Introduction to Heparin-induced Thrombocytopenia (HIT)

Introduction Heparin-induced thrombocytopenia, the degree of heparin-induced thrombocytopenia is not clearly related to the dose of heparin, the route of injection and the history of previous heparin exposure, but with heparin preparation Source related. Causes (1) Causes Heparin can induce thrombocytopenia in various dosage forms. Experimental studies have shown that high molecular weight heparin is more likely to interact with platelets, leading to thrombocytopenia, which is compared with the use of low molecular weight heparin observed in the clinic. The results of patients with lower rates of thrombocytopenia were consistent. (B) the pathogenesis of heparin-induced thrombocytopenia may be related to the immune mechanism, some patients may have a specific antibody IgG, the antibody can be combined with heparin-PF4 (platelet factor 4) complex, PF4 also known as "heparin Binding to cationic proteins". It is secreted by platelet alpha particles and then bound to the surface of platelets and endothelial cells. It is secreted by platelet alpha particles and then bound to the surface of platelets and endothelial cells. The antibody-heparin-PF4 forms a 3-molecular complex that binds to the Fcγ IIa receptor on the surface of the platelet. The immune complex activates platelets and produces procoagulant substances, which is a possible cause of heparin-induced thrombocytopenia with thrombotic complications. mechanism. Thrombocytopenia caused by other drugs generally has no thrombotic complications and can be used as an identification. The immune complex activates platelets by cross-linking with the FcyR IIa molecule on the surface of the platelets. The His/Arg polymorphism at position 131 of the amino acid chain of FcγR IIa can influence its ability to bind to IgG, and thus can be used as a predictor to predict the individual risk of heparin-induced thrombocytopenia. Symptoms can be classified into transient thrombocytopenia and persistent thrombocytopenia according to the course of clinical course of thrombocytopenia induced by heparin therapy. 1. Most of the temporary thrombocytopenia occurs after the start of heparin treatment, and the platelets are immediately reduced, but generally not less than 50 × 109 / L. It may be related to the induced aggregation of platelets by heparin, which can cause temporary aggregation of platelets and increased platelet adhesion, and platelets are retained in the blood vessels, resulting in transient thrombocytopenia. 2. Persistent thrombocytopenia is less common than the former, usually occurs 5 to 8 days after heparin treatment. If the patient has been treated with heparin, thrombocytopenia may occur immediately, and the number of platelets may be less than 50×109/L. Below 10 × 109 / L. In addition to thrombocytopenia, thrombosis and disseminated intravascular coagulation can be accompanied. Hemorrhagic symptoms are rare, mainly manifested as thrombosis. A history of drugs with heparin can be diagnosed in conjunction with laboratory tests for thrombocytopenia. Treatment (1) Treatment For patients with heparin-induced thrombocytopenia, if the platelet count is not less than 50 × 109 / L, and there is no obvious clinical symptoms, heparin treatment can continue to be used, and the total number of platelets can be recovered by itself. Heparin therapy is discontinued when the number of platelets is less than 50 x 109/L or there is a manifestation of thrombosis. Within a few days of discontinuation of heparin, all changes in platelet and coagulation caused by heparin were corrected, but heparin-dependent antiplatelet antibodies were still detectable. If severe thrombocytopenia is associated with thrombosis, plasma exchange can be performed, platelet transfusion is ineffective, and even thrombosis may be aggravated, causing symptoms similar to thrombotic thrombocytopenic purpura. Prevention is fully aware of the potential for heparin therapy to induce thrombocytopenia, and frequent review of platelet counts is the primary preventive measure. The application of low molecular weight heparin can reduce the incidence of this disease.

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