Endothelial cell hyperplasia contributes to thrombosis in heparin- induced thrombocytopenia

Hau C. Kwaan*, Shumpei Sakurai

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Heparin-induced thrombocytopenia (HIT), a well recognized complication of heparin administration, is associated with thrombotic complications. An immunologic mechanism is believed to be responsible for the thrombocytopenia, but the cause of thrombosis is not fully understood. We report a histological and immunohistochemical study of thrombosed vessels in surgically removed ischemic tissues in patients with HIT complicated by gangrene of the lower limbs. Tissue sections were studied by: (1) hematoxylin and eosin staining and immunoperoxidase staining using a monoclonal antibody against platelet surface glycoprotein Ib(GPIb) for the identification of platelets, and (2) polyclonal antibodies against tissue-type plasminogen activator (tPA) and factor VIII for the identification of endothelial cells. We observed small arteries occluded by multiple small platelet thrombi surrounded by proliferative endothelial cells. In addition, depositions of IgG, IgA, and IgM were found in the occluded arteries. We postulate that the endothelial cell hyperplasia is caused by immunologic injury to endothelial cells as a result of immunoglobulin deposition, and by various mitogens derived from the activated platelets in the thrombi. Such endothelial cell hyperplasia is a major contributory factor, in addition to the microthrombi, of the occlusive vasculature in this disease.

Original languageEnglish (US)
Pages (from-to)23-27
Number of pages5
JournalSeminars in thrombosis and hemostasis
Issue number2 SUPPL. 1
StatePublished - 1999


  • Endothelial cell hyperplasia
  • Heparin
  • Heparin-induced thrombocytopenia
  • Platelet thrombus
  • Platelets
  • Thrombocytopenia

ASJC Scopus subject areas

  • Hematology
  • Cardiology and Cardiovascular Medicine


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