Evaluation of Endostatin Levels in COVID-19 Patients Admitted to the Emergency Department

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Published Nov 9, 2025
https://doi.org/10.62438/tunismed.v103i9.6017
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Vol. 103 No. 9 (2025): Tunis Med sept 2025

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Gokhan Akdur
Departments of Emergency Medicine, Canakkale Onsekiz Mart University Faculty of Medicine,Turkey
Okan Bardakci
Departments of Emergency Medicine, Canakkale Onsekiz Mart University Faculty of Medicine,Turkey
Murat Das
Departments of Emergency Medicine, Canakkale Onsekiz Mart University Faculty of Medicine,Turkey
Canan Akman
Departments of Emergency Medicine, Canakkale Onsekiz Mart University Faculty of Medicine,Turkey
Hilal Sehitoglu
Departments of of Biochemistry, Canakkale Onsekiz Mart University Faculty of Medicine,Turkey
Okhan Akdur
Departments of Emergency Medicine, Canakkale Onsekiz Mart University Faculty of Medicine,Turkey

Abstract

Introduction: The COVID-19 is defined as a respiratory and endothelial disease caused by Severe Acute Respiratory Syndrome Coronavirus 2. Endostatin is a molecule bound to collagen in the basal membrane of endothelial cells.


Objective: The aim of this study was to measure the serum endostatin levels of patients diagnosed with COVID-19 in the emergency department.


Methods: This study was conducted in the emergency department with two groups: COVID-19 PCR-positive patients and healthy adults. Complete blood count, serum biochemistry values, and radiological imaging results were evaluated. Serum endostatin levels were measured from venous blood samples collected during the emergency department visits. Data were analyzed using the SPSS 19.0 software.


Results: A total of 148 COVID-19 patients and 35 healthy controls were included in the study. The serum endostatin levels of the COVID-19 patient group were significantly lower compared to the healthy control group (p<0.05). The Chest CT Severity Score, 4C-Mortality Score, Quick SOFA, and Quick COVID-19 Severity Index were significantly higher in the patients with a fatal outcome compared to those who survived (p<0.001). Although serum endostatin levels were slightly higher in the fatal outcome group, no statistically significant difference was observed (p>0.05).


Conclusion: There is no increase in serum endostatin levels in patients with COVID-19 presenting to the emergency department. While a slight increase in endostatin levels was observed in patients with a fatal outcome, it is believed that endostatin will not be effective in predicting prognosis.

Keywords:

COVID-19, Emergency Department, Endostatin, Pulmonary Injury, Prognosis

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References

  1. Debuc B, Smadja DM. Is COVID-19 a New Hematologic Disease? Stem Cell Rev Rep. 2021;17:4-8.
  2. Libby P, Lüscher T. COVID-19 is, in the end, an endothelial disease. Eur Heart J. 2020;1:41:3038-3044.
  3. Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet 2020;395:1054–62.
  4. Singhal T. A Review of Coronavirus Disease-2019 (COVID-19). Indian J Pediatr 2020;87:281–6.
  5. Rodriguez-Morales AJ, Cardona-Ospina JA, Gutiérrez-Ocampo E, Villamizar-Peña R, Holguin-Rivera Y, Escalera-Antezana JP, et al. Clinical, laboratory and imaging features of COVID-19: A systematic review and meta-analysis. Travel Med Infect Dis 2020;34:101623.
  6. Ni W, Yang X, Yang D, Bao J, Li R, Xiao Y, et al. Role of angiotensin converting enzyme 2 (ACE2) in COVID-19. Crit Care 2020;24:422.
  7. Teuwen LA, Geldhof V, Pasut A, Carmeliet P. COVID-19: the vasculature unleashed. Nat Rev Immunol 2020;20:389.
  8. Lowenstein CJ, Solomon SD. Severe COVID-19 Is a Microvascular Disease. Circulation 2020;142:1609.
  9. Goshua G, Pine AB, Meizlish ML, Chang CH, Zhang H, Bahel P, et al. Endotheliopathy in COVID-19-associated coagulopathy: Evidence from a single-centre, cross-sectional study. Lancet Haematol. 2020; 7: e575–e582.
  10. Helms J, Tacquard C, Severac F, Leonard-Lorant I, Ohana M, Delabranche X, et al. High risk of thrombosis in patients with severe SARS - CoV - 2 infection: A multicenter prospective cohort study. Intensive Care Med. 2020; 46: 1089-1098.
  11. Philippe A, Chocron R, Gendron N, Bory O, Beauvais A, Peron N, Khider L, et al. Circulating Von Willebrand factor and high molecular weight multimers as markers of endothelial injury predict COVID-19 in-hospital mortality. Angiogenesis. 2021; 24: 505-517.
  12. Digtyar AV, Pozdnyakova NV, Feldman NB, Lutsenko SV, Severin SE. Endostatin: current concepts about its biological role and mechanisms of action. Biochemistry 2007; 72: 235-246.
  13. O'Reilly MS, Boehm T, Shing Y Fukai N, Vasios G, Lane WS, et al. Endostatin: an endogenous inhibitor of angiogenesis and tumor growth. Cell. 1997; 24; 277-85.
  14. Ruge T, Carlsson AC, Larsson A, J Ärnlöv. Endostatin: a promising biomarker in the cardiovascular continuum?. Biomarkers in Medicine. 2017; 11: 905-916.
  15. Hang YC, Yu CJ, Chang SC Galvin JR, Liu HM, Hsiao CH, et al. Pulmonary sequelae in convalescent patients after severe acute respiratory syndrome: evaluation with thin-section CT. Radiology. 2005 ;236 :1067-75.
  16. Churpek MM, Snyder A, Han X Sokol S, Pettit N, Howell MD, et al. Quick Sepsis-related Organ Failure Assessment, Systemic Inflammatory Response Syndrome, and Early Warning Scores for Detecting Clinical Deterioration in Infected Patients outside the Intensive Care Unit. Am J Respir Crit Care Med. 2017; 195: 906-911.
  17. Haimovich AD, Ravindra NG, Stoytchev S, Young HP, Wilson FP, van Dijk D, et al. Development and Validation of the Quick COVID-19 Severity Index: A Prognostic Tool for Early Clinical Decompensation. Ann Emerg Med. 2020; 76: 442-453.
  18. Knight SR, Ho A, Pius R, Buchan I, Carson G, Drake TM, et al. Risk stratification of patients admitted to hospital with COVID-19 using the ISARIC WHO Clinical Characterisation Protocol: development and validation of the 4C Mortality Score. BMJ. 2020; 9: 370:m3339.
  19. World Health Organization Data [Internet]. [cited 2025 Jan 16]. Avalaible from: https://data.who.int/dashboards/covid19/deaths?n=o.
  20. Sun Y, Heng BH, Tay SY, Seow E. Predicting hospital admissions at emergency department triage using routine administrative data. Acad Emerg Med. 2011; 18: 844-50.
  21. Bernstein SL, Aronsky D, Duseja R, Epstein S, Handel D, Hwang U, et al. The Effect of Emergency Department Crowding on Clinically Oriented Outcomes. Acad Emerg Med. 2009; 16: 1-10.
  22. Carlsson AC, Wessman T, Larsson A, Leijonberg G, Tofik R, Ärnlöv J, et al. Endostatin predicts mortality in patients with acute dyspnea - A cohort study of patients seeking care in emergency departments. Clin Biochem. 2020; 75: 35-39.
  23. Shah I, Malik MO, Khan MJ, Fatima S, Baxendale RH, Habib SH. Endostatın concentratıon in plasma of healthy human volunteers. J Ayub Med Coll Abbottabad 2017; 29: 200-6.
  24. Deininger MH, Wybranietz WA, Graepler FT, Lauer UM, Meyermann R, Schluesener HJ. Endothelial endostatin release is induced by general cell stress and modulated by the nitric oxide/cGMP pathway. FASEB J. 2003; 17: 1267-76.
  25. Asif S, Ruge T, Larsson A, Anderberg SB, Lipcsey M, Frithiof R, et al. Plasma endostatin correlates with hypoxia and mortality in COVID-19-associated acute respiratory failure. Biomark Med. 2021; 15: 1509-1517.
  26. Suhr F, Brixius K, de Marées M, Bölck B, Kleinöder H, Achtzehn S, et al. Effects of short-term vibration and hypoxia during high-intensity cycling exercise on circulating levels of angiogenic regulators in humans. J Appl Physiol. 2007; 103: 474-483.