Definition
A decrease in the number of platelets due to the administration of heparin is called heparin-induced thrombocytopenia (HIT). A distinction is made between two forms, the non-immunological form (HIT type I) and the antibody induced form (HIT type II).
Introduction
The word thrombocytopenia refers to a deficiency of thrombocytes, i.e. blood platelets. The word components “thrombos”, “kytos” and “penia” come from the Greek and mean translated: clot, vessel/shell and deficiency. Thrombocytes play an important role in blood clotting because they attach themselves to injured parts of the blood vessels and close the injury by attaching themselves to each other.
In addition, they release substances that promote clotting. Normally, humans have between 150 000 and 450 000 platelets per microliter of blood. If fewer platelets are present, one speaks of thrombocytopenia. A heparin-induced thrombocytopenia (abbreviated: HIT) is a rare but dreaded possible side effect of the anticoagulant heparin, in which the number of thrombocytes is reduced by the heparin.
Frequency
Exact information about the frequency is difficult to obtain. However, it can be assumed that every tenth patient treated with heparin will produce antibodies. A type II reaction occurs in about 3% of patients treated with unfractionated heparin and only in 0.1% of patients treated with low molecular weight fractionated heparin. Thus, heparin-induced type II thrombocytopenia is 30 times less frequent in patients treated with fractionated heparin than in patients treated with unfractionated heparin. Therefore, patients should preferably be treated with fractionated heparin to avoid HIT II.
Forms of heparin-induced thrombocytopenia
This form is the most common HIT with an early start and a rather mild course. It affects about 1-5% of patients treated with unfractionated heparin. In the non-immunological early form of heparin-induced thrombocytopenia, there is no massive drop in platelets; they decrease by a maximum of 30% of the initial value.
This is due to the effect of heparin on the blood platelets, as it directly activates the platelets. In this way, they release coagulation-promoting messenger substances, which lead to the attachment of further thrombocytes. As a rule, the platelet count returns to normal spontaneously after a few days, even if therapy with heparin is continued.
With this form of HIT, thrombosis usually does not occur and the number of platelets does not drop below 80,000 per microliter. Patients treated with fractionated, low-molecular-weight heparins instead of unfractionated ones show significantly less HIT type I. The second type of heparin-induced thrombocytopenia usually manifests itself somewhat later, but can be life-threatening.
Approximately 1% of patients treated by infusion with unfractionated heparins are affected. Untreated, 30% of patients die as a result of heparin-induced thrombocytopenia type II. With alternative anticoagulant drugs, the figure is still comparatively high at eight to twenty percent.
Type II is based on the formation of antibodies against the complex formed in the body between heparin and the protein platelet factor 4. In patients who are not yet sensitized, symptoms occur between the fifth and twentieth day after the start of heparin administration. If sensitization is pre-existing, the antibodies from previous heparin therapy and the corresponding reaction are already present and type II heparin-induced thrombocytopenia manifests itself within a few hours. The platelet drop is much more severe than in heparin-induced thrombocytopenia type I, because the drop is usually greater than 50% of the initial value and only less than 100 000 platelets per microliter remain. When treated with fractionated heparins, HIT type II occurs about 30 times less than unfractionated heparin.
