What is pathophysiology of acquired antithrombin III (ATIII) deficiency?

Updated: Mar 04, 2020
  • Author: James L Harper, MD; Chief Editor: Hassan M Yaish, MD  more...
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Acquired deficiencies are commonly due to increased coagulation activity secondary to endothelial injury or the presence of antiphospholipid (AP) antibodies (eg, lupus anticoagulant). In both of these situations, antithrombin III is consumed at increased rates because of excessive activation of the coagulation pathway. Other reported mechanisms of acquired antithrombin III deficiency include chronic liver disease, with resultant synthetic failure, and protein loss due to ascites or nephrotic syndrome, as indicated earlier.

A study by Di Minno et al indicated that in patients with unprovoked VTE, even mild antithrombin deficiency significantly increases the risk of VTE recurrence. In the report, which involved 823 patients who had suffered a first VTE, the investigators found that after adjusting for major VTE risk factors and anticoagulation duration, patients with antithrombin levels as high as 80% had a significantly higher risk of VTE recurrence than did those with antithrombin levels above 80%. [7]

A study by Sokol et al further supported evidence that mild antithrombin deficiency can be linked to recurrent VTE. The report found that when patients with antithrombin activity of less than 70% were compared with those with antithrombin activity of over 80%, VTE recurrence in the lower group had a hazard ratio of 3.7. [8]

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