Do we need to worry about pre-existing heparin-induced thrombocytopenia antibodies in people admitted with pulmonary embolism / deep venous thrombosis? Or can we keep happily slinging heparin at first sight?
Warkentin et al analyze data from the Matisse VTE studies, which enrolled 3,994 patients with DVT or PE. All had ELISA HIT antibodies collected at entry, and 127 (3.2%) were “HIT-positive.” (Remember that you are not supposed to do this routinely due to the high false positive rate. Instead, use the 4Ts.) Only 14 of the 127 (0.4% of the 3,994) had the more specific platelet-activating antibodies.
Of those 14:
- 4 of the 4 who were treated with heparin developed HIT (but only one developed thrombosis – a recurrent DVT). 1 of the 4 was already thrombocytopenic at study entry.
- 10 of the 10 treated with fondaparinux had maintenance or improvement of their platelet count; 3 of the 10 were already thrombocytopenic at baseline.
So 1 of 3,994 people definitively had clinical HIT with thrombosis. (That person had been continued on heparin even after platelet counts fell, by the way.) CHEST 2011;140:366-373.
What do you think? Is the described risk of HIT worth doing what the implication is here — that we should test everyone for HIT antibodies, and probably use more fondaparinux?