The Factor v G1691A, Factor v H1299R, prothrombin G20210A polymorphisms in children with family history of premature coronary artery disease


Çiftdoǧan D. Y., COŞKUN Ş., ULMAN C., Tkz H.

Coronary Artery Disease, cilt.20, sa.7, ss.435-439, 2009 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 20 Sayı: 7
  • Basım Tarihi: 2009
  • Doi Numarası: 10.1097/mca.0b013e32832bdb8c
  • Dergi Adı: Coronary Artery Disease
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.435-439
  • Anahtar Kelimeler: child, coronary artery disease, Factor V G1691A, family history, prothrombin G20210A
  • Manisa Celal Bayar Üniversitesi Adresli: Evet

Özet

Atherosclerosis, the major cause of coronary artery disease (CAD), has a very long asymptomatic development phase, which begins in childhood. In this study, we describe the Factor V G1691A, Factor V H1299R and prothrombin G20210A gene polymorphisms in children with a family history of premature CAD. Evidence of these polymorphisms in these children may predict the probability of having atherosclerosis in the future. Our study included a total of 140 children, 72 males and 68 females between the ages of 4.9 and 15.7 years. Among these children, 73 had a parental history of premature CAD and the remaining 67 belonged to our control group. The participants were screened for the mutations Factor V G1691A, Factor V H1299R and prothrombin G20210A by polymerase chain reaction amplified DNA products with specific oligonucleotide probes. Our results suggested that frequencies of the mutated allele of Factor V G1691A and prothrombin G20210A are higher in children with a parental history of premature CAD. In conclusion, Factor V G1691A and prothrombin G20210A polymorphisms which were detected in higher frequencies in children with a parental history of premature CAD may indicate a risk for developing atherosclerosis and might be useful in screening for CAD in children; however, large population-based research is necessary to investigate further genetic risk assessment for CAD. © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.