Study of Platelet Aggregation Function in Children Undergoing COVID-19. Initial Results

Background. There is evidence that platelet dysfunction in new-type coronavirus infection can lead to both thrombotic and hemorrhagic events: hypercoagulation syndrome leading to thrombosis is one of the most threatening complications of COVID-19; equally important is the hemorrhagic syndrome that can be observed after this disease. The study of platelet aggregation function in children with new-onset coronavirus infection is highly relevant: the results of aggregometry in pediatric practice may help to predict the development of complications from vascular and platelet hemostasis.

Aims — to evaluate the direction of changes in platelet haemostasis in children undergoing COVID-19.

Methods. In the first phase of the work, we clarified the normal values of platelet aggregation in children with different inducers in whole blood by impedance testing (based on examination data from 105 conditionally healthy children who had not had COVID-19). At the second (main) phase of the study we conducted a single-stage prospective study including 250 pediatric patients residing in the Russian Federation: 143 children suffered mild COVID-19, while the comparison group consisted of 107 patients who had not been ill with a new-type coronavirus infection. All children (those who had COVID-19 and those who had no disease) underwent a comprehensive examination, which included: physical examination, aggregometry and laboratory tests (to rule out acute inflammatory process and hemogram abnormalities potentially affecting platelet aggregation rates).

Results. Almost half of the patients after COVID-19 had platelet aggregation abnormalities. At the same time, in every third child there were combined multidirectional disorders in the form of hypo- and hyperaggregation with different inducers, in contrast to the group of children who did not have COVID19 (p < 0.05). In the COVID19 group aggregation abnormalities with arachidonic acid were most frequently detected: almost every second patient had hyperaggregation and every fourth patient had hypoaggregation, which was statistically significantly different from the non-disease group (p < 0.05). Analysis of the results depending on the time interval after the disease (1–3 months, 3–6, 6–12 months, more than 12 months) showed platelet hyperaggregation with all inducers at 1–3 months, and there was a tendency to reduce aggregation with thrombin and ADP, but hyperaggregation with arachidonic acid persisted for one year after the disease. At an interval of more than one year after COVID-19 every second patient showed a decrease in platelet function (hypoaggregation with all inducers). No statistically significant differences by gender were observed depending on the time interval after the infection.

Conclusions. The results of the study demonstrate the vectors of impaired vascular and platelet hemostasis in children with mild COVID-19: The time intervals of platelet dysfunction after the disease have been determined. The results of the study may help to develop a surveillance strategy for children who have had a new type of coronavirus infection to prevent the development of complications from vascular and platelet hemostasis.