Iintroduction

Almost as soon as heparin was introduced into clinical medicine, the new drug was reported to cause immediate small, but consistent, reductions in platelet count (Sappington, 1939). Later it was also found to produce platelet dysfunction (Heiden et al., 1977), accounting for at least some of its hemorrhagic risk (Hirsh, 1984; John et al., 1993). These effects, which most likely result from direct contact between heparin and platelets, are distinct from the role heparin plays in immune-mediated, heparin-induced thrombocytopenia (HIT). However, direct heparin-platelet binding is critical in the pathogenesis of HIT as well (Horne and Hutchison, 1998). Therefore, the various "nonimmune" heparin-platelet interactions will be reviewed.

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