Antithrombin iii deficiency acquired D68.5

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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In addition to congenital, primary antithrombin III deficiency, there are also acquired AT III deficiencies:

  • in the context of disseminated intravascular coagulation
  • for liver diseases
  • in the case of advanced liver parenchyma damage in the context of liver cirrhosis or toxic liver failure
  • after blood transfusion
  • in sepsis
  • in nephrotic syndrome (loss of AT-III as part of the protein loss in ascites and urine)
  • under continuous heparin therapy
  • after major surgery or severe trauma, burns.

In the case of an antithrombin III deficiency, the risk can be estimated by means of the so-called hypercoagulability index. Normally this is between 1 and 1.2. Hypercoagulability is present when the Hi value is < 0.7. Hypocoagulability is present when the Hi value is >1.2.
The activity of AT-III is pH dependent. The activity of antithrombin III decreases in an acidic environment.

For patients with both protein C and protein S deficiency, the incidence of thromboembolic events increases with age. At 28 years, the probability of suffering a thromboembolic event is 50%.
In case of a threatening deficiency, there is an indication for substitution with AT-III (e.g. Kybernin HS, Abinex, Atenativ, AT-III Imuno). 1 IU/kg increases the AT-III level by 1.0-1.5%.

This section has been translated automatically.

  1. HA Neumann (2014) The coagulation system. ABW-Wissenschaftsverlag GmbH Berlin S. 224f.


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Last updated on: 29.10.2020