Antiplatelet factor 4-heparin antibodies in patients with antiphospholipidantibodies

Citation
Me. Martinuzzo et al., Antiplatelet factor 4-heparin antibodies in patients with antiphospholipidantibodies, THROMB RES, 95(6), 1999, pp. 271-279
Citations number
27
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
THROMBOSIS RESEARCH
ISSN journal
00493848 → ACNP
Volume
95
Issue
6
Year of publication
1999
Pages
271 - 279
Database
ISI
SICI code
0049-3848(19990915)95:6<271:AF4AIP>2.0.ZU;2-G
Abstract
Antibodies directed against platelet factor 4-heparin are present in patien ts with heparin-induced thrombocytopenia (HIT). Additionally, it has been s uggested that heparin can be an antigenic target of antiphospholipid antibo dies (aPL). We investigated the presence of heparin-platelet factor 4-induc ed antibodies (HPIA) in 33 patients with aPL, There were 30 patients with l upus anticoagulant, 25 with anticardiolipin antibodies, 21 with anti-beta(2 ) glycoprotein I, and 18 with antiprothrombin antibodies. 20 patients had a history of thrombosis and 19 had received heparin during the last 60 month s. We found 7 (21.2%) who had HPIA; 5 of them also had anti-beta(2) glycopr otein I antibodies. Four patients had severe thrombocytopenia and suspicion of HIT. Among them, two presented high positive HPIA results, one of them with positive platelet aggregation test. The third patient showed grey zone HPIA and borderline aggregation test and the fourth one had negative resul ts. Among patients without a history of HIT, 2 who had never received hepar in presented high positive, one a moderate positive, and one a grey zone HP IA result; all of them with negative aggregation tests. Five positive sera samples were incubated with cardiolipin liposomes in the presence of beta(2 ) glycoprotein I, and whereas an inhibition greater than 50% was achieved i n anticardiolipin and anti-beta(2) glycoprotein I activities, HPIA results did not change. We demonstrate that HPIA could be frequently found in patie nts with aPL, They are responsible for HIT in some cases but can also be fo und in patients who have not received heparin. Whether they predispose pati ents with aPL to HIT is not known; nevertheless, a close follow-up of hepar in treatment in these patients seems to be mandatory. (C) 1999 Elsevier Sci ence Ltd. All rights reserved.