Evidence of Thrombogenesis Recurrence Induced by IgA Antiphospholipid Antibody β2 Glycoprotein I-Dependent in Early Adulthood.

Antiphospholipid antibodies (aPLs) against Beta-2 glycoprotein-I (βGPI) are considered to be the center of pathogenesis of antiphospholipid syndrome (APS). Autoimmune aPLs are pathogenic as patients are at increased risk of enhancing thrombin generation at a young age. There are only three aPLs considered as diagnostic laboratory markers for APS - IgM, IgG, and IgA isotypes. However, the association of the IgA isotypes with clinical thrombosis remains highly controversial. A 30-year-old male with a past medical history of childhood asthma initially presented to the hospital with acute left middle cerebral artery ischemic stroke, which did not get resolved with tissue plasminogen activator (tPA) but was successfully resolved with thromboembolectomy. It was speculated to be associated with a clot from mitral valve prolapse found subsequently on echocardiogram. Twenty-eight days later, the patient presented again with a high-grade luminal narrowing of his mid- and distal left internal carotid artery with 80% narrowing and an acute dissection of his left internal carotid artery. The recurrence of thrombosis was evaluated through hypercoagulable state workup, which demonstrated evidence of antiphospholipid syndrome with elevated beta-2 glycoprotein IgA antibody titers of more than 150 U/mL. This is one of the first cases reported nationwide as evidence of thrombogenesis recurrence induced by IgA antiphospholipid antibody β glycoprotein I-dependent in early adulthood. IgA anti- βGPI antibodies are found to have an association with many clinical manifestations of antiphospholipid syndrome and thrombotic events, particularly arterial thrombosis. To determine the link between the IgA-aβGPI antibodies and APS-events in asymptomatic individuals before recommending preventive treatments, there needs to be a broader intention to standardize IgA-aβGPI assays as a diagnostic criterion for APS.