Related Experiment Videos
Changes of antithrombin III (AT III) in AT III deficient patients during long-term anticoagulant treatment
1First Department of Internal Medicine, Medical School, Medical University of Pécs, Hungary.
Insights
Long-term coumarin treatment in antithrombin III deficient patients did not alter AT III levels in Type I deficiency. Other AT III deficiency types normalized during coumarin therapy.
Area of Science:
- Hematology
- Clinical Biochemistry
- Pharmacology
Background:
- Antithrombin III (AT III) deficiency predisposes individuals to thromboembolic events.
- Long-term anticoagulation with coumarin derivatives is standard for these patients.
- Previous studies show conflicting results regarding AT III levels during coumarin therapy.
Purpose of the Study:
- To investigate the effect of long-term coumarin treatment on Antithrombin III (AT III) levels in patients with different types of AT III deficiency.
- To clarify the impact of coumarin therapy on AT III function and antigen levels.
Main Methods:
- Assessed AT III function using Gerendás-Rák method and chromogenic substrate assays.
- Measured AT III antigen levels via Behring M-Partigen and Laurell rocket electrophoresis.
- Utilized crossed immunoelectrophoresis for comprehensive analysis in all patients.
Main Results:
- In patients with Type I AT III deficiency, AT III levels remained unchanged over extended treatment periods (>10 years).
- Patients with functional AT III abnormalities or pathological heparin binding showed normalization of AT III levels.
- Pathological heparin binding characteristics did not alter during coumarin treatment.
Conclusions:
- Long-term coumarin therapy does not affect Antithrombin III levels in Type I deficiency.
- Coumarin treatment can normalize AT III levels in patients with functional AT III abnormalities.
- These findings provide crucial insights into managing anticoagulation in AT III deficient patients.
Abstract:
Antithrombin III deficient patients with manifest thromboembolic diseases need long term coumarin treatment. There are contradictory data on the change of AT III during this therapy. The authors observed 5 patients with severe AT III decrease type I, 3 with functional abnormality and 2 with a pathological heparin binding. AT III function was determined by the Gerendás-Rák method and with chromogenic substrate. AT III antigen was measured with Behring M-Partigen and Laurell rocket electrophoresis. Crossed immunoelectrophoresis was carried out in all patients. In patients with type I AT III decrease, AT III hasn't changed even in a long period of more than 10 years. In the other types AT III became normal. The pathological heparin binding wasn't changed.