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Thromb Haemost 1994; 71(01): 068-072
DOI: 10.1055/s-0038-1642386
Review Article
Schattauer GmbH Stuttgart

The Prevalence of Moderate and Severe FXII (Hageman Factor) Deficiency among the Normal Population: Evaluation of the Incidence of FXII Deficiency among 300 Healthy Blood Donors

Walter-Michael Halbmayer
1   The Central Laboratory, Municipal Hospital Vienna-Lainz, Vienna, Austria
,
Alexander Haushofer
1   The Central Laboratory, Municipal Hospital Vienna-Lainz, Vienna, Austria
,
Renate Schön
1   The Central Laboratory, Municipal Hospital Vienna-Lainz, Vienna, Austria
,
Christine Mannhalter
2   Clinical Institute of Medical and Chemical Laboratory Diagnostics, University of Vienna, Vienna, Austria
,
Ernst Strohmer
3   The Blood Donation Center of the Austrian Red Cross for Vienna, Lower Austria and Burgenland, Vienna, Austria
,
Kurt Baumgarten
3   The Blood Donation Center of the Austrian Red Cross for Vienna, Lower Austria and Burgenland, Vienna, Austria
,
Michael Fischer
1   The Central Laboratory, Municipal Hospital Vienna-Lainz, Vienna, Austria
› Author Affiliations
Further Information

Publication History

Received: 28 June 1993

Accepted after revision 14 September 1993

Publication Date:
12 July 2018 (online)

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Summary

Factor XII (FXII) deficiency has been reported to be a risk factor for the development of arterial and venous thromboembolism. However, no data are available on the prevalence of FXII deficiency within the normal population. Measuring APTT and FXII activity, seven FXII deficiencies could be detected among 300 healthy blood donors. This corresponds to an incidence of FXII deficiency of 2.3%. On the basis of these data the prevalence of severe and mild FXTT deficiency in the normal population can be estimated to be 1.5-3.0%. Assessment of FXII antigen levels revealed, that all seven FXII deficient individuals had FXII antigen levels matching the activity. One presented a severe FXII deficiency (1/300, 0.3%) without detectable FXII activity and an APTT prolongation of more than 120 s. The remaining six FXII deficiencies (6/300, 2.0%) were moderate variations with FXII activities ranging from 20-45% and less prolonged APTTs. Among the 300 healthy donors 16 (5.3%) subjects with prolonged APTTs were identified. Causes for APTT-prolongation were FXII deficiency (7/16), lupus anticoagulant (6/16), mild FVIII deficiency (1/16) and hepatic disorder (1/16). In the remaining sample (1/16) the cause for the prolongation of the APTT remained unexplained. Although 8.7% (26/300) of the donors had a positive family-history of thromboembolism (TE-FHX), none of the FXII deficient subjects were among those with positive TE-FHX.

 

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