Table 1.

Treatment controversies and paradoxes in HIT and VITT.

Treatment controversy or paradox	Comment
Heparin vs non-heparin anticoagulation	Heparin may promote platelet activation if heparin-dependent antibodies are present (characteristic of HIT); however, VITT features PF4-dependent, rather than heparin-dependent, platelet activation (rather, heparin in pharmacological concentrations can inhibit VITT serum-induced platelet activation)
IVIG—prothrombotic or antithrombotic	IVIG inhibits platelet activation in HIT and VITT, and thus helps to deescalate antibody-induced hypercoagulability (in contrast, IVIG treatment of ITP and drug-induced ITP is rarely complicated by acute thrombosis)
Treatment of “isolated” HIT and VITT	As per recommendations for treatment of “isolated” HIT (ie, strongly suspected HIT without apparent thrombosis), patients with strongly suspected VITT recognized by thrombocytopenia alone should receive therapeutic-dose anticoagulation; high-dose IVIG is also indicated for VITT
Corticosteroid therapy	Corticosteroids decrease reticuloendothelial (macrophage) clearance of antibody-coated platelets, and thus their use could shift platelet clearance towards platelet activation (theoretical deleterious effect of corticosteroids)
Avoidance of vitamin K antagonist therapy in acute HIT and VITT	Increased risk of venous limb gangrene and skin necrosis due to depletion of protein C and ongoing thrombin generation

References for this table are found in the relevant sections of the text.