Heparin in plasma
Last reviewed: 23.04.2024
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The activity of heparin in plasma is normal at 0.24-0.6 cfd / l.
Heparin is a sulfated polysaccharide, synthesized in mast cells, does not penetrate the placenta. A lot of it is found in the liver and lungs. Turns antithrombin III into an immediate anticoagulant. With fibrinogen, plasmin and adrenaline forms complexes possessing anticoagulant and fibrinolytic action. At 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 certain functions of platelets. Exogenous heparin is inactivated mainly in the liver, but 20% of it is excreted in the urine. Therefore, after the appointment of patients with liver and kidney damage, it is necessary to monitor the effectiveness of anticoagulant treatment and, if necessary (increase the coagulation time and thrombin time by more than 2-3 times), reduce its dose.
Heparin exerts its effect only if there is a complete antithrombin III in the blood.
Determination of heparin is necessary both for monitoring heparin therapy, and for identifying the resistance of patients to heparin. The main forms of heparin resistance are:
- deficiency of antithrombin III. At the core of the mechanisms of development of the deficit of antithrombin III are its increased intake (for example, in the ICD syndrome), heparin-induced depletion, a synthesis disorder, loss of urine in massive proteinuria;
- functional anomalies of antithrombin III: a decrease in sensitivity to heparin, a decrease in the inactivating effect on thrombin. At the heart of this pathology of antithrombin III lie the inherent qualitative defects of the molecule of antithrombin III;
- disturbance of interaction of antithrombin III with heparin. At the heart of the pathology is the competitive interaction of immune complexes, acute phase proteins of inflammation, antiheparin factor of platelets, 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 causes of ineffective use of heparin in patients.
An increase in the amount of heparin is observed in diffuse diseases of connective tissue, leukemia, radiation sickness, with anaphylactic and posttransfusion shock.
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