Platelet and monocyte antigenic complexes in the pathogenesis of heparin-induced thrombocytopenia (HIT).

Published

Journal Article (Review)

Heparin-induced thrombocytopenia (HIT) is an iatrogenic disorder that occurs in a small subset of patients receiving heparin. Twenty-five per cent (or higher) of affected patients develop limb or life-threatening thrombosis. The effectiveness of therapy is incomplete and may be complicated by bleeding. HIT is caused by antibodies that recognize the platelet chemokine, Platelet Factor 4 (PF4), complexed to heparin or to cellular glycosaminoglycans (GAGs). However, antibodies with the same apparent specificity are found in many more patients without clinical disease and the reason why so few develop HIT is uncertain. We propose that HIT antibodies recognize cell surface PF4/GAG complexes on intravascular cells, including platelets and monocytes that are dynamic and mutable. Heparin removes cell surface-bound PF4 in most individuals, but removal is incomplete in those with high pre-exposure surface-bound PF4 levels. Such individuals retain critically localized cellular antigenic complexes at the time antibodies develop and are at risk to develop HIT. This article reviews the scientific basis for this model and its clinical implications.

Full Text

Duke Authors

Cited Authors

  • Rauova, L; Arepally, G; McKenzie, SE; Konkle, BA; Cines, DB; Poncz, M

Published Date

  • July 2009

Published In

Volume / Issue

  • 7 Suppl 1 /

Start / End Page

  • 249 - 252

PubMed ID

  • 19630810

Pubmed Central ID

  • 19630810

Electronic International Standard Serial Number (EISSN)

  • 1538-7836

Digital Object Identifier (DOI)

  • 10.1111/j.1538-7836.2009.03373.x

Language

  • eng

Conference Location

  • England