Distinctive Biomarker Features in the Endotheliopathy of COVID-19 and Septic Syndromes
| Autor: | Ferran Segui, Helena Ventosa, Paul G. Richardson, Enric Carreras, Carmelo Carlo-Stella, Gines Escolar, Sara Fernández, Pedro Castro, Ana Belen Moreno-Castaño, Sergi Torramade-Moix, Edward Richardson, Maribel Diaz-Ricart, Marta Palomo, José M. Moraleda, Julia Martinez-Sanchez, Josep M. Nicolás, Adrián Téllez, David García-Bernal |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Male
medicine.medical_specialty endothelium Thrombomodulin medicine.medical_treatment ADAMTS13 Protein Vascular Cell Adhesion Molecule-1 Complement Membrane Attack Complex Critical Care and Intensive Care Medicine Clinical Science Aspects Gastroenterology sepsis Endothelial activation Sepsis Von Willebrand factor Coagulopathy Internal medicine Plasminogen Activator Inhibitor 1 von Willebrand Factor Fibrinolysis Humans Medicine Prospective Studies Aged alpha-2-Antiplasmin biology SARS-CoV-2 business.industry Septic shock Patient Acuity COVID-19 DNA Middle Aged medicine.disease Systemic inflammatory response syndrome Receptors Tumor Necrosis Factor Type I Emergency Medicine biology.protein septic shock Biomarker (medicine) Female Heparitin Sulfate business Biomarkers |
| Zdroj: | Shock (Augusta, Ga.) Shock r-IGTP. Repositorio Institucional de Producción Científica del Instituto de Investigación Germans Trias i Pujol instname |
| ISSN: | 1540-0514 1073-2322 |
| Popis: | Background: Endotheliopathy is a key element in COVID-19 pathophysiology, contributing to both morbidity and mortality. Biomarkers distinguishing different COVID-19 phenotypes from sepsis syndrome remain poorly understood. Objective: To characterize circulating biomarkers of endothelial damage in different COVID-19 clinical disease stages compared with sepsis syndrome and normal volunteers. Methods: Patients with COVID-19 pneumonia (n = 49) were classified into moderate, severe, or critical (life-threatening) disease. Plasma samples were collected within 48 to 72 h of hospitalization to analyze endothelial activation markers, including soluble Vascular Cell Adhesion Molecule-1 (sVCAM-1), von Willebrand Factor (VWF), A disintegrin-like and metalloprotease with thrombospondin type 1 motif no. 13 (ADAMTS-13) activity, thrombomodulin (TM), and soluble TNF receptor I (sTNFRI); heparan sulfate (HS) for endothelial glycocalyx degradation; C5b9 deposits on endothelial cells in culture and soluble C5b9 for complement activation; circulating dsDNA for neutrophil extracellular traps (NETs) presence, and alpha 2-antiplasmin and PAI-1 as parameters of fibrinolysis. We compared the level of each biomarker in all three COVID-19 groups and healthy donors as controls (n = 45). Results in critically ill COVID-19 patients were compared with other intensive care unit (ICU) patients with septic shock (SS, n = 14), sepsis (S, n = 7), and noninfectious systemic inflammatory response syndrome (NI-SIRS, n = 7). Results: All analyzed biomarkers were increased in COVID-19 patients versus controls (P < 0.001), except for ADAMTS-13 activity that was normal in both groups. The increased expression of sVCAM-1, VWF, sTNFRI, and HS was related to COVID-19 disease severity (P < 0.05). Several differences in these parameters were found between ICU groups: SS patients showed significantly higher levels of VWF, TM, sTNFRI, and NETS compared with critical COVID-19 patients and ADAMTS-13 activity was significantly lover in SS, S, and NI-SIRS versus critical COVID-19 (P < 0.001). Furthermore, alpha 2-antiplasmin activity was higher in critical COVID-19 versus NI-SIRS (P < 0.01) and SS (P < 0.001), whereas PAI-1 levels were significantly lower in COVID-19 patients compared with NI-SIRS, S, and SS patients (P < 0.01). Conclusions: COVID-19 patients present with increased circulating endothelial stress products, complement activation, and fibrinolytic dysregulation, associated with disease severity. COVID-19 endotheliopathy differs from SS, in which endothelial damage is also a critical feature of pathobiology. These biomarkers could help to stratify the severity of COVID-19 disease and may also provide information to guide specific therapeutic strategies to mitigate endotheliopathy progression. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|