Increased plasma level of soluble P-selectin in non-hospitalized COVID-19 convalescent donors

ABSTRACT

Background: COVID-19 has severe implications on the vascular and coagulation system. A procoagulant platelet phenotype has been reported for the acute disease phase. Soluble P-selectin (sP-sel) in the plasma is a surrogate biomarker of platelet activation. Increased plasma levels of sP-sel have been reported in hospitalized COVID-19 patients associated with disease severity. In a longitudinal study we evaluated the sP-sel plasma concentration in blood donors who previously suffered from moderate COVID-19. Method(s) 154 COVID-19 convalescent and 111 non-infected control donors were recruited for plasma donations and for participation in the CORE research trial. First donations were performed 6 to 56 weeks after COVID-19 diagnosis. Blood samples were taken at up to three plasma donations (T1, T2, T3) within a time period of 8-12 weeks. Baseline characteristics including COVID-19 symptoms of the donors were recorded based on a questionnaire. Platelet function was measured at T1 by flow cytometry and light transmission aggregometry in a subset of 25 COVID- 19 convalescent and 28 control donors. The sP-sel plasma concentration was determined in a total of 704 samples by using a commercial ELISA. Result(s) In vitro platelet function was comparable in COVID-19 convalescent and control donors at T1 (3-9 months after disease diagnosis). Plasma samples from COVID-19 convalescent donors revealed a significantly higher sP-sel level compared to controls at T1 (1.05 +/- 0.42 ng/mL vs. 0.81 +/- 0.30 ng/mL;p<0.0001) and at T2 (0.96 +/- 0.39 ng/mL vs. 0.83 +/- 0.38 ng/mL;p=0.0098). At T3 the sP-sel plasma level was comparable in both study groups. Most of the COVID-19 convalescent donors showed a continuous decrease of sP-sel from T1 to T3. Conclusion(s) Increased sP-sel plasma concentration as a marker for platelet activation could be demonstrated even weeks after moderate COVID- 19, whereas, in vitro platelet function was comparable with non-infected controls. We conclude that COVID-19 and additional individual factors could lead to an increase of the sP-sel plasma level.