Genetic predictors of fibrin D-dimer levels in healthy adults.

نویسندگان

  • Nicholas L Smith
  • Jennifer E Huffman
  • David P Strachan
  • Jie Huang
  • Abbas Dehghan
  • Stella Trompet
  • Lorna M Lopez
  • So-Youn Shin
  • Jens Baumert
  • Veronique Vitart
  • Joshua C Bis
  • Sarah H Wild
  • Ann Rumley
  • Qiong Yang
  • Andre G Uitterlinden
  • David J Stott
  • Gail Davies
  • Angela M Carter
  • Barbara Thorand
  • Ozren Polašek
  • Barbara McKnight
  • Harry Campbell
  • Alicja R Rudnicka
  • Ming-Huei Chen
  • Brendan M Buckley
  • Sarah E Harris
  • Annette Peters
  • Drazen Pulanic
  • Thomas Lumley
  • Anton J M de Craen
  • David C Liewald
  • Christian Gieger
  • Susan Campbell
  • Ian Ford
  • Alan J Gow
  • Michelle Luciano
  • David J Porteous
  • Xiuqing Guo
  • Naveed Sattar
  • Albert Tenesa
  • Mary Cushman
  • P Eline Slagboom
  • Peter M Visscher
  • Tim D Spector
  • Thomas Illig
  • Igor Rudan
  • Edwin G Bovill
  • Alan F Wright
  • Wendy L McArdle
  • Geoffrey Tofler
  • Albert Hofman
  • Rudi G J Westendorp
  • John M Starr
  • Peter J Grant
  • Mahir Karakas
  • Nicholas D Hastie
  • Bruce M Psaty
  • James F Wilson
  • Gordon D O Lowe
  • Christopher J O'Donnell
  • Jacqueline C M Witteman
  • J Wouter Jukema
  • Ian J Deary
  • Nicole Soranzo
  • Wolfgang Koenig
  • Caroline Hayward
چکیده

BACKGROUND Fibrin fragment D-dimer, one of several peptides produced when crosslinked fibrin is degraded by plasmin, is the most widely used clinical marker of activated blood coagulation. To identity genetic loci influencing D-dimer levels, we performed the first large-scale, genome-wide association search. METHODS AND RESULTS A genome-wide investigation of the genomic correlates of plasma D-dimer levels was conducted among 21 052 European-ancestry adults. Plasma levels of D-dimer were measured independently in each of 13 cohorts. Each study analyzed the association between ≈2.6 million genotyped and imputed variants across the 22 autosomal chromosomes and natural-log–transformed D-dimer levels using linear regression in additive genetic models adjusted for age and sex. Among all variants, 74 exceeded the genome-wide significance threshold and marked 3 regions. At 1p22, rs12029080 (P=6.4×10(-52)) was 46.0 kb upstream from F3, coagulation factor III (tissue factor). At 1q24, rs6687813 (P=2.4×10(-14)) was 79.7 kb downstream of F5, coagulation factor V. At 4q32, rs13109457 (P=2.9×10(-18)) was located between 2 fibrinogen genes: 10.4 kb downstream from FGG and 3.0 kb upstream from FGA. Variants were associated with a 0.099-, 0.096-, and 0.061-unit difference, respectively, in natural-log–transformed D-dimer and together accounted for 1.8% of the total variance. When adjusted for nonsynonymous substitutions in F5 and FGA loci known to be associated with D-dimer levels, there was no evidence of an additional association at either locus. CONCLUSIONS Three genes were associated with fibrin D-dimer levels. Of these 3, the F3 association was the strongest, and has not been previously reported.

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عنوان ژورنال:
  • Circulation

دوره 123 17  شماره 

صفحات  -

تاریخ انتشار 2011