CLINICAL APPROACH TO HEPARIN-INDUCED THROMBOCYTOPENIA

Abstract number: SYM-W-055

Alberio¹ L.

¹Division of Haematology and Central Haematology Laboratory, Inselspital, University of Berne, Berne, Switzerland

How-to-cite Alberio L. CLINICAL APPROACH TO HEPARIN-INDUCED THROMBOCYTOPENIA. J Thromb Haemost 2007; 5 Supplement 2: SYM-W-055

Abstract

Heparin-induced thrombocytopenia (HIT) represents a biologically fascinating and clinically challenging haemostatic paradox: Patients anticoagulated with (unfractionated or low molecular weight) heparin develop thrombocytopenia and yet, instead of bleeding, they suffer from an increased thrombotic risk, threatening their limbs and lives. This is caused by an immune reaction leading to the formation of ternary complexes (heparin/PF4/HIT-antibodies), that activate platelets by cross-linking their Fc-gamma receptors. The final steps of the pathogenic sequence lead to platelet aggregation and procoagulant activity with unbalanced in vivo thrombin generation.

Because of the protean clinical manifestations (e.g. "typical", "early", "delayed-onset") the primary challenge for the clinician is to think of HIT as a possible reason for the clinical problem of the patient he/she is caring for. Then, when HIT is clinically suspected, the pre-test probability (4⁺¹ T) should be assessed before performing laboratory assays and combined with the quantitative test result in order to confirm or refute the diagnosis of HIT. Functional platelet activation assays have a high specificity for clinically relevant HIT antibodies (abs). Immunoassays are much more sensitive but detect non-pathogenic abs as well. However, their specificity can be increased either by detecting only IgG-abs and/or by considering the magnitude of a positive result.

Treatment of HIT resides on following principles. 1) Stop heparin, 2) Administer an alternative anticoagulant (Approved: lepirudin, argatroban, danaparoid. Hypothetical: fondaparinux?), 3) Postpone Vitamin K antagonists (VKA) until the platelet count has substantially recovered, 4) Individualized decision regarding the length of therapeutic anticoagulation with VKA, 5) Since HIT abs are transient, HIT patients can be re-treated with heparin provided that the previous heparin treatment is remote (> 100 days) and that anti-heparin/PF4 abs are undetectable.

To cite this abstract use the following format:

Journal of Thrombosis and Haemostasis 2007; Volume 5, Supplement 2: abstract number

Session Details

Date:	01/08/2007
Time:	00:00-00:00
Session name:	XXIst ISTH Congress
Subject:
Location:	Oxford, UK
Presentation type:
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