Genetic factors are thought to contribute to the pathogenesis of acute myocardial infarction (AMI). A common variant of factor XIII (FXIII), FXIII Val34Leu, may be protective against developing an AMI, but various studies show conflicting results. We performed a meta-analysis to determine whether the FXIII Val34Leu variant is associated with a decreased risk of AMI.
View Article and Find Full Text PDFThe substitution of leucine for valine at amino acid position 34 of the factor XIII gene is commonly referred to as FXIII Val34Leu polymorphism. The homozygous leucine/leucine genotype has been reported to confer protection against venous thromboembolism, but previous studies have not evaluated a population limited to those with idiopathic venous thromboembolism. The primary objective of the study was to determine whether the FXIII Val34Leu polymorphism is independently associated with the occurrence of idiopathic venous thromboembolism.
View Article and Find Full Text PDFIt has been suggested that a G-to-T transition in exon 2 of the factor XIIIA gene resulting in a substitution of leucine for valine at amino acid 34 (FXIII Val34Leu) protects against venous thromboembolism (VTE). However, the evidence to date is insufficient to incorporate testing for the FXIII Val34Leu variant into clinical practice. To determine whether genotypes with the FXIII Val34Leu variant are protective against VTE, the authors performed a meta-analysis of 12 studies with genotyping for the FXIII Val34Leu variant (3,165 objectively diagnosed VTE cases and 4,909 controls).
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