What Is Heparin-Induced Thrombocytopenia?

Heparin-induced thrombocytopenia (heparin-induced thrombocytopenia), the degree of thrombocytopenia caused by heparin has no clear relationship with the dose of heparin, the route of injection, and previous history of exposure to heparin, but it is related to the source of the heparin preparation related.

Heparin-induced thrombocytopenia

Overview of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia (heparin-induced thrombocytopenia), the degree of thrombocytopenia caused by heparin has no clear relationship with the dose of heparin, the route of injection, and previous history of exposure to heparin, but it is related to the source of the heparin preparation related.

Causes of heparin-induced thrombocytopenia

Causes of heparin-induced thrombocytopenia

Heparin in various dosage forms can induce thrombocytopenia. Experimental studies have shown that high molecular weight heparin is more likely to interact with platelets, leading to thrombocytopenia, which is observed in patients with thrombocytopenia treated with low molecular weight heparin. The lower rate results are consistent.

Pathogenesis of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia may be related to the immune mechanism. Some patients may have a specific antibody IgG, which can bind to the heparin-PF4 (platelet 4 factor) complex. PF4 is also called "heparin-binding cationic protein". Secreted by platelet alpha particles and then bound to the surface of platelets and endothelial cells. 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, which then binds to the Fc a receptor on the surface of platelets. The immune complex can activate platelets and produce procoagulant substances. It is a possible heparin-induced thrombocytopenia with thrombotic complications. mechanism. Thrombocytopenia caused by other drugs generally has no thrombotic complications and can be used for identification.
Immune complexes activate platelets by cross-linking with FcyR IIa molecules on the surface of platelets. The His / Arg polymorphism of the 131th amino acid chain of FcR a molecule affects its ability to bind to IgG, which can be used as a predictor to predict the individual risk of heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia symptoms

According to the course of thrombocytopenia induced by the clinical application of heparin treatment, it can be divided into temporary thrombocytopenia and persistent thrombocytopenia.

Heparin-induced Thrombocytopenia

Most of them occur immediately after the initiation of heparin treatment, but the platelet decreases, but generally it is not less than 50 × 109 / L. It may be related to the induced aggregation effect of heparin on platelets. Heparin can cause temporary aggregation of platelets and increased platelet adhesion, and platelets are blocked in blood vessels, resulting in transient thrombocytopenia.

Heparin-induced thrombocytopenia

It is rarer than the former. It usually occurs 5 to 8 days after heparin treatment. If the patient has previously received heparin treatment, thrombocytopenia may occur immediately. The number of platelets can be less than 50 × 109 / L, and no less than 10 × 109 / L person. In addition to thrombocytopenia, it can be accompanied by thrombosis and disseminated intravascular coagulation. Bleeding symptoms are rare, mainly manifested by thrombosis.
A history of heparin in combination with laboratory tests for thrombocytopenia can be diagnosed.

Heparin-induced thrombocytopenia treatment

For patients with heparin-induced thrombocytopenia, if the number of platelets is not less than 50 × 109 / L, and there are no obvious clinical symptoms, heparin treatment can continue to be used, and the number of platelets can generally recover by itself. Heparin therapy should be discontinued when the number of platelets is less than 50 × 109 / L or there are signs of thrombosis. Within a few days of discontinuing heparin, all changes in platelets and coagulation caused by heparin could be corrected, but heparin-dependent antiplatelet antibodies could still be detected.
If severe thrombocytopenia is accompanied by thrombosis, plasma exchange can be performed, platelet transfusion is ineffective, and even thrombosis may be exacerbated, causing symptoms similar to thrombotic thrombocytopenic purpura.

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