Advances in the pathophysiology and treatment of heparin-induced thrombocytopenia.

ABSTRACT:

Purpose of review

To review the recent developments in understanding the pathophysiology of heparin-induced thrombocytopenia (HIT) and in applying this knowledge to the treatment of patients with suspected and proven HIT.

Recent findings

HIT pathophysiology is dynamic and complex. HIT pathophysiology is initiated by four essential components--heparin (Hep), platelet factor 4 (PF4), IgG antibodies against the Hep-PF4 complex, and platelet FcγRIIa. HIT is propagated by activated platelets, monocytes, endothelial cells, and coagulation proteins. Insights into the unique HIT antibody response continue to emerge, but without consensus as to the relative roles of B cells, T cells, and antigen-presenting cells. Platelet activation via FcγRIIa, the sine qua non of HIT, has become mu

SUBMITTER: McKenzie SE 

PROVIDER: S-EPMC4232774 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature