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HIT, or Heparin Induced Thrombocytopenia or HIT is one of the undesirable side effects that characterizes this anticoagulant drug. Why is HIT developing? Who is predisposed to give HIT? How is heparin-induced thrombocytopenia treated?

HIT , i.e.heparin-induced thrombocytopeniaorpost-heparin-induced thrombocytopenia(for heparin-induced thrombocytopenia - HIT), can occur in anyone who is treated with heparin.

Physiologically, heparin is a substance produced by various cells in our body, especially the immune system, such as mast cells and macrophages. It works by activating antithrombin and inhibiting blood clotting. At higher concentrations, it also influences the function of platelets (thrombocytes) and cholesterol levels. Of course, the amounts produced by our body are minimal. In larger amounts, heparin is used as a drug in diseases caused by excessive clotting and in their prophylaxis with the aim of "thinning the blood", i.e. reducing the clotting capacity. It is administered subcutaneously or intravenously, and the indications for its use include: treatment and prevention of venous thromboembolism (venous thrombosis, pulmonary embolism), treatment of recent myocardial infarction, antiphospholipid syndrome, the topical ointment, e.g. . in thrombophlebitis of superficial veins or varicose veins of the lower limbs.

HIT (heparin-induced thrombocytopenia, heparin-induced thrombocytopenia) - causes

U about 8 percent patients receiving heparin develop antibodies to this substance. Why does this happen when heparin is also produced by our body? This drug is a protein of animal origin, so it has a slightly different structure of the molecule and therefore can be recognized as a foreign protein. How does HIT develop? In some people, administration of heparin causes the platelets to secrete a substance called platelet factor 4. It binds to the medicine and forms a complex against which the lymphocytes produce IgG antibodies. They, in turn, attach to the plates and activate them. In the process, freed byThrombocytes remain the next group of factors that activate clotting, and they themselves are stimulated to connect with each other. This results in the formation of blood clots in the circulation which are then removed. The number of thrombocytes decreases, and hence the blood's ability to clot decreases. At the same time, there are both bleeding and thrombotic complications, in the treatment of which - paradoxically - heparin is administered. When thrombotic complications occur - and the risk of their occurrence increases up to 40 times - when the number of platelets decreases, the disease is called HITT, or heparin-induced thrombocytopenia with thrombosis. Fortunately, not all of them have the same consequences as mentioned. Approx. 8 percent of patients produces antibodies, but only in 1 to 5 percent. this will result in a decrease in the number of plaques, while in about 30 percent. of them, it will have the further described consequences. The development of the disease can be prevented by monitoring platelet levels at the beginning of heparin treatment, by stopping it and by taking appropriate medications.

HIT (heparin-induced thrombocytopenia, heparin-induced thrombocytopenia) - factors that increase the risk of HIT

HIT can occur in anyone treated with heparin, but several predisposing conditions have been found.

The risk of developing heparin-induced thrombocytopenia depends on various factors, such as the state in which heparin is administered. A greater frequency of HIT was observed in patients after major surgery, e.g. cardiosurgical or orthopedic surgery, as well as in cases where a malignant neoplasm was diagnosed.

Due to these risk factors, the platelet count is usually checked quite frequently at the start of treatment. In addition to the conditions listed above, the indication for platelet determination is treatment with heparin for more than 4 days. The remaining people do not need to be controlled. Other, slightly less significant risk factors are:

  • type of heparin administered - in the treatment, the doctor has the so-called unfractionated heparin and low molecular weight heparin, and its choice depends largely on other diseases (e.g. kidney failure)
  • dose used, which in turn is forced to be recognized
  • sex - HIT is worse in women
  • origin and structure of heparin molecule (mass and number of sulphate groups)
Worth knowing

Two types of heparin-induced thrombocytopenia are observed:

  • HIT type I, milder- here the reduction in the number of platelets has a non-immune mechanism and is much smaller. It does not cause the consequences described previously, and the thrombocyte counts return to the correct number, even if treatment is not discontinuedheparin
  • HIT type II, immunological- in this case the number of platelets is reduced even by more than 50%, usually to 30-50 thousand (the norm is 150-400 thousand) most often after 4-10 days, therefore it is important to monitor blood counts during this time and check their number

HIT (heparin-induced thrombocytopenia, heparin-induced thrombocytopenia) - diagnosis

It is not easy to make a diagnosis, because a drop in the number of platelets alone does not necessarily mean an HIT. This laboratory deviation is also found in pseudo-thrombocytopenia (when blood is collected in a test tube with an anticoagulant that destroys the platelets), in autoimmune diseases, and in sepsis. The diagnosis takes into account the risk of disease occurrence, which is assessed on various scales, as well as the duration of heparin treatment, and the severity of the decrease in platelets.

HIT is suspected if

  • heparin has been or has been administered for more than 5 days
  • there will be a decrease in the number of platelets by more than 50%
  • there is a thromboembolic episode
  • other causes of thrombocyte decline will be excluded

This thromboembolic event is a disease associated with blockage of blood flow in various organs by clumps of platelets in the circulation. In HIT, we observe both venous clots (which are more frequent and appear as deep vein thrombosis, adrenal vein thrombosis and pulmonary embolism) and arterial embolism. The latter are less common, but they cause a heart attack, stroke or acute limb ischemia, and in patients after surgery, by-pass implantation may cause their closure. Thrombosis is associated with relatively high morbidity and mortality, even when properly treated.

If the above-mentioned conditions are met, there is usually no need for further HIT diagnostics and treatment of this syndrome is started immediately. Confirmation of the production of anti-platelet antibodies is rarely required. However, this can be done with the help of functional tests that assess the activation of platelets in the presence of heparin and the patient's serum (Platelet Serotonin Release Test, the so-called "gold standard" and heparin-induced platelet activation test) and serological tests (detection of antibodies by ELISA). In the case of a thromboembolic episode, it is often necessary to more accurately diagnose and treat it specific to it.

HIT (heparin-induced thrombocytopenia, post-heparin-induced thrombocytopenia) - treatment

The therapy is initiated immediately after the diagnosis of the disease, and often even only in the case of suspicion. The first step isheparin withdrawal. After discontinuation of this therapy - within a few days, sometimes several weeks - the number of platelets in the blood returns to normal, and their functions also improve. The produced antibodies, on the other hand, remain in the circulation 60-80 days after the administration of heparin, but they do not cause further symptoms. Anticoagulant therapy is continued with other drugs, but their availability is quite limited - these are: bivalirudin or fondaparinux. Therapy should continue at least until the platelet count returns to the baseline values, most often around 4 weeks in asymptomatic patients, and 3 months when thrombotic changes have occurred. Oral anticoagulants (warfarin, acenocoumarol) are often discontinued in HIT, and their administration is resumed at low doses when the number of platelets returns to normal. Occasionally, in the event of major bleeding, a platelet concentrate is required. However, their administration may be associated with an increase in thrombosis, as thrombocytes are delivered that are the target of the produced antibodies. If in the course of HIT there are: infarction, stroke, limb embolism, pulmonary embolism, specific treatment is implemented.

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