[Heparin-induced thrombopenia. Clinical manifestations and physiopathology]

Heparin-induced thrombocytopenia is a clinically interesting model of immunological thrombocytopenia because thrombus formation occurs much more frequently than hemorrhage, in some patients, major thrombocytopenia is observed with signs of consumption coagulopathy. HIGH INCIDENCE OF THROMBUS FORMATION: Venous thrombi predominate with severe consequences such as pulmonary emboli or more rarely distal gangrene. Artenal thrombi are less frequent but are highly suggestive and often lead to acute ischemia in the lower limbs. IMMUNOLOGICAL MECHANISM: Severe forms of heparin-induced thrombocytopenia result from an immunological mechanism and are associated with IgG antibody production. The Fc fragment of these antibodies activate platelets. Heparin-dependent antibodies preferentially recognize antigenic complexes formed by the heparin-platelet facto 4 association although certain other antigens (IL-8 or NAP-2 are also recognized. Thrombus formation results from platelet activation and enhanced coagulability which can be favored by antibody binding to endothelial cells and synthesis of tissue factor. PRACTICAL ASPECTS: Severe heparin-induced thrombocytopenia is particularly frequent in medical and surgical situations involving platelet activation and treatments by infractionated heparins. No particular phenotype of the IgG Fc receptor has been identified. Likewise no specific risk factors have been found. As effective antithrombin therapy is required in most cases, Xa inhibitors or thrombin inhibitors are useful.