A patient with systemic lupus erythematosus (SLE) has recurrent thromboses and recurrent foetal loss. Serological tests show prolonged APTT (not corrected by mixing study), anti-cardiolipin antibodies (IgG, high titre), and positive lupus anticoagulant. What mechanism underlies the thrombotic tendency in this patient?

• A Reduced production of coagulation factors due to liver disease in SLE
• B Type I hypersensitivity reaction causing mast cell degranulation and platelet aggregation
• C Antiphospholipid antibodies bind to beta-2 glycoprotein I on phospholipid surfaces of platelets/endothelium, promoting platelet activation, tissue factor expression, and inhibition of protein C pathway — thrombogenic state ✓
• D Complement-mediated lysis of endothelial cells exposing subendothelial collagen

Explanation

Antiphospholipid syndrome (APS) is characterised by antiphospholipid antibodies (aPL) — including anti-cardiolipin antibodies, lupus anticoagulant, and anti-beta-2 glycoprotein I antibodies. These antibodies bind to beta-2 glycoprotein I on phospholipid-rich surfaces, activating platelets, inducing endothelial tissue factor expression, and inhibiting the protein C anticoagulant pathway — creating a prothrombotic state. Paradoxically, the in vitro APTT is prolonged (aPL interferes with phospholipid-dependent clotting assays) but in vivo thrombosis occurs. Recurrent arterial/venous thrombosis and obstetric complications (fetal loss) are the hallmark clinical features.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.