Abstract
Coronavirus disease (COVID-19) is threatened our societies and the need for personalized medicine and efficient drugs are compulsory. COVID-19 can lead to systemic coagulation activation and thrombotic complications. Excessive cytokine release and activation of coagulation are key drivers of COVID-19 pneumonia and associated mortality. Contact activation has been linked to pathologic upregulation of both inflammatory mediators and coagulation. Congenital factor XI (FXI) deficiency is more frequent than previously expected, as it has been demonstrated in numerous reports and all over the world. Although it was first described prevalent in exclusively etnias (Ashkenazy or Iraqi-Jewish), it seems to be misdiagnosed and not so exclusive, with a potential high prevalence at least in heterozygosis, also in Europe.[1] Moreover, acquired deficiency can occur with the presence of inhibitors or antibodies such as antiphospholipid as β2-glycoprotein I.[2] Whether or not COVID-19 contributing to the appearance of antiphospholipid antibodies, is still unclear and requires further studies.
Highlights
factor XI (FXI) is a pleiotropic molecule whose role is extended from coagulation to inflammation
FXI is involved in the inflammatory system as part of the contact activation pathway with FXII
The description and characterization of COVID-19 patients with congenital or acquired FXI deficiency, as the one presented by Andreani et al in this issue,4 could help to understand the disease and to identify new targets in this disease
Summary
FXI is a pleiotropic molecule whose role is extended from coagulation to inflammation. The main role in the clot cascade is to amplify the thrombin activation.
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