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RASSEGNE - Reviews

Volume:

Biochimica Clinica 2020; 44(4) 015-016

Pubblicato on-line:

June 1, 2020

DOI:

10.19186/BC_2020.056

Scarica in PDF:

Alterazioni dei meccanismi dell’emostasi in corso di infezione da SARS-CoV-2 (COVID-19)
Alterations of hemostasis during SARS-CoV-2 infection (COVID-19)

AUTORI

Benedetto Morelli1*, Barbara Montaruli2*, Mario Bazzan3*, Paola Calzoni4*, Paolo Fassina5*, Paola Pradella6, per il Gruppo di Studio SIBioC Emostasi*
1Synlab Castenedolo, Castenedolo (BS)
2Laboratorio Analisi Chimico Cliniche e Microbiologiche, Azienda Ospedaliera Ordine Mauriziano, Torino
3CMID, Centro Malattie Rare, San Giovanni Bosco, Torino
4Laboratorio Patologia Clinica, Azienda Ospedaliera Universitaria Senese, Siena
5Servizio di Medicina di Laboratorio, ULSS7 Pedemontana, Santorso, Vicenza
16Servizio di Medicina Trasfusionale, Azienda Sanitaria Universitaria Integrata, Trieste

ABSTRACT

Alterations of hemostasis during SARS-CoV-2 infection (COVID-19)

The corona virus infection (named COVID-19), first identified in December 2019 in Wuhan, China, has contributed to significant mortality in several countries with the number of infected cases increasing exponentially worldwide, in particular in Italy and in the USA. The majority of the most severely ill patients initially presents with single organ failure (i.e. severe respiratory syndrome), but some of them progress to more systemic disease and multiple organ failure (MOF). One of the most significant poor prognostic features in these patients is the development of coagulopathy, similarly to patients who develop sepsis from various infectious agents. Coagulopathy in patients with COVID-19 may be asymptomatic but, in some cases, the septic state may evolve into Sepsis-Induced Coagulopathy (SIC) and overt Disseminated Intravascular Coagulopathy (DIC). In patients with severe clinical manifestations, a cytokine storm occurs that contributes to triggering a greater imbalance of the hemostatic mechanisms by promoting the development of microthrombosis at the level of the pulmonary endothelium. The effectiveness of anticoagulant therapies, performed primarily with low-molecular weight heparin, is greater the earlier the diagnosis is made. This is possible through the adoption of diagnostic protocols that include laboratory tests and clinical scores. The laboratory tests suggested for this purpose by the available Guidelines are prothrombin time, platelet count, D-dimer and fibrinogen. D-dimer appears to be the parameter with the greatest prognostic significance since it also allows a stratification of the thrombotic risk.

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