PATHOMORPHOLOGICAL ASPECTS OF HEPARIN-INDUCED THROMBOCYTOPENIA-II (HIT-II SYNDROME)

The therapeutic use of heparin results in thrombocytopenia in 5-30% of patients. In 0.1-1% of patients treated with heparin, the platelet co unt decreases to between 100 x 10(9)/1 and 50 x 10(9)/1 and leads to s evere synchronous central arterial and venous thrombosis with a mortal ity of 18-36%. This is known as ''white-clot syndrome'' or heparin-ind uced thrombocytopenia II (HIT-II syndrome). Whilst the clinical aspect s and the central type of thrombosis in HIT-II syndrome are well docum ented, the histomorphology and differential diagnosis of thrombosis ar e not. We report three cases of HIT-II syndrome with thrombosis of the central arteries and veins. The HIT-II thrombi could be differentiate d from thrombi of other origins, particularly from mural thrombi. Hepa rin-induced thrombi were seen on microscopical examination to be like onion skin in structure, and immunohistochemistry showed that they had a markedly reduced content of fibrin and clearly enhanced amounts of IgG and IgM. The layered structure thus implied appositional growth. T he thrombi in HIT-II syndrome do not seem to be induced by activation of the coagulation cascade, but by platelet aggregation mediated by an ti-platelet antibodies.