Heparin-induced thrombocytopenia: molecular pathogenesis.

Abstract:

:Heparin-induced thrombocytopenia (HIT) is a common and often serious complication of heparin therapy [1,2]. Although the reduction in platelet levels associated with HIT is usually not severe, about 10% of patients experience arterial and/or venous thromboses (HITT), which can be incapacitating or fatal [3]. Recent work done in our laboratory [4] and by others [5-7] has shown that patients with HIT/T* almost invariably have antibodies specific for complexes consisting of heparin and platelet factor 4 (PF4), a heparin-binding protein found normally in platelet alpha granules. We [4] and others [8] have developed hypotheses to explain how these antibodies cause HIT/T in patients given heparin, but knowledge of the disease process is far from complete. An unusual feature of HIT/T is that antibodies important in pathogenesis are specific for complexes made up of two normal body constituents: PF4 and heparin. These antibodies are produced by a high percentage of certain patient populations treated with heparin, but only a minority of antibody formers are adversely affected. We postulate that a fuller understanding of the molecular basis for this immune response could lead to improved diagnosis, treatment and prevention of HIT/T and to the identification of risk factors that predispose to this complication.

journal_name

Int J Hematol

authors

Lee SH,Liu CY,PaoloVisentin G

doi

10.1007/BF03165283

subject

Has Abstract

pub_date

2002-08-01 00:00:00

pages

346-51

eissn

0925-5710

issn

1865-3774

journal_volume

76 Suppl 1

pub_type

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