key: cord-0735690-ygc4yq77
authors: Mezgebe, Michael; Jacobson, Barry Frank; Mayne, Elizabeth Sarah; Louw, Susan
title: Change in platelet indices in patients with Coronavirus disease‐2019 (COVID‐19): A reflection of platelet activation and contribution to immunothrombosis?
date: 2021-09-24
journal: Int J Lab Hematol
DOI: 10.1111/ijlh.13705
sha: 9ea821dc71ae03409b713377e0c202c87c900aef
doc_id: 735690
cord_uid: ygc4yq77

In December 2019, several cases of pneumonia of unknown aetiology were reported in Wuhan, China. The causative Coronavirus was subsequently isolated and named the Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) and the disease, Coronavirus disease-2019 (COVID-19).1 COVID-19 related coagulopathy is a poor prognostic feature and reflects an underlying pathological process termed immunothrombosis.2 This process differs from infection-related disseminated intravascular coagulation (DIC) as it manifests primarily with thrombosis while thrombocytopenia and bleeding remain modest.3 The coagulation activation in COVID-19 relates to endothelial dysfunction, complement activation and ensuing cytokine storm with contributions from secondary infections and organ dysfunction.1,2 D-dimer values above 0.5 mg/L signifies poor patient outcomes.

while thrombocytopenia and bleeding remain modest. 3 The coagulation activation in COVID-19 relates to endothelial dysfunction, complement activation and ensuing cytokine storm with contributions from secondary infections and organ dysfunction. 1,2 D-dimer values above 0.5 mg/L signify poor patient outcomes. 3, 4 Platelets are essential for normal haemostasis and become activated when exposed to the sub-endothelial matrix at sites of vessel injury with the formation of platelet plugs, which support coagulation factor rich thrombi. 5 Platelets are however also inflammatory cells with key innate and adaptive functions displaying several pattern recognition receptors (PRR) and serve as first-line responders in the defence against pathogens, including viruses. 6 Viral infections cause platelet activation through different pathophysiological processes including direct interactions with the viral pathogen, effects of inflammatory mediators such as interleukin-3 and interleukin-6 and exposure to viral antigen-antibody complexes. 6 Platelets in turn release chemokines which promote endothelial signalling and leukocyte tissue migration. 6 There are several ways to monitor platelet activation in the laboratory including flow cytometric analysis of platelet activation markers. Platelet activation however also alters routine laboratory platelet indices such as mean platelet volume (MPV), platelet-large cell ratio (P-LCR), platelet distribution width (PDW) and platelet crit (PCT). 7 A proportion of platelets also consists of "young," hyper-reactive reticulated platelets, which can be quantified in the laboratory as the immature platelet fraction (%IPF). 8 Changes in these indices reflect an increased average size and density of platelets as the proportion of immature platelets with greater prothrombotic activity increases in response to infection. 7, 9 Deranged laboratory platelet parameters reflecting platelet activation are potential prognostic biomarkers in multiple disease processes including malignancies, critical illness and venous and arterial thromboses. 10 The role of platelets in COVID-19-related immunothrombosis is an area of active research and thrombocytopenia is a biomarker of poor outcome and increased disease severity. 2, 8 The current study aimed to determine whether changes in 

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