Heparin-induced thrombocytopenia (HIT) type II is paradoxically associated with thrombosis rather than bleeding. The antibody involved targets:

• A IgG antibodies against the GP IIb/IIIa receptor–fibrinogen complex on platelets
• B IgM antibodies against thrombin-heparin complexes, consuming thrombin
• C IgG antibodies against the complex of heparin and platelet factor 4 (PF4), activating platelets via FcgammaRIIA receptors ✓
• D IgG antibodies against antithrombin, reducing its heparin-binding capacity

Explanation

In HIT type II, the immune system generates IgG antibodies against the complex of PF4 (a platelet alpha-granule protein) bound to heparin. These antibody–PF4–heparin complexes bind to FcγRIIA (Fc receptor) on platelets, causing widespread platelet activation, aggregation, and thrombocytopenia. Paradoxically, activated platelets release more PF4 and generate thrombin, precipitating a hypercoagulable, prothrombotic state (venous and arterial thrombosis). Management requires stopping heparin and starting a non-heparin anticoagulant (argatroban, fondaparinux, or a DOAC).

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.