No association of interleukin-6 gene polymorphism (-174 G/C) with premature coronary artery disease in a Turkish cohort


Sekuri C., ÇAM F. S., Sagcan A., Ercan E., Tengiz I., Alioglu E., ...Daha Fazla

Coronary Artery Disease, cilt.18, sa.5, ss.333-337, 2007 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 18 Sayı: 5
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1097/mca.0b013e32820588ae
  • Dergi Adı: Coronary Artery Disease
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.333-337
  • Anahtar Kelimeler: gene, interleukin-6, polymorphism, premature coronary artery disease
  • Manisa Celal Bayar Üniversitesi Adresli: Evet

Özet

OBJECTIVES: Interleukin-6 (IL-6) may contribute to the inflammatory response by activating endothelial cells and stimulating the synthesis of fibrinogen. It might thus be important in the pathogenesis of inflammation associated with coronary artery disease (CAD). Several studies suggested that the -174 C allele was associated with an increased prevalence of coronary heart disease. The aim of this study was to investigate further the association of the IL-6 -174 G/C allele status with premature CAD. METHODS: A total of 120 patients and 105 controls were included in the study. The IL-6 -174 G/C polymorphism was genotyped using PCR-restriction fragment length polymorphism. RESULTS: The genotype distribution of the -174 G/C polymorphism was not different in premature CAD patients (GG: 53%; GC: 42.6%; CC: 4.3%) and controls (GG: 54.3%; GC: 39%; CC: 6.7%) (P=0.72). The prevalence of the C allele was 25.6% in patients and 26.1% in controls. By multiple regression analysis, family history, smoking, diabetes, and hypertension were independent risk factors of premature CAD, but not IL-6 genotype. CONCLUSIONS: We conclude that the IL-6 -174 G/C polymorphism is not associated with the risk of premature CAD, and does not contribute to cardiovascular risk stratification. © 2007 Lippincott Williams & Wilkins, Inc.