Heparin-induced Thrombocytopenia PF4 Antibody
- Also Known As:
- Heparin-PF4 Antibody
- HIT Antibody
- HIT PF4 Antibody
- Heparin Induced Antibody
- Heparin Associated Antibody
- Formal Name:
- Heparin-induced Thrombocytopenia Platelet Factor 4 Antibody

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.At a Glance
Why Get Tested?
To detect antibodies against the anticoagulant heparin, to help diagnose immune-mediated heparin-induced thrombocytopenia (HIT II)
When To Get Tested?
When you are receiving heparin therapy and your platelet count significantly decreases (thrombocytopenia), especially when you also have new blood clots (thrombosis)
Sample Required?
A blood sample drawn from a vein in your arm
Test Preparation Needed?
None
What is being tested?
Heparin-induced thrombocytopenia is a complication of treatment with the blood-thinner (anticoagulant) heparin that can cause low platelets in the blood and an increased risk of excessive blood clotting. This test detects and measures antibodies that may be produced by your immune system when or after you are treated with heparin.
Heparin is a common anticoagulant that is given intravenously or through injections to prevent the formation of inappropriate blood clots (thrombosis) or as an initial treatment when you have a blood clot, to prevent the clot from enlarging. It is often given during some surgeries, such as heart surgery (cardiopulmonary bypass), when the risk for developing blood clots is high. Small amounts of heparin are frequently used to flush out catheters and intravenous lines to keep clots from forming in them.
Sometimes, when you are given heparin, the drug can combine with a substance found in platelets called platelet factor 4 (PF4) and form a complex. In some people, the body’s immune system recognizes the heparin-PF4 complex as “foreign” and produces an antibody directed against it. This antibody in turn can activate your platelets and lead to a drop in the number of platelets, a condition known as heparin-induced thrombocytopenia (HIT). It may also lead to the development of new thrombosis or worsening thrombosis, which is a potentially life-threatening complication of heparin use.
Platelets are cell fragments that are an important part of your blood clotting system. When a blood vessel is injured and leaks blood, platelets are activated and clump together at the site of the injury, and work with coagulation factors to promote clot formation and stop the bleeding.
Not everyone on heparin produces HIT antibodies, and not everyone with HIT antibodies develops a low platelet count, but about 1% to 5% of those with the antibodies do.
- In HIT, the antibodies bind to the heparin-PF4 complexes, which then attach to the surface of platelets. If this happens, it activates your platelets, which in turn, triggers the release of more PF4.
- This starts a cycle that can cause a rapid and significant drop (e.g., 50% or more) in the number of platelets in your blood.
- Usually, a decrease in platelets results in a higher risk of bleeding, but in HIT, the activation of platelets by HIT antibodies can paradoxically lead to new and progressive blood clot formation in your veins and arteries.
- This cycle occurs in about 30% to 50% of those who develop the HIT antibody and thrombocytopenia.
This condition, associated with the presence of HIT antibody, low platelet count, and excessive clotting, is formally called immune-mediated heparin-induced thrombocytopenia or HIT type II. If this happens, it typically develops about 5-10 days after you start heparin therapy but may also develop rapidly, within 1-2 days, if you have been treated with heparin in the last 3 months and start heparin treatment again.
There is also a non-immune mediated HIT (type I) that occurs when heparin binds directly to platelets, causing activation. It is more common than type II but is temporary and a milder form and is of no clinical significance.
Common Questions
View Sources
Sources Used in Current Review
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