Thromb Haemost 2005; 94(01): 132-135
DOI: 10.1160/TH04-12-0825
Platelets and Blood Cells
Schattauer GmbH

Clinical features of heparin-induced thrombocytopenia including risk factors for thrombosis

A retrospective analysis of 408 patients
Andreas Greinacher
1   Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald, Germany
,
Beate Farner
1   Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald, Germany
,
Hartmut Kroll
2   Institut für Klinische Immunologie und Transfusionsmedizin, Justus-Liebig-Universität Giessen, Germany
,
Thomas Kohlmann
3   Institut für Community Medicine, Ernst-Moritz-Arndt Universität Greifswald, Germany
,
Theodore E. Warkentin
4   Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
,
Petra Eichler
1   Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald, Germany
› Author Affiliations
Financial support: This study has been supported by the Deutsche Forschungsgemeinschaft Gr 1096/2–4; by the German Federal Ministry for Education and Research (NBL3 program, reference 01 ZZ 0103); and from the German Federal Ministry for Education and Research (CAN04/006; NBL3 program, reference 01-ZZ0103) and is part of the research activities of the Department of Cardiovascular Medicine at the Medical Faculty of the Ernst-Moritz-Arndt-University-Greifswald.
Further Information

Publication History

Received 20 December 2004

Accepted after resubmission 20 April 2005

Publication Date:
05 December 2017 (online)

Summary

Immune mediated heparin induced thrombocytopenia (HIT) is a prothrombotic adverse effect of heparin. However, only a subgroup of patients with HIT develops thromboembolic complications. We aimed to identify risk factors for developing HITassociated thrombosis. We analyzed a registry of patients with clinical suspicion of HIT who tested positive using a sensitive functional assay. Patient information was obtained by a standardized questionnaire. By multivariate analysis the association of age, gender, type of patient population, and magnitude of the platelet count decline with the frequency, type (venous or arterial), and temporal pattern of thrombotic events was assessed. In 408 HIT patients we observed predominance of venous thrombosis (2.4:1), with 40% of patients developing a pulmonary embolism. However, in the subgroup of post-cardiovascular surgery patients there was predominance of arterial thrombosis (1:8.5). The type of arterial thrombosis (limb artery thrombosis > thrombotic stroke > myocardial infarction) was the converse of that observed with typical atherothrombotic clots in non-HIT populations. In 59.8% of patients HIT-related thrombosis manifested either on the same day a platelet count decrease >50% was documented (26.3%) or before the decrease in platelet counts (33.5%).The most important risk factors for thrombosis were orthopedic/trauma surgery and the magnitude of platelet count decrease. HIT-associated thrombosis occurs in a considerable proportion of patients before platelet counts decrease by more than 50%.

* The sponsors of the study had no role in study design, data analysis or interpretation, or the writing of the report. None of the authors declare a conflict of interest or financial interest.


 
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