Your browser doesn't support javascript.
Adverse Outcome in COVID-19 Is Associated With an Aggravating Hypo-Responsive Platelet Phenotype.
Schrottmaier, Waltraud C; Pirabe, Anita; Pereyra, David; Heber, Stefan; Hackl, Hubert; Schmuckenschlager, Anna; Brunnthaler, Laura; Santol, Jonas; Kammerer, Kerstin; Oosterlee, Justin; Pawelka, Erich; Treiber, Sonja M; Khan, Abdullah O; Pugh, Matthew; Traugott, Marianna T; Schörgenhofer, Christian; Seitz, Tamara; Karolyi, Mario; Jilma, Bernd; Rayes, Julie; Zoufaly, Alexander; Assinger, Alice.
  • Schrottmaier WC; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Pirabe A; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Pereyra D; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Heber S; Department of General Surgery, Division of Visceral Surgery, Medical University of Vienna, General Hospital Vienna, Vienna, Austria.
  • Hackl H; Institute of Physiology, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Schmuckenschlager A; Institute of Bioinformatics, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
  • Brunnthaler L; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Santol J; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Kammerer K; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Oosterlee J; Department of General Surgery, Division of Visceral Surgery, Medical University of Vienna, General Hospital Vienna, Vienna, Austria.
  • Pawelka E; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Treiber SM; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Khan AO; Department of Medicine IV, Clinic Favoriten, Vienna, Austria.
  • Pugh M; Department of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
  • Traugott MT; Institute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
  • Schörgenhofer C; Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
  • Seitz T; Department of Medicine IV, Clinic Favoriten, Vienna, Austria.
  • Karolyi M; Department of Clinical Pharmacology, Medical University of Vienna, General Hospital Vienna, Vienna, Austria.
  • Jilma B; Department of Medicine IV, Clinic Favoriten, Vienna, Austria.
  • Rayes J; Department of Medicine IV, Clinic Favoriten, Vienna, Austria.
  • Zoufaly A; Department of Clinical Pharmacology, Medical University of Vienna, General Hospital Vienna, Vienna, Austria.
  • Assinger A; Institute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Front Cardiovasc Med ; 8: 795624, 2021.
Article in English | MEDLINE | ID: covidwho-1597865
ABSTRACT
Thromboembolic complications are frequently observed in Coronavirus disease 2019 (COVID-19). While COVID-19 is linked to platelet dysregulation, the association between disease outcome and platelet function is less clear. We prospectively monitored platelet activation and reactivity in 97 patients during the first week of hospitalization and determined plasma markers of platelet degranulation and inflammation. Adverse outcome in COVID-19 was associated with increased basal platelet activation and diminished platelet responses, which aggravated over time. Especially GPIIb/IIIa responses were abrogated, pointing toward impeded platelet aggregation. Moreover, platelet-leukocyte aggregate formation was diminished, pointing toward abrogated platelet-mediated immune responses in COVID-19. No general increase in plasma levels of platelet-derived granule components could be detected, arguing against platelet exhaustion. However, studies on platelets from healthy donors showed that plasma components in COVID-19 patients with unfavorable outcome were at least partly responsible for diminished platelet responses. Taken together this study shows that unfavorable outcome in COVID-19 is associated with a hypo-responsive platelet phenotype that aggravates with disease progression and may impact platelet-mediated immunoregulation.
Keywords

Full text: Available Collection: International databases Database: MEDLINE Type of study: Prognostic study Language: English Journal: Front Cardiovasc Med Year: 2021 Document Type: Article Affiliation country: Fcvm.2021.795624

Similar

MEDLINE

...
LILACS

LIS


Full text: Available Collection: International databases Database: MEDLINE Type of study: Prognostic study Language: English Journal: Front Cardiovasc Med Year: 2021 Document Type: Article Affiliation country: Fcvm.2021.795624