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G‐455A polymorphism of the fibrinogen beta gene and deep vein thrombosis
Author(s) -
Renner W.,
Cichocki L.,
Forjanics A.,
Köppel H.,
Gasser R.,
Pilger E.
Publication year - 2002
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2002.01070.x
Subject(s) - fibrinogen , genotype , thrombosis , venous thrombosis , deep vein , medicine , gastroenterology , polymorphism (computer science) , allele , gene polymorphism , endocrinology , biology , gene , genetics
Abstract Background Elevated fibrinogen levels have been linked to increased risk for deep venous thrombosis, although it is not clear whether fibrinogen is causal or rather a marker for the presence of other risk factors. A common G/A polymorphism in the gene for the fibrinogen beta‐chain (FGB G‐455A) is associated with elevated fibrinogen levels. The present study was designed to analyze the role of this genetic marker for deep venous thrombosis. Materials and Methods We performed a case–control study including 307 patients with documented deep venous thrombosis and 316 control subjects. β‐fibrinogen genotypes were determined by allele‐specific polymerase chain reaction. Results GG, GA and AA genotype frequencies were similar among the patients (53·1%, 41·0, 5·9) and controls (51·6%, 42·1, 6·3; P = 0·92). Fibrinogen levels of the patients (median 3·72 g l −1 ; range 1·93–11·6) did not differ significantly from those of the controls (3·76; 2·17–9·99). Carriers of the homozygous AA genotype had significantly higher fibrinogen levels than noncarriers (patients: 5·32 vs. 3·59; P = 0·024; controls: 6·29 vs. 3·72; P = 0·048). Conclusion Our data suggest that the fibrinogen‐elevating FGB G‐455A gene polymorphism is not linked to an increased risk for deep venous thrombosis.