Pathomorphological aspects of heparin-induced thrombocytopenia II (HIT-II syndrome)

Virchows Arch. 1998 Jun;432(6):541-6. doi: 10.1007/s004280050203.

Abstract

The therapeutic use of heparin results in thrombocytopenia in 5-30% of patients. In 0.1-1% of patients treated with heparin, the platelet count decreases to between 100 x 10(9)/l and 50 x 10(9)/l and leads to severe synchronous central arterial and venous thrombosis with a mortality of 18-36%. This is known as "white-clot syndrome" or heparin-induced thrombocytopenia II (HIT-II syndrome). Whilst the clinical aspects and the central type of thrombosis in HIT-II syndrome are well documented, the histomorphology and differential diagnosis of thrombosis are not. We report three cases of HIT-II syndrome with thrombosis of the central arteries and veins. The HIT-II thrombi could be differentiated from thrombi of other origins, particularly from mural thrombi. Heparin-induced thrombi were seen on microscopical examination to be like onion skin in structure, and immunohistochemistry showed that they had a markedly reduced content of fibrin and clearly enhanced amounts of IgG and IgM. The layered structure thus implied appositional growth. The thrombi in HIT-II syndrome do not seem to be induced by activation of the coagulation cascade, but by platelet aggregation mediated by anti-platelet antibodies.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Autoantibodies / analysis
  • Fatal Outcome
  • Female
  • Fibrin / metabolism
  • Heparin / adverse effects*
  • Humans
  • Immunoglobulin G / analysis
  • Immunoglobulin M / analysis
  • Immunohistochemistry
  • Thrombocytopenia / chemically induced
  • Thrombocytopenia / pathology*
  • Thrombosis / immunology
  • Thrombosis / metabolism
  • Thrombosis / pathology*

Substances

  • Autoantibodies
  • Immunoglobulin G
  • Immunoglobulin M
  • Fibrin
  • Heparin