HIGH HEPARANASE LEVEL IN SURVIVORS OF COVID-19 — INDICATOR OF VASCULAR AND PULMONARY RECOVERY?

Autor: Neb, Holger, Talbot, Steven Roger, Ruskowski, Katharina, Brkic, Djurdjina, Sonntagbauer, Michael, Adam, Elisabeth Hannah, Knethen, Andreas von, Zacharowski, Kai D., Heinicke, Ulrike
Přispěvatelé: Publica
Rok vydání: 2022
Předmět:
i.S. - in serum
DM - diabetes mellitus
ICU - intensive care unit
SD - standard deviation
severe acute respiratory syndrome
Critical Care and Intensive Care Medicine
CRT - capillary refill time
intensive care unit
aHT - arterial hypertension
ARDS - acute respiratory distress syndrome
Cohort Studies
SARS-CoV-2 - severe acute respiratory syndrome coronavirus 2
Humans
i.U. - in urine
endothelial barrier dysfunction
Prospective Studies
Survivors
Enoxaparin
anticoagulation
CRP - C-reactive protein
low-molecular-weight heparin
HPSE - heparanase
MV - mechanical ventilation
Inflammation
Heparin
COVID-19
LDH - lactate dehydrogenase
NE - noradrenaline
Heparin
Low-Molecular-Weight

HBP - heparin-binding protein
HS - heparan sulfate
LMWH
LMWH - low-molecular-weight heparin
CARDS - COVID-19-associated acute respiratory distress syndrome
ECMO - extracorporeal membrane oxygenation
Emergency Medicine
COPD - chronic obstructive pulmonary disease
endothelitis
NIV - noninvasive ventilation
COVID-19 - coronavirus disease 2019
PCT - procalcitonin
Zdroj: Shock. 58:514-523
ISSN: 1073-2322
DOI: 10.1097/shk.0000000000002021
Popis: Background: Severe progression of coronavirus disease 2019 (COVID-19) causes respiratory failure and critical illness. Recently, COVID-19 has been associated with heparanase (HPSE)-induced endothelial barrier dysfunction and inflammation, so called endothelitis, and therapeutic treatment with heparin or low-molecular-weight heparin (LMWH) targeting HPSE has been postulated. Because, up to this date, clinicians are unable to measure the severity of endothelitis, which can lead to multiorgan failure and concomitant death, we investigated plasma levels of HPSE and heparin-binding protein (HBP) in COVID-19 intensive care patients to render a possible link between endothelitis and these plasma parameters. Therefore, a prospective prolonged cohort study was conducted, including 47 COVID-19 patients from the intensive care unit. Plasma levels of HPSE, and HBP were measured daily by enzyme-linked immunosorbent assay in survivors (n = 35) and nonsurvivors (n = 12) of COVID-19 from admission until discharge or death. All patients were either treated with heparin or LMWH, aiming for an activated partial thromboplastin time of ≥60 seconds or an anti-Xa level of >0.8 IU/mL using enoxaparin, depending on the clinical status of the patient (patients with extracorporeal membrane oxygenation or >0.1 μg/kg/min noradrenaline received heparin, all others enoxaparin). Results: We found significantly higher plasma levels of HPSE and HBP in survivors and nonsurvivors of COVID-19, compared with healthy controls. Still, interestingly, plasma HPSE levels were significantly higher (P < 0.001) in survivors compared with nonsurvivors of COVID-19. In contrast, plasma HBP levels were significantly reduced (P < 0.001) in survivors compared with nonsurvivors of COVID-19. Furthermore, when patients received heparin, they had significantly lower HPSE (P = 2.22e - 16) and significantly higher HBP (P = 0.00013) plasma levels as when they received LMWH. Conclusion: Our results demonstrated that patients, who recover from COVID-19-induced vascular and pulmonary damage and were discharged from the intensive care unit, have significantly higher plasma HPSE level than patients who succumb to COVID-19. Therefore, HPSE is not suitable as marker for disease severity in COVID-19 but maybe as marker for patient's recovery. In addition, patients receiving therapeutic heparin treatment displayed significantly lower heparanse plasma level than upon therapeutic treatment with LMWH.
Databáze: OpenAIRE