Platelets and Thrombotic Antiphospholipid Syndrome

Ibrahim Tohidi-Esfahani; Prabal Mittal; David Isenberg; Hannah Cohen; Maria Efthymiou

doi:10.3390/jcm13030741

Platelets and Thrombotic Antiphospholipid Syndrome

J Clin Med. 2024 Jan 27;13(3):741. doi: 10.3390/jcm13030741.

Authors

Ibrahim Tohidi-Esfahani^{1

2}, Prabal Mittal^{3

4}, David Isenberg⁵, Hannah Cohen^{3

4}, Maria Efthymiou⁴

Affiliations

¹ Haematology Department, Concord Repatriation General Hospital, Sydney, NSW 2139, Australia.
² Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, NSW 2050, Australia.
³ Department of Haematology, University College London Hospitals NHS Foundation Trust, London NW1 2BU, UK.
⁴ Haemostasis Research Unit, Department of Haematology, University College London, London WC1E 6DD, UK.
⁵ Centre for Rheumatology, Division of Medicine, University College London, London WC1E 6JF, UK.

Abstract

Antiphospholipid antibody syndrome (APS) is an autoimmune disorder characterised by thrombosis and the presence of antiphospholipid antibodies (aPL): lupus anticoagulant and/or IgG/IgM anti-β2-glycoprotein I and anticardiolipin antibodies. APS carries significant morbidity for a relatively young patient population from recurrent thrombosis in any vascular bed (arterial, venous, or microvascular), often despite current standard of care, which is anticoagulation with vitamin K antagonists (VKA). Platelets have established roles in thrombosis at any site, and platelet hyperreactivity is clearly demonstrated in the pathophysiology of APS. Together with excess thrombin generation, platelet activation and aggregation are the common end result of all the pathophysiological pathways leading to thrombosis in APS. However, antiplatelet therapies play little role in APS, reserved as a possible option of low dose aspirin in addition to VKA in arterial or refractory thrombosis. This review outlines the current evidence and mechanisms for excessive platelet activation in APS, how it plays a central role in APS-related thrombosis, what evidence for antiplatelets is available in clinical outcomes studies, and potential future avenues to define how to target platelet hyperreactivity better with minimal impact on haemostasis.

Keywords: antiphospholipid antibodies; antiphospholipid syndrome; antiplatelets; platelets; thrombosis.

Publication types

Review

Grants and funding

This research received no external funding. I.T.-E. was supported by a Haematology Society of Australia and New Zealand New Investigator Clinical Fellowship.