WEIGHT-LOSS INDUCED CHANGES IN PLASMA FACTOR-VII COAGULANT ACTIVITY AND RELATION TO THE FACTOR-VII ARG GLN(353) POLYMORPHISM IN MODERATELY OBESE ADULTS/

Citation
Js. Pankow et al., WEIGHT-LOSS INDUCED CHANGES IN PLASMA FACTOR-VII COAGULANT ACTIVITY AND RELATION TO THE FACTOR-VII ARG GLN(353) POLYMORPHISM IN MODERATELY OBESE ADULTS/, Thrombosis and haemostasis, 79(4), 1998, pp. 784-789
Citations number
38
Categorie Soggetti
Hematology,"Peripheal Vascular Diseas
Journal title
ISSN journal
03406245
Volume
79
Issue
4
Year of publication
1998
Pages
784 - 789
Database
ISI
SICI code
0340-6245(1998)79:4<784:WICIPF>2.0.ZU;2-X
Abstract
Elevated plasma factor VII coagulant activity (factor VIIc) may be an independent risk factor for coronary heart disease. Several cross-sect ional studies suggest that a polymorphism of the factor VII gene (Arg- Gln(353)) interacts with plasma triglyceride level in determining fact or VIIc, but prospective data are lacking. Factor VII genotype, factor VIIc, and triglyceride level were measured in moderately obese adults aged 25 to 45 who underwent a six-month clinical trial to evaluate st rategies for weight loss. A total of 48 men and 50 women who experienc ed substantial weight loss (mean: 10 kg) provided samples for genetic analysis. Overall, 78% of participants were homozygous for the Arg(353 ) allele, while the remaining 22% were heterozygous (Arg/Gln(353)). At the baseline examination, heterozygotes had lower mean factor VIIc th an Arg(353) homozygotes (92% vs. 112%; p<0.001), and genotype explaine d 18% of the variance of factor VIIc. Average six-month weight loss wa s similar in both genotypes; mean reductions in factor We following we ight loss were greatest among Arg(353) homozygotes with high initial v alues (>120%). Cross-sectional and longitudinal associations between p lasma factor VIIc and triglyceride level were not dependent on genotyp e. These data confirm that the Gln(353) allele is associated with lowe r factor Vn coagulant activity in moderately obese adults, but they do not support the hypothesis that the Arg-Gln(353) polymorphism interac ts with plasma triglyceride level in determining factor VIIc.