: Thrombosis associated with thrombocytopenia is an apparent paradox that is present across a wide spectrum of disorders. While thrombocytopenia has been a controversial clinical classification criterion for antiphospholipid syndrome because initial reports failed to demonstrate a relation between low platelet count with other clinical or laboratory manifestations of the syndrome, recent data highlight the association between mild to moderate thrombocytopaenia and the risk of thrombosis. Although antiphospholipid antibodies may induce platelet activation in vitro, additional stimuli may contribute to their activation in vivo, amongst which reactive oxygen and nitrogen species and lipid peroxidation products, elevated in patients with the antiphospholipid syndrome: an excess of the same stimuli may induce megakaryocyte and platelet apoptosis that leads to decreased platelet production and increased destruction, exposure resulting ultimately in thrombocytopaenia. Herein we provide a novel plausible framework involving free radicals that could add to the understanding of the thrombocytopenia/thrombosis paradox in the antiphospholipid syndrome.
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