Searches were limited to English language. We carried out a systematic search of the literature from Medline, Embase, PubMed, Web of Science, the Cochrane Central Register of Controlled Trials (CENTRAL) for all literature published up to 27th March 2021. The review is reported in line with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The aim of this rapid evidence review is to assess the potential association of increased MPV, PDW and P-LCR with disease severity and mortality in patients with COVID-19.Ī review protocol was published on PROSPERO (ID: CRD42021242848). Platelet morphological parameters include mean platelet volume (MPV), platelet distribution width (PDW) and platelet-large cell ratio (P-LCR) ( Table 1). There are several methods on automated analysers for measuring platelet size and count, including aperture impedance, optical scattering, and fluorescence. Platelet size can be assessed during a routine clinical blood test using automated haematology analysers. Ĭirculation of larger, younger platelets reflect platelets activity and seem to be useful predictors and prognostic biomarker of thrombotic events. While there are many methods used to test platelet activation for research purposes, most of the existing techniques are expensive, require trained personnel and take time to perform, limiting their use in clinical practice.
Platelet activation markers are useful tools in evaluating risk factors of thrombosis in a variety of clinical conditions such as acute myocardial infarction, atherosclerosis, type 2 diabetes mellitus and other inflammatory diseases. Since the lung is considered an active site of megakaryopoiesis, a prothrombotic status leading to platelet activation, aggregation and consumption may trigger a compensatory pulmonary response. Moreover, pulmonary megakaryocytes are increased in COVID-19 patients with acute lung injury. In addition, mild thrombocytopenia is observed in COVID-19 patients, and a progressive decline of platelet counts was significantly associated with increased mortality. Platelet hyperreactivity may contribute to immunothrombosis often seen in patients with COVID-19.
COVID-19 patients have higher levels of P-selectin expression in resting and activated platelets, elevated circulating platelet-leukocyte aggregates, increased aggregation, and thromboxane generation. Ĭirculating platelets play a central role in haemostasis and thrombosis, and platelets significantly contribute to immune responses during viral infection in a process termed “immunothrombosis”. Moreover, COVID-19 autopsies have shown evidence of widespread microthrombosis in the lungs and other organs. Unexpectedly high incidence of thrombosis have been reported, and severity of COVID-19 disease is associated with elevated inflammatory markers and markers of coagulation such as d-Dimer, fibrinogen and von Willebrand factor. Severe disease is predominantly observed in the elderly and those with underlying health conditions such as hypertension, diabetes and coronary heart disease. While most cases of COVID-19 are mild, some develop severe viral pneumonia with respiratory failure, that can result in death. Coronavirus disease 2019 (COVID-19) disease is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
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