Semin Thromb Hemost 2021; 47(05): 506-511
DOI: 10.1055/s-0041-1725098
Review Article

Impaired Fibrinolysis in the Antiphospholipid Syndrome

Aleksandra Antovic
1   Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden
2   Division of Rheumatology, Karolinska University Hospital, Stockholm, Sweden
,
Maria Bruzelius
1   Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden
3   Department of Hematology, Karolinska University Hospital, Stockholm, Sweden
› Author Affiliations

Abstract

The pathogenesis of the antiphospholipid syndrome (APS) is complex and involves the persistent presence of antiphospholipid antibodies (aPL) in the bloodstream causing a prothrombotic condition. aPL induce excessive activation of the endothelium, monocytes, and platelets in consort with aberrations in hemostasis/clotting, fibrinolytic system, and complement activation. Impaired fibrinolysis has been found in APS patients with thrombotic as well as obstetric manifestations. Increased levels of plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor, together with the presence of aPL against annexin-2, tissue-type plasminogen activator, and plasminogen contribute to the compromised fibrinolytic activity in these patients. Furthermore, unfavorably altered fibrin morphology, less amenable to fibrinolysis, has been proposed as a novel prothrombotic mechanism in APS. This review aims to summarize the present knowledge of the mechanisms involved in impaired fibrinolysis in APS patients. We also present a case from clinical practice as an illustration of fibrinolysis impairment in APS patients from a real-life setting.



Publication History

Article published online:
20 April 2021

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