Carrier-state of the A allele of – 455G>A polymorphism within the beta fibrinogen gene increases the risk of coronary artery disease in the presence of elevated concentration of serum triacylglycerols

• Authors: Beata Sarecka-Hujar , Iwona Zak , Jolanta Krauze

Title variants

PL

Nosicielstwo allela A polimorfizmu – 455G>A genu fibrynogenu beta zwiększa ryzyko choroby wieńcowej przy jednoczesnym podwyższonym stężeniu triglicerydów w surowicy

• Languages of publication: EN

Abstracts

EN

BACKGROUND Fibrinogen promotes development of atherosclerosis by directed integration in atherosclerotic lesions where it is converted into fi brin. The aim of the study was to assess a relationship between –455G>A polymorphism of beta fi brinogen (FGB) gene and coronary artery disease (CAD) in the Polish patients from Upper Silesia region and to establish whether there are any interactions between this polymorphism and traditional risk factors that infl uence the risk of CAD. METHODS We analyzed 191 patients with angiographically documented CAD and 203 blood donors. Genetic analysis was performed using PCR-RFLP method. RESULTS The frequency of FGB -455G>A genotypes was compatible with Hardy- Weinberg equilibrium. There was no signifi cant diff erences in the distribution of A allele and A allele carriers of FGB polymorphism between cases and controls. We observed a tendency to higher level of plasma fibrinogen in subjects with AA or GA genotypes than in GG homozygotes. We also found strong synergistic eff ects between A allele carrier-state and increased level of triacylglycerols (TG) in determining the risk of CAD (SI=5.97, SIM=2.63). Carriers of A allele with elevated level of TG were 3-fold more frequent among cases than in control group (12.0% vs 3.9%, p=0.003,OR=3.34). CONCLUSIONS There is a synergistic eff ect between –455G>A polymorphism of FGB gene and elevated concentration of serum triacylglycerols which determine the risk of CAD.

PL

WSTĘP Fibrynogen promuje rozwój zmian miażdżycowych przez przyleganie do zmienionej ściany tętnic gdzie jest przekształcany w fibrynę. Celem niniejszej pracy była ocena związku między polimorfi zmem –455G>A genu kodującego łańcuch beta fibrynogenu (FGB) a ryzykiem choroby wieńcowej (CAD, ang. coronary artery disease) w grupie pacjentów z Górnego Śląska i ustalenie czy istnieją interakcje między tym polimorfi zmem a tradycyjnymi czynnikami ryzyka miażdżycy w determinowaniu ryzyka CAD. MATERIAŁ I METODY Grupę badaną stanowiło: 191 pacjentów z potwierdzoną koronarografi cznie CAD oraz 203 krwiodawców bez obciążeń chorobami sercowo-naczyniowymi. Polimorfi zm –455G>A genu FGB genotypowano metodą RFLP-PCR. Wyniki. Częstości genotypów polimorfi zmu -455G>A genu FGB były zgodne z równowagą Hardy-Weinberg’a. Nie stwierdzono znamiennych różnic w częstości allela A i nosicieli allela A polimorfi zmu genu FGB między pacjentami a grupą kontrolną. Obserwowano tendencję do występowania wyższego poziomu fi brynogenu w osoczu osób z genotypami AA i GA w porównaniu do poziomu fibrynogenu w osoczu osób z genotypem GG. Stwierdzono również silny synergiczny efekt między nosicielstwem allela A a podwyższonym poziomem triglicerydów w determinowaniu ryzyka CAD (indeksy synergii SI=5.97, SIM=2.63). Nosiciele allela A charakteryzujący się podwyższonym poziomem triglicerydów występowali trzykrotnie częściej w grupie chorych niż w kontroli (12.0% vs 3.9%, p=0.003,OR=3.34). WNIOSKI Przedstawione wyniki wskazują na synergiczny związek nosicielstwa allela A polimorfi zmu – 455G>A genu FGB z ponadnormatywnym stężeniem triglicerydów w surowicy krwi w kształtowaniu ryzyka CAD w populacji pacjentów z Górnego Śląska.

Keywords

EN

choroba wieńcowa; coronary artery disease; fi brinogen beta; fibrynogen beta; gene polymorphism; lipids; lipidy; polimorfi zm; traditional risk factors; tradycyjne czynniki ryzyka

Discipline

• MEDICINE: MEDICINE

• Publisher: Śląski Uniwersytet Medyczny w Katowicach
• Journal: Annales Academiae Medicae Silesiensis
• Year: 2009
• Volume: 63
• Issue: 5
• Pages: 41-49

Contributors

author

Beata Sarecka-Hujar

• Department of Biochemistry and Medical Genetics, School of Health Care Medical University of Silesia, Kasztanowa Str. 3, 41-200 Sosnowiec, Poland; phone: [phone]

author

Iwona Zak

• Department of Biochemistry and Medical Genetics, School of Health Care, Medical University of Silesia, Katowice, Poland

author

Jolanta Krauze

• The First Department of Cardiac Surgery, School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland

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• Document Type: article