Heparin-induced thrombocytopenia overview: Difference between revisions
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==Causes== | ==Causes== | ||
[[Heparin-induced thrombocytopenia]] is caused by a variety of factors. It is typically caused by unfractionated heparin (moreso than low-molecular weight heparin). Females are more likely to develop HIT. Patients undergoing cardiac surgery are more likely to develop HIT. | |||
==Differentiating Heparin-induced thrombocytopenia from other Diseases== | ==Differentiating Heparin-induced thrombocytopenia from other Diseases== | ||
Revision as of 16:14, 18 August 2017
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Heparin-induced thrombocytopenia |
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Differentiating Heparin-induced thrombocytopenia from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Heparin-induced thrombocytopenia overview On the Web |
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American Roentgen Ray Society Images of Heparin-induced thrombocytopenia overview |
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Directions to Hospitals Treating Heparin-induced thrombocytopenia |
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Risk calculators and risk factors for Heparin-induced thrombocytopenia overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2] Shyam Patel [3]
Overview
Historical Perspective
The association between heparin and thrombosis with thrombocytopenia was noted in the 1950s. In the 1970s, it was noted that heparin exposure resulted in development of antibodies. In 2000, argatroban became available on the market for treatment of HIT. As of 2012, the American College of Chest Physicians (ACCP) updated their guidelines for management of HIT.
Classification
Heparin-induced thrombocytopenia is diagnosed when the platelet count falls by > 50% typically after 5-10 days of heparin therapy. There are two forms of HIT: type I and type 2. Type II HIT is the main adverse effect of heparin use.
Pathophysiology
Heparin-induced thrombocytopenia is diagnosed when the platelet count falls by > 50% typically after 5-10 days of heparin therapy. Heparin exposure triggers the release of PF4 from endothelial surfaces. Complexes of heparin and PF4 serve as neoepitopes, or new antigens, and can induce production of antibodies, since this large complex serves as an unfamiliar antigen to the body. Binding of IgG from the large complexes into the Fc gamma RII receptors triggers activation of the target cells containing the receptors and eventual release of platelet microparticles. This results in production of thrombin, which is highly thrombogenic and contributes to clot formation. Ultimately, this leads to thrombotic complications in the venous and arterial systems.
Causes
Heparin-induced thrombocytopenia is caused by a variety of factors. It is typically caused by unfractionated heparin (moreso than low-molecular weight heparin). Females are more likely to develop HIT. Patients undergoing cardiac surgery are more likely to develop HIT.
Differentiating Heparin-induced thrombocytopenia from other Diseases
Heparin-induced thrombocytopenia is diagnosed when the platelet count falls by > 50% typically after 5-10 days of heparin therapy. It should be differentiated by other causes of thrombocytopenia like hemolytic uremic syndrome, thrombotic thrombocytopenia, disseminated intravascular coagulation, post-transfusion purpura, and systemic lupus erythematosis.
Epidemiology and Demographics
Worldwide, the prevalence of HIT (in persons exposed to heparin) ranges from a low of 200 per 100,000 persons to a high of 5,000 per 100,000 persons. In pediatric populations, the prevalence of HIT (in persons exposed to heparin) ranges from a low of 1,500 per 100,000 persons to a high of 3,700 per 100,000 persons with an average prevalence of 2,600 per 100,000 persons. In neonatal populations, the prevalence of HIT (in persons exposed to heparin) is as low as 330 per 100,000 persons. HIT is more prevalent in the African American race than the Caucasian race and occurs more commonly in females compared to males.