Heparin‐induced Thrombocytopenia: Effect of Heparin Platelet Antibody on Platelets

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Abstract
The plasma of 2 patients with heparin-induced thrombocytopenia caused platelet aggregation in the presence of heparin. The platelet aggregating factor was isolated in the IgG fraction of the patients'' sera suggesting that it was an antibody. This heparin anti-platelet antibody (HAP-Ab) induced platelet aggregation and release but did not cause platelet lysis, although it fixed complement. Platelet aggregation was inhibited by EDTA and by inactivation of complement. There was a significant production of malondialdehyde (MDA) and thromboxane B2 (TXB2) implying a role of the prostaglandin synthesis pathway in HAP-Ab induced aggregation. ADP release was also involved as apyrase blocked aggregation while hirudin, a thrombin inhibitor, had no effect. The thrombotic complications recently reported in patients with heparin-induced thrombocytopenia may be explained by some effects of HAP-Ab on platelets: antibody mediated platelet factor 3 release, prostaglandin endoperoxides and thromboxane A2 (TXA2) production and platelet aggregation in vivo. These HAP-Ab mediated effects were inhibited by anti-platelet drugs such as aspirin, indomethacin and dipyridamole and may have therapeutic implications.

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