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The – 148 C/T fibrinogen gene polymorphism and fibrinogen levels in ischaemic stroke: a case–control study
  1. M P J van Goor1,
  2. E B Gómez-García2,
  3. F W G Leebeek2,
  4. G J Brouwers2,
  5. P J Koudstaal1,
  6. D W J Dippel1
  1. 1Department of Neurology, Erasmus Medical Centre Rotterdam, Rotterdam, Netherlands
  2. 2Department of Haematology, Erasmus Medical Centre Rotterdam
  1. Correspondence to:
 Dr Mary-Lou P J van Goor
 Erasmus MC Rotterdam, Department of Neurology, PO Box 2040, 3000 CA Rotterdam, Netherlands;


Background: To determine whether −148 C/T fibrinogen gene promoter polymorphism increases stroke risk by modifying the fibrinogen level.

Design: A case–control study of patients with first ever ischaemic stroke, confirmed by computed tomography.

Methods: Venous blood samples were collected for fibrinogen and routine coagulation tests one week after the stroke, and after three months in about half the patients. Population controls were age and sex matched. −148 C/T fibrinogen polymorphism was determined by polymerase chain reaction followed by digestion with restriction enzymes HindIII/AluI.

Results: There were 124 patients and 125 controls, mean age 56 years (range 18 to 75); 34 patients (27%) and 41 controls (33%) were heterozygous for −148 C/T fibrinogen polymorphism; six patients (5%) and five controls (4%) had the T/T genotype. The odds ratio of ischaemic stroke associated with CC homozygotes v T carriers was 0.8 (95% confidence interval, 0.5 to 1.4). Relative risk for ischaemic stroke associated with fibrinogen levels in the highest quartile was 3.9 (1.9 to 8.4) at one week, decreasing to 1.4 (0.6 to 3.3) at three months.

Conclusions: −148 C/T fibrinogen gene polymorphism was not a strong risk factor for ischaemic stroke. High fibrinogen levels early after acute stroke probably represent an acute phase response.

  • ischaemic stroke
  • −148 C/T fibrinogen gene
  • fibrinogen

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  • Competing interests: none declared