AKUT PULMONER EMBOLİ HASTALARINDA GALECTİN-3 Galectin-3 in Patients with Acute Pulmonary Embolism

Year 2020, Volume: 10 Issue: 1, 75 - 82, 25.03.2020

Mustafa Çelik Ahmet Avcı Recep Karataş Ahmet Erseçgin Fikret Keleş Ahmet Yılmaz Fatmagül Can Erdoğan Sökmen Murat Erer

Abstract

ÖZET
Amaç: Pulmoner emboli (PE) göreceli olarak yaygın bir kardiyovasküler acil durumdur ve spesifik olmayan
klinik tablo nedeniyle gözden kaçırılabilecek zor bir tanıdır. PE patogenezi iyi tanımlanmış olmasına rağmen,
PE teşhisine yardımcı olabilecek klinik bir biyobelirteçlere ihtiyaç vardır. Teorik olarak, Galectin-3'ün (Gal-3)
prokoagülan etkisinden dolayı, PE patogenezinde rol alabileceği düşünülebilir. Bu çalışmanın amacı, akut
PE hastalarında Gal-3 düzeyinin önemini göstermek ve PE'nin ekokardiyografik özellikleri ile ilişkisini tanımlamaktır.
Yöntem: 2013 - 2014 tarihleri arasında ardışık 40 PE hastası (26 kadın, ort. Yaş 60.93 ± 14.28 yıl) ve 40 yaş
uyumlu sağlıklı kontrol çalışmaya dahil edildi. Gal-3, D-dimer ve Troponin I düzeyleri ölçüldü. PE ve kontrol
grubundaki tüm hastalara transtorasik ekokardiyografik inceleme yapıldı.
Bulgular: Gal-3 ve D-dimer düzeyleri PE' li hastalarda kontrollere göre anlamlı derecede yüksek bulundu.
(17.04 ± 6.6 ve 8.22 ± 4.9, p <0.001) Gal-3 seviyeleri, D- dimer (r = 0.595, p <0.001) ve Troponin I değerleri
(r = 0.452, p <0.001) ile anlamlı bir korelasyon gösterdi. Gal-3 seviyeleri ekokardiyografik parametrelerle
anlamlı korelasyon gösterdi. ROC eğrisi analizinde, %82.5 duyarlılık ve %82.7 özgüllük ile akut PE tanısı için
gereken seviye 11.43 ng / ml idi. Eğri altındaki alan % 95 CI 0.79-0.96 (p <0.001) ile 0.88 idi.
Sonuç: Bu çalışmada akut PE' li hastalarda Gal-3'ün rolü gösterilmiştir. Gal-3, akut PE' yi teşhis etmek için
kullanılabilecek biyobelirteçler arasında yer alabilir. Ancak daha kapsamlı çalışmalara ihtiyaç vardır.
Anahtar Kelimeler: Galectin-3; D-dimer; Akut pulmoner emboli; Biyomarker; Ekokardiyografi
ABSTRACT
Background: Pulmonary embolism (PE) is a relatively common cardiovascular emergency and it is a difficult
diagnosis that may be missed because of non-specific clinical presentation. Although the pathogenesis
of PE has been well described, there is a clinical need for biomarkers that can aid the diagnosis of PE.
Theoretically, because of the procoagulant effect of Galectin-3 (Gal-3), this marker may play a role in the
pathogenesis of PE. The aim of the present study is to show the significance of the level of Gal-3 in patients
with acute PE and identify a relation to the echocardiographic features of PE.
Methods: Between 2013-2014, 40 consecutive PE patients (26 females, mean age 60.93±14.28 years) and
40 age-matched healthy controls were included in this study. Gal-3, D-dimer, and Troponin I were measured.
All patients with PE and control subjects underwent transthoracic echocardiographic examination.
Results: Gal-3 and D-dimer levels were significantly higher in patients with PE when compared with
controls (17.04±6.6 vs 8.22±4.9, p<0.001). Gal-3 levels showed a significant correlation with D-dimer
(r=0.595, p<0.001) and Troponin I values (r=0.452, p<0.001). Gal-3 levels showed significant correlation
with echocardiographic parameters. In the receiver operating characteristics (ROC) curve analysis, the level
required for a diagnosis of acute PE with a sensitivity of 82.5% and specificity of 82.7% was 11.43 ng/ml. The
area under the curve was 0.88 with a 95% CI of 0.79-0.96 (p < 0.001).
Conclusion: In the present study, we demonstrated the role of Gal-3 in patients with acute PE. Gal-3 can be
used to diagnose acute PE.
Keywords: Galectin-3; D-dimer; Acute pulmonary embolism; Biomarker; Echocardiography

Keywords

AKUT PULMONER EMBOLİ HASTALARINDA GALECTİN-3 Galectin-3 in Patients with Acute Pulmonary Embolism

References

• 1. Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest 2002;121:877–905. 2. Konstantinides S. Pulmonary embolism: impact of right ventricular dysfunction. Curr Opin Cardiol 2005;20: 496–501. 3. Alikhan R, Peters F, Wilmott R, and Cohen AT. Fatal pulmonary embolism in hospitalised patients: a necropsy review. J Clin Pathol 2004;57: 1254–57. 4. Heit JA, O’Fallon WM, Petterson TM, Lohse CM, Silverstein MD, Mohr DN, et al. Relative impact of risk factors for deep vein thrombosis and pulmonary embolism: a population-based study. Arch Intern Med 2002;162:1245–48. 5. de Boer RA, Yu L, and van Veldhuisen DJ. Galactin-3 in cardiac remodeling and heart failure. Curr Heart Fail Rep 2010;7: 1-8. 6. Kimura Y, Izumiya Y, Hanatani S, Yamamoto E, Kusaka H, Tokitsu T, et al. High serum levels of thrombospondin-2 correlate with poor prognosis of patients with heart failure with preserved ejection fraction. Heart Vessels 2014; DOI: 10.1007/s00380-014-0571-y. 7. Pacienza N, Pozner RG, Bianco GA, D'Atri LP, Croci DO, Negrotto S, et al. The immunoregulatory glycan-binding protein galectin-1 triggers human platelet activation. FASEB J 2008;22:1113-23. 8. Falcone C, Lucibello S, Mazzucchelli I, Bozzini S, D'Angelo A, Schirinzi S, al. Galectin-3 plasma levels and coronary artery disease: a new possible biomarker of acute coronary syndrome. Int J Immunopathol Pharmacol 2011;24:905 9. Grandin EW, Jarolim P, Murphy SA, Ritterova L, Cannon CP, Braunwald E, et al. Galectin-3 and the Development of Heart Failure after Acute Coronary Syndrome: Pilot Experience from PROVE IT-TIMI 22. Clin Chem 2012;58: 267-73. 10. Ramacciotti E, Hawley AE, Wrobleski SK, Myers DD Jr, Strahler JR, Andrews PC, et al. Proteomics of microparticles after deep venous thrombosis. Thromb Res 2010;125:269-74.