35 kontrol hastası değerlendirildi, ayrıntılı anamnezleri, spirometrik ölçümleri ve galektin-3 sonuçları kaydedildi. Hastalar antifibrotik tedavilerine göre gruplandırıldı. Hasta grubunun galektin-3 düzeyi ortalama 8,4 ng/ml iken, kontrol grubunun ortalaması 8,2 ng/ml idi. Pirfenidon alanlarda serum 8.9 ng/ml iken nintedanib alanlarda 8.2 ng/ml idi. Yine pirfenidon kullanan hastalarda da nintedanibe göre gal-3 yüksek saptanmıştır. Ancak gruplar arasında istatistiksel olarak anlamlı bir farklılık izlenmedi. Galektin-3 düzeyleri ile eş zamanlı bakılan diğer parametreler arasında ilişki saptanmadı. Ayrıca hastalarımız antifibrotik kullanırken spirometrik takiplerinde başlangıca göre bir miktar FVC ve DLCO kaybı izlenmiştir. Ek olarak çalışmamızdaki İPF hastalarında takip süresi arttıkça gal-3 düzeyleri azaldığı görülmüş. Hastalar takipleri süresinde pirfenidon ya da nintedanib tedavisi kullanmakta olup belki de bu ilaçlara maruziyet arttıkça hastaların galektin-3 seviyelerinde azalma izlenmiş olabilir. Bu mekanizmaları netleştirebilmek için ileri çalışmalara ihtiyaç vardır.
Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease of unknown cause, poor prognosis, characterized by progressive fibrosis. In this disease, which is known to have a survival rate of 3-5 years after diagnosis, early diagnosis is important, but the diagnosis is usually made late since there is no biomarker that can be used in the diagnosis. Galectin 3 is a B-galactoside binding lectin that plays a central role in inflammation and fibrosis, expressed in various cells. We aimed to define the levels of serum galectin-3 protein in patients by grouping them according to the antifibrotic treatment they use and comparing them with healthy subjects. In addition, we aimed to show that galectin-3 concentrations can be used as diagnostic and prognostic biomarker in the serum of IPF patients and that the use of galectin-3 inhibitors in combination with antifibrotic treatments can be beneficial in the therapeutic management of fibrosis. In our study, 44 patients and 35 control patients who were followed up with the diagnosis of IPF in our outpatient clinic between 2016 and 2022 were evaluated, and their detailed anamnesis, spirometric measurements and galectin-3 results were recorded. While the mean galectin-3 level of the patient group was 8.4 ng/ml, the mean galectin-3 level of the control group was 8.2 ng/ml. The serum gal-3 level was 8.9 ng/ml in those receiving pirfenidone treatment, while it was 8.2 ng/ml in those receiving nintedanib. Again, gal-3 was found to be higher in patients using pirfenidone compared to nintedanib. However, no statistically significant difference was observed between the groups. No correlation was found between galectin-3 levels and other parameters measured simultaneously. While our patients were using antifibrotic treatment, some loss of FVC and DLCO was observed in their spirometric follow-up compared to baseline. In addition, gal-3 levels were found to decrease as the follow-up period increased in IPF patients in our study. These patients were using pirfenidone or nintedanib treatment during their follow-up, and perhaps as the exposure to these drugs increased, a decrease in the galectin-3 levels of the patients may have been observed. Further studies are needed to clarify these mechanisms.
Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease of unknown cause, poor prognosis, characterized by progressive fibrosis. In this disease, which is known to have a survival rate of 3-5 years after diagnosis, early diagnosis is important, but the diagnosis is usually made late since there is no biomarker that can be used in the diagnosis. Galectin 3 is a B-galactoside binding lectin that plays a central role in inflammation and fibrosis, expressed in various cells. We aimed to define the levels of serum galectin-3 protein in patients by grouping them according to the antifibrotic treatment they use and comparing them with healthy subjects. In addition, we aimed to show that galectin-3 concentrations can be used as diagnostic and prognostic biomarker in the serum of IPF patients and that the use of galectin-3 inhibitors in combination with antifibrotic treatments can be beneficial in the therapeutic management of fibrosis. In our study, 44 patients and 35 control patients who were followed up with the diagnosis of IPF in our outpatient clinic between 2016 and 2022 were evaluated, and their detailed anamnesis, spirometric measurements and galectin-3 results were recorded. While the mean galectin-3 level of the patient group was 8.4 ng/ml, the mean galectin-3 level of the control group was 8.2 ng/ml. The serum gal-3 level was 8.9 ng/ml in those receiving pirfenidone treatment, while it was 8.2 ng/ml in those receiving nintedanib. Again, gal-3 was found to be higher in patients using pirfenidone compared to nintedanib. However, no statistically significant difference was observed between the groups. No correlation was found between galectin-3 levels and other parameters measured simultaneously. While our patients were using antifibrotic treatment, some loss of FVC and DLCO was observed in their spirometric follow-up compared to baseline. In addition, gal-3 levels were found to decrease as the follow-up period increased in IPF patients in our study. These patients were using pirfenidone or nintedanib treatment during their follow-up, and perhaps as the exposure to these drugs increased, a decrease in the galectin-3 levels of the patients may have been observed. Further studies are needed to clarify these mechanisms.
Açıklama
Anahtar Kelimeler
İdiyopatik Pulmoner Fibrozis, Galektin-3, Biyobelirteç, Idiopathic Pulmonary Fibrosis, Galectin-3, Biomarker, Göğüs Hastalıkları, Chest Diseases
