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Blood, Vol. 93 No. 3 (February 1), 1999:
pp. 906-908
Association of a Common Polymorphism in the Factor XIII Gene With
Venous Thrombosis
Andrew J. Catto,
Hans P. Kohler,
Julie Coore,
Michael W. Mansfield,
Max H. Stickland, and
Peter J. Grant
From the Unit of Molecular Vascular Medicine, Research School of
Medicine, University of Leeds, Leeds, UK.
We have shown an association between a common mutation in the factor
XIII a-subunit gene, coding for an amino acid change, 3 amino acids
from the thrombin activation site (factor XIII Val34Leu) that may
protect against myocardial infarction and predisposes to intracranial
hemorrhage. To investigate the possible role of factor XIII Val34Leu in
the pathogenesis of venous thromboembolism (VTE) and potential
interactions with factor V Leiden (FV:Q506) and prothrombin
G  A 20210, we studied 221 patients with a history of VTE and
254 healthy controls. Patients with VTE showed an increased frequency
of the FXIII Val/Val genotype (63% v 49%) and a lower
frequency of the Val/Leu genotype (31% v 42%) than controls
(P = .007). FV:Q506 heterozygotes were more
frequent in VTE patients (11%) than controls (5%; P = .04).
The prothrombin G A 20210 mutation was present in only 3 patients and no controls (P = .10). In a logistic regression model for a history of VTE, the odds ratio (95% confidence interval) for FXIII Val/Leu or Leu/Leu genotype was 0.63 (0.38 to 0.82) and for
possession of FV:Q506 2.40 (1.17 to 4.90). There was no
evidence for an interaction between factor XIII Val34Leu genotype and
FV:Q506, prothrombin G A 20210, sex, or age. It
is concluded that possession of the Leu allele at factor XIII Val34Leu
is protective against deep venous thrombosis.
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