Venous thromboembolism in COVID-19 and inherited thrombophilia

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In December 2019, the first cases of a severe acute respiratory syndrome caused by coronavirus 2 (SARS-CoV-2; COVID-19) were detected in Wuhan, China.1 SARS-coV-2 is a highly infectious virus which leads to heterogeneous clinical manifestations.1 Some individuals remain asymptomatic, while others, especially individuals with comorbidities, are more prone to develop severe manifestations of the disease.2 SARSCoV-2 leads to extensive inflammation, endothelial damage, platelet activation and hypercoagulability, characterizing a prothrombotic state.2 Advanced age, diabetes, obesity and hypertension are associated with a higher risk of thromboembolic complications in COVID-19.2 However, little is known about potential interaction between COVID-19 and hereditary thrombophilia and its effect on thrombotic risk.3 Antithrombin (AT) is a physiological inhibitor of coagulation, mainly of thrombin, but also of factors Xa, IXa and others.4 AT deficiency is an autosomal dominant hereditary disorder, with variable penetrance and equal distribution between sexes.4 Patients with AT deficiency are at significantly increased risk of thromboembolism, especially venous (VTE).4 Of all hereditary thrombophilias, AT deficiency is the one with the highest risk of VTE.4 The aim of this article is to report a case of a young man with AT deficiency and prothrombin mutation G20210A who, 7 days after the onset of COVID-19, developed an episode of deep venous thrombosis (DVT) in the right leg.

Abstract

Assunto

Tromboembolia Venosa, COVID-19

Palavras-chave

Venous thromboembolism, Inherited thrombophilia, COVID-19

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Endereço externo

https://www.sciencedirect.com/science/article/pii/S2531137922013074?via%3Dihub

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