Gender differences in the expression of erythrocyte aggregation in relation to B β -fibrinogen gene polymorphisms in apparently healthy individuals
Einor Ben Assayag1 , Irena Bova1 , Shlomo Berliner 2 , Hava Peretz 3 , Sali Usher 3 , Itzhak Shapira 2 , Natan M. Bornstein1
1 Department of Neurology, 2 Department of Medicine “D“, 3 Laboratory of Clinical Biochemistry, Tel Aviv Sourasky Medical Center, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Keywords
Erythrocyte aggregation, fibrinogen, gene polymorphism
Summary
An increased erythrocyte aggregation (EA) is associated with
capillary slow flow, tissue hypoxemia and endothelial dysfunction.
Fibrinogen is a major determinant in the formation of aggregated
red blood cells. It has been suggested that the B ß -fibrinogen
–455G/A polymorphism is associated with erythrocyte
hyperaggregability in men with coronary artery disease.The purpose
of this study was to investigate the influence of the ß -fibrinogen
–455G/A polymorphism on erythrocyte aggregation in
apparently healthy individuals. Plasma fibrinogen, red blood cell
count, serum lipids, erythrocyte sedimentation rate, and the genotype
of the B ß -fibrinogen –455G/A polymorphism were
examined in a cohort of 545 apparently healthy individuals and
those with atherothrombotic risk factors.A whole blood erythrocyte
aggregation test was performed by using a simple slide test and image analysis. In men, EA levels and plasma fibrinogen
levels were significantly higher in subjects carrying the –455A allele
compared to subjects with the –455 GG genotype.This association
did not exist in women carrying the fibrinogen –455A
allele.The –455GA/AA men presented significantly higher correlation
between the plasma fibrinogen concentrations and EA.
This observation raises the prospect of possible change in the
functional properties of the –455GA/AA fibrinogen, enhancing
its ability to induce EH. This study suggests that the B ß -fibrinogen
–455A allele is related to EH in men only. Putative mechanism
could be hyperfibrinogenemia and a functional change in
the fibrinogen molecule that alters its ability to interact with red
blood cells and supports the aggregability of these cells.