Abstract
Coronavirus Disease 2019 (COVID-19), caused by the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), has affected over 30 million globally to date. Although high rates of venous thromboembolism and evidence of COVID-19-induced endothelial dysfunction have been reported, the precise aetiology of the increased thrombotic risk associated with COVID-19 infection remains to be fully elucidated. Therefore, we assessed clinical platelet parameters and circulating platelet activity in patients with severe and nonsevere COVID-19. An assessment of clinical blood parameters in patients with severe COVID-19 disease (requiring intensive care), patients with nonsevere disease (not requiring intensive care), general medical in-patients without COVID-19, and healthy donors was undertaken. Platelet function and activity were also assessed by secretion and specific marker analysis. We demonstrated that routine clinical blood parameters including increased mean platelet volume (MPV) and decreased platelet:neutrophil ratio are associated with disease severity in COVID-19 upon hospitalisation and intensive care unit (ICU) admission. Strikingly, agonist-induced ADP release was 30- to 90-fold higher in COVID-19 patients compared with hospitalised controls and circulating levels of platelet factor 4 (PF4), soluble P-selectin (sP-selectin), and thrombopoietin (TPO) were also significantly elevated in COVID-19. This study shows that distinct differences exist in routine full blood count and other clinical laboratory parameters between patients with severe and nonsevere COVID-19. Moreover, we have determined all COVID-19 patients possess hyperactive circulating platelets. These data suggest abnormal platelet reactivity may contribute to hypercoagulability in COVID-19 and confirms the role that platelets/clotting has in determining the severity of the disease and the complexity of the recovery path.
Highlights
Over 30 million people globally have been infected since the outbreak of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) in December 2019, with over 1 million fatalities reported to date [1]
Higher levels of D-dimer were observed on the day of hospital admission among the patients who subsequently developed severe COVID-19 in comparison (p = 0.0.012) to that observed in the nonsevere COVID-19 group (1.01 ± 0.75 mg/ L) (Table 1)
We have demonstrated that distinct platelet-related patterns in full blood count and other clinical laboratory parameters appear to be associated with the development of a more severe disease course in our cohort of COVID-19 patients, reflecting other recently published data [2,46,51]
Summary
Over 30 million people globally have been infected since the outbreak of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) in December 2019, with over 1 million fatalities reported to date [1]. Coronavirus Disease 2019 (COVID-19) is characterised by a marked pro-inflammatory response with fever, elevated inflammatory markers, and clinical and radiological features of pneumonitis being evident among affected individuals [2]. A complex interplay is known to exist between pro-inflammatory pathway activity and blood coagulation activation; this interplay appears to represent a source of morbidity among SARS-CoV-2–infected patients, among those with severe disease [3]. High levels of venous thromboembolism (VTE) [4,5,6,7,8,9,10] have been reported in this patient group and levels of D-dimer (a marker of increased blood coagulation activation) have been shown to correlate with disease severity and appear to be predictive of mortality [11,12]. Recent postmortem studies have shown evidence of widespread thrombosis in pulmonary vasculature and other organs [17,18]
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