In a patient with suspected antiphospholipid syndrome, the activated partial thromboplastin time is prolonged and does not correct with a 1:1 mix with normal plasma. Why does the same patient suffer venous thrombosis despite this laboratory 'anticoagulant' effect?

• A The antibody inhibits factor VIII in vivo but not in vitro
• B The antibody binds tissue plasminogen activator, causing fibrinolysis resistance
• C The antibody degrades protein C rapidly in vivo
• D The antibody interferes with phospholipid-dependent clotting tests in vitro while activating platelets and endothelium in vivo ✓

Explanation

Lupus anticoagulant antibodies bind phospholipid-bound proteins such as beta2-glycoprotein I, prolonging phospholipid-dependent assays like aPTT and failing to correct on mixing because the antibody persists in vitro. In vivo the same antibodies activate endothelium, platelets, and complement, tipping the balance to thrombosis. This paradox of bleeding tests with clotting behaviour is the defining feature tested here.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.