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HIT typically develops 4-14 days after the administration of heparin. Heparin (UFH) is used in cardiovascular surgery, as prevention or treatment for deep-vein thrombosis and pulmonary embolism and in various other clinical scenarios. LMWH is increasingly used in outpatient prophylaxis regimes.
There are two forms of HIT. Type II HIT is the main adverse effect of heparin use.
Additional recommended knowledge
Patients have a transient decrease in platelet count (down to 50% normal) without any further symptoms. Platelet counts recover even if heparin continues to be administered. Platelet counts rarely fall below 100,000. It occurs in 10-20% of all patients on heparin. Type I HIT is not due to an auto-immune disorder (as Type II is).
This form is due to an autoimmune reaction where antibodies form against platelet factor 4 (PF4), neutrophil-activating peptide 2 (NAP-2) and/or interleukin 8 (IL-8). These reactive complexes then bind with heparin (heparin-PF4 complex being the most common). Research suggests that when heparin complexes with platelet factor 4, the heparin molecule undergoes a conformational change that renders it antigenic and different antibodies then clear the heparin from the bloodstream. IgG class antibodies are the most commonly found, reactive against heparin, whereas IgM and IgA class antibodies may or may not form. IgM and IgA are rarely found without IgG antibodies. Type II HIT develops in 3-5% of all patients on unfractionated heparin (UFH), and only 0.1% of patients on low molecular weight heparin (LMWH). Arterial and venous thromboses occur in 30% to 40% of patients with type II HIT. The remaining patients seem able to compensate for the activation of hemostasis that leads to thrombosis. Clot formation is mainly arterial and rich in platelets ("white clot syndrome"), in contrast with fibrin-rich clots (which are red due to trapped red blood cells). Most thrombotic events are in the lower limbs; skin lesions and necrosis may also occur at the site of the heparin infusion.
The most important enzyme in type II HIT is thrombin, the generation of which is increased following platelet activation. Platelet activation follows the binding of heparin to PF4 and the cross linking of receptors on the platelet surface.
Genetic risk factors for thrombosis such as factor V Leiden, prothrombin gene mutation, methylenetetrahydrofolate reductase (MTHFR) polymorphism and platelet-receptor polymorphisms do not increase the risk of developing HIT associated thrombosis.
Risk for HIT is higher in women than in men, and HIT occurs more commonly in surgical settings rather than non-surgical settings.
The sensitivity and specificity of Enzyme Immunoassay-Serotonin Release assay (EIA-SRA) was 100% and 97.4%, respectively and for 14C-SRA was 100% and 92.9% in HITS patients. No false positive results were found in patients receiving heparin (n=28), in patients with elevated levels of bilirubin (n=5), in patients w/ Antiphospholipid Antibody Syndrome (n=10), or in non-HIT patients (n=78) w/ both assays. 
Treatment is by prompt withdrawal of heparin and replacement with a suitable alternative anticoagulant. To block the thrombotic state, lepirudin, fondaparinux, bivalirudin, argatroban, danaparoid or other direct thrombin inhibitors are used. Low molecular weight heparin is contraindicated in HIT.
According to systematic review, patients treated with lepirudin for heparin-induced thrombocytopenia showed a relative risk reduction of clinical outcome (death, amputation, etc.) to be 0.52 and 0.42 when compared to patient controls. In addition, patients treated with argatroban for HIT showed a relative risk reduction of the above clinical outcomes to be 0.20 and 0.18. 
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Heparin-induced_thrombocytopenia". A list of authors is available in Wikipedia.|