Abstract

BACKGROUND:

Factor XIII catalyzes crosslinking of fibrin in the last steps of the coagulation process. A common polymorphism in the gene for factor XIII A subunit (F13A1 V34L) has been associated with a decreased risk for coronary artery disease, cerebrovascular disease, and deep venous thrombosis.

METHODS:

To analyze the role of this polymorphism in peripheral arterial disease (PAD) we performed a case-control study including 873 patients with documented PAD and a total of 523 controls without vascular disease. The F13A1 genotype was determined by an allele-specific polymerase chain reaction.

RESULTS:

Genotype distribution and allele frequencies were not significantly different between patients (VV: 51.9%; VL: 40.7%; LL: 7.4%) and controls (VV: 54.7%; VL: 39.2%; LL: 6.1%). Mean age at onset of the disease was significantly higher in LL homozygous subjects than in VV homozygous subjects (67.3 versus 64.1 years, p=0.017). Heterozygous subjects had an intermediate age at onset (65.1 years), suggesting a gene-dose effect. The association of the L34 variant with onset of PAD remained significant after adjustment for other risk factors. The effect was stronger in men than in women.

CONCLUSIONS:

We conclude that the F13A1 V34L polymorphism was not associated with the presence of PAD in our study, but may be linked to a later onset of the disease.