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Thromb Haemost 1992; 67(05): 542-544
DOI: 10.1055/s-0038-1648490
Original Articles
Schattauer GmbH Stuttgart

Measurement of Markers of Activated Coagulation in Antithrombin III Deficient Subjects

Christine Demers
The Departments of Medicine and Pathology, McMaster University and the Canadian Red Cross Society, Hamilton, Canada
,
Jeffrey S Ginsberg
The Departments of Medicine and Pathology, McMaster University and the Canadian Red Cross Society, Hamilton, Canada
,
Penny Henderson
The Departments of Medicine and Pathology, McMaster University and the Canadian Red Cross Society, Hamilton, Canada
,
Fred A Ofosu
The Departments of Medicine and Pathology, McMaster University and the Canadian Red Cross Society, Hamilton, Canada
,
Jeffrey I Weitz
The Departments of Medicine and Pathology, McMaster University and the Canadian Red Cross Society, Hamilton, Canada
,
Morris A Blajchman
The Departments of Medicine and Pathology, McMaster University and the Canadian Red Cross Society, Hamilton, Canada
› Author Affiliations
Further Information

Publication History

Received 02 September 1991

Accepted after revision 28 November 1991

Publication Date:
03 July 2018 (online)

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Summary

Functional antithrombin III levels were measured by factor Xa inhibition in 63 members of a large family with type 2 antithrombin III deficiency and individuals were classified as antithrombin III deficient or non-deficient according to the results. FI+2 and TAT complexes were measured using an ELISA and FPA levels were measured by radioimmunoassay.

Thirty subjects (48%) were classified as antithrombin III deficient and 33 (52%) as antithrombin III non-deficient. The mean level of FI+2 was significantly higher in the deficient adults (0.87 ± 0.26) compared to both the non-deficient adults (0.70 ± 0.21) (p = 0.03) and the deficient adults receiving warfarin (0.16 ± 0.01) (p <0.001). The differences in the mean values of TAT complexes and FPA between deficient and non-deficient individuals were not statistically significant.

These findings suggest that untreated antithrombin III deficient subjects generate more thrombin than their non-deficient family members and that warfarin inhibits this thrombin formation. In this cross-sectional study, it is not possible to correlate the levels of the surrogate makers with future clinical outcome.

 

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