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Heparin‐induced Thrombocytopenia: Effect of Heparin Platelet Antibody on Platelets
Author(s) -
Chong B. H.,
Grace C. S.,
Rozenberg M. C.
Publication year - 1981
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1981.tb07261.x
Subject(s) - platelet , heparin , chemistry , platelet factor 4 , pharmacology , thrombin , thromboxane , hirudin , apyrase , platelet activation , heparin induced thrombocytopenia , immunology , biochemistry , medicine
S ummary . 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 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 B 2 (TXB 2 ) 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 A 2 (TXA 2 ) 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.