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Heparin-induced thrombocytopenia (HIT) without or with thrombosis (HITT) is the development of thrombocytopenia (low platelet counts) due to the administration of the anticoagulant (blood clotting inhibitor) heparin, either in its “unfractionated” or “low molecular weight” form. It predisposes to thrombosis, the formation of abnormal blood clots inside a blood vessel. If someone receiving heparin develops new or worsening thrombosis, or if the platelet count falls, HIT can be confirmed with specific blood tests.[1]
The treatment of HIT requires both protection from thrombosis and choice of an agent that will not reduce the platelet count further. Several agents exist for this purpose, mainly lepirudin and argatroban.[1] While heparin was discovered in the 1930s, HIT was not reported until the 1960s and 1970s.[2]
Heparin may be used for both prevention and the treatment of thrombosis. It exists in two main forms: an “unfractionated” form that can be injected under the skin or through an intravenous infusion, and a “low molecular weight” form that is always administered under the skin. Commonly used low molecular weight heparins are enoxaparin, dalteparin and tinzaparin.[3]
In HIT, the platelet count in the blood falls below the normal range. However, it is generally not low enough to lead to an increased risk of bleeding. Most people with HIT will therefore not experience any symptoms. Typically the platelet count will fall 5–14 days after heparin is first commenced; if someone has received heparin in the previous three months, the fall in platelet count may occur much quicker, sometimes within a day.[1] The most common symptom of HIT is enlargement (extension) of a previously diagnosed blood clot, or the development of a new blood clot elsewhere in the body. This may take the form of clots either in arteries (arterial thrombosis) or veins (venous thrombosis). Examples of arterial thrombosis are stroke, myocardial infarction (heart attack) and acute leg ischemia. Venous thrombosis may occur in the leg or arm in the form of deep vein thrombosis (DVT) and in the lung in the form of a pulmonary embolism (PE–these usually originate in the leg but migrate to the lung).[1][4]
In those receiving heparin through an intravenous infusion, a complex of symptoms (“systemic reaction”) may occur when the infusion is commenced: fever, chills, high blood pressure, a fast heart rate, shortness of breath and chest pain. This happens in about a quarter of people with HIT. Others may develop a skin rash consisting of red spots.[1][4]
Heparin does not occur naturally in the human body, and is therefore sometimes treated as a foreign “non-self” substance by the immune system. In HIT, the immune system forms antibodies against heparin when it is bound to a protein called platelet factor 4 (PF4). These antibodies are usually of the IgG class. This process takes about five days. However, those who have been exposed by heparin in the last few months may still have circulating IgG, as IgG continues to be produced even when the precipitant has been removed. This is similar to immunity against certain viruses, with the difference that the HIT antibody does not persist longer than 3 months.[1][4]
The IgG antibodies form a complex with heparin and PF4 in the bloodstream. The tail of the antibody then binds to the Fc?IIa receptor, a protein on the surface of the platelet. This results in platelet activation and the formation of platelet microparticles, which initiate the formation of blood clots; the platelet count falls as a result.[1][4]
Formation of PF4-heparin antibodies is common in people receiving heparin, but only a proportion of these develop thrombocytopenia or thrombosis.[1] This has been referred to as an “iceberg phenomenon”.[2]
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