Antiphospholipid syndrome (APS) and Heparin-induced Thrombocytopenia (HIT)

Both have antibodies that target vascular sites and platelets.

Antibodies in both processes induce a hypercoagulable state, inflammation, thrombocytopenia, and thrombosis.

Both processes are autoimmune in nature.

In both disorders the antibody targets a bound protein.

Cryptic epitopes on the protein beta-2-GPI for APS and PF4 for HIT are exposed after it binds with a natural substrate, that is phospholipid for APS and heparin for HIT.

The new epitopes induce antibody formation, and the antigen-antibody complex bind to and activates Fc gamma IIa receptors causing platelet activation and endothelial vascular perturbations.

In both cases there is enhanced thrombin generation.

In both cases there is a significant increase in platelet activation.

In both cases there are increased levels of soluble thromobomodulin and tissue factor.

Thromobomodulin levels are higher in HIT than APS and tissue factor levels are higher in APS than in HIT patients.

Both processes share increased vascular damage caused by excess immune complex formation leading to thrombin generation and thrombosis.

Both processes associated with platelet activation, fibrinolysis defect and thrombin generation.

Both processes have poor correlation in clinical laboratory testing and clinical findings.

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