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Heparin in plasma
Last reviewed: 05.07.2025
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The normal heparin activity in plasma is 0.24-0.6 kU/l.
Heparin is a sulfated polysaccharide, synthesized in mast cells, does not penetrate the placenta. It is found in large quantities in the liver and lungs. It converts antithrombin III into an immediate-action anticoagulant. It forms complexes with fibrinogen, plasmin and adrenaline that have anticoagulant and fibrinolytic effects. In low concentrations, it inhibits the reaction between factors 1Xa, VIII, autocatalytic activation of thrombin and the action of factor Xa. In high concentrations, it inhibits coagulation in all phases, including thrombin-fibrinogen. It inhibits some functions of platelets. Exogenous heparin is inactivated mainly in the liver, but 20% of it is excreted in the urine. Therefore, after prescribing it to patients with liver and kidney damage, it is necessary to monitor the effectiveness of anticoagulant treatment and, if necessary (increase in blood clotting time and thrombin time by more than 2-3 times), reduce its dose.
Heparin has an effect only in the presence of complete antithrombin III in the blood.
Determination of heparin is necessary both for monitoring heparin therapy and for identifying patients' resistance to heparin. The main forms of heparin resistance are:
- antithrombin III deficiency. The mechanisms underlying the development of antithrombin III deficiency include increased consumption (for example, in DIC syndrome), heparin-induced depletion, impaired synthesis, and loss in urine in massive proteinuria;
- functional abnormalities of antithrombin III: decreased sensitivity to heparin, decreased inactivating effect on thrombin. This pathology of antithrombin III is based on congenital qualitative defects of the antithrombin III molecule;
- disruption of the interaction of antithrombin III with heparin. The pathology is based on the competitive interaction of immune complexes, acute phase proteins of inflammation, platelet antiheparin factor, fibronectin with antithrombin III;
- discirculatory metabolic forms (stasis, acidosis, microcirculatory disorders);
- mixed forms.
The development of these forms of heparin resistance is one of the main reasons for the ineffective use of heparin in patients.
An increase in the amount of heparin is observed in diffuse connective tissue diseases, leukemia, radiation sickness, anaphylactic and post-transfusion shock.
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