Heparin-Induced Thrombocytopenia

Perfusfind S.L.
Artículos, Coagulation Jan 1, 1970 0

Abstract

Heparin-induced thrombocytopenia is an immune-mediated disorder caused by antibodies that recognize complexes of platelet factor 4 and heparin. Thrombosis is a central and unpredictable feature of this syndrome. Despite optimal management, disease morbidity and mortality from thrombosis remain high. The hypercoagulable state in heparin-induced thrombocytopenia is biologically distinct from other thrombophilic disorders in that clinical complications are directly attributable to circulating ultra-large immune complexes. In some individuals, ultra-large immune complexes elicit unchecked cellular procoagulant responses that culminate in thrombosis. To date, the clinical and biologic risk factors associated with thrombotic risk in heparin-induced thrombocytopenia remain elusive. This review will summarize our current understanding of thrombosis in heparin-induced thrombocytopenia with attention to its clinical features, cellular mechanisms, and its management.

Unfractionated heparin remains the mainstay of anticoagulation for indications for which there are no effective substitutes, such as anticoagulation for cardiopulmonary bypass surgery, extracorporeal membrane oxygenator circuits, dialysis, and mechanical prosthetic valves. The continued use of unfractionated heparin in clinical practice places patients at risk for developing heparin-induced thrombocytopenia (HIT), a potentially devastating immune disorder caused by antibodies to complexes of PF4 (platelet factor 4) and heparin (anti-PF4/H Abs).

Thrombosis is the most serious and life-threatening complication of HIT. Thrombosis occurs at presentation or complicates the course of illness in 20% to 64%.1,2 Disease morbidity is further compounded by high rates of bleeding (≈40%) associated with use of potent nonheparin anticoagulants for the prevention or treatment of HIT thrombosis.2 Even with use of alternative anticoagulants, thrombosis contributes to fatal outcomes in ≈6% to 26% of patients with HIT.2–5

As thrombosis is central to disease morbidity and mortality in HIT, this review will summarize our current understanding of its risk factors, mechanisms, and treatment. For topics related to other aspects of the disease, such as the epidemiology,3,6 diagnosis,7 or laboratory testing8,9 in HIT the reader is referred to corresponding reviews on these topics.

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