The plasma of two patients with heparin-induced thrombocytopenia has been shown to cause platelet aggregation in the presence of heparin. The platelet aggregating factor was isolated in the IgG reaction 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 also appeared to be involved as apyrase blocked aggregation while hirudin, a thrombin inhibitor, had no effect. The thrombotic complications that have recently been reported in patients with heparin-induced thrombocytopenia may be explained by some effects of HAP-Ab on platelets, namely: the antibody mediated platelet factor 3 release, prostaglandin endoperoxides and thromboxane A2 (TXA2) production and platelet aggregation in vivo. These HAP-Ab mediated effects could be inhibited by anti-platelet drugs such as aspirin, indomethacin and dipyridamole and thus may have therapeutic implications.

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Surgically removed spleens from 14 subjects were perfused to determine their platelet content. Some patients had Cr51 labeled platelets prior to surgery, and radioactive platelet recoveries were also obtained. A sizable pool of splenic platelets has been demonstrated, which seems dependent on splenic size only. Increase in size of this pool in splenomegaly (and not suppression of thrombopoiesis) may be the sole reason for thrombocytopenia. A dynamic exchange between splenic and circulating platelets appears to be present. Awareness of the existence of a splenic platelet pool is important in considering variation in platelet survival and other platelet dynamic studies, especially in the presence of splenomegaly.