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[Significance of disordered antithrombin III function in disseminated intravascular coagulation and deep venous thrombosis for anticoagulant therapy].

In patients with acute deep vein thrombosis of the pelvis and limbs and in patients with decompensating course of DICFS considerable defects in AT III function are regularly demonstrated by laboratory tests, while in groups including patients with old or less pronounced venous thrombosis or in patients with compensated or overcompensated consumption coagulopathy normal AT III values might frequently be expected. This seems to be of interest for the interpretation of laboratory data on AT III. However, from these findings AT III replacement cannot be deduced and they cannot be used as a criterion to assess the prognostic value of AT III deficiency for the course of the underlying disease. In acquired AT III defects the anticoagulant activity of heparin is not necessarily decreased. After continuous infusion of doses below 500 USP in patients with DICFS and after administration of heparin doses of 750 USP/h/70 kg in patients undergoing fibrinolytic therapy the AT III content rather increases continuously. After extremely high heparin doses during extracorporeal circulation in the heart-lung machine transitorily decreased AT III values return to normal. In certain risk situations, however, such as after bolus injection of comparatively high heparin doses in patients with greatly reduced AT III values, a lowered anticoagulant effect of high heparin doses must be expected. In these cases AT III replacement is indicated. However, when enhanced heparin resistance is suspected or diagnosed, treatment with AT III concentrates is justified only when the diagnosis is based on laboratory findings. Cortisone and protamine chloride were found to exert direct effects on AT III function and concentration independent of the AT III defects mentioned.