(Stroke. 2000;31:2661.)
© 2000 American Heart Association, Inc.
Original Contributions |
From the Departments of Neurology (D.I., N.T., H.S., Y.F.), Laboratory Medicine (M.M., A.S., K.W.), Hematology (M.M.), and Health Center (I.S.), School of Medicine, Keio University, Tokyo, Japan.
Correspondence to Daisuke Ito, MD, Department of Neurology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Background and PurposeA growing
amount of evidence suggests that infectious and inflammatory processes
may be involved in the initiation of
arteriosclerosis, but the mechanisms are
conceivably multifactorial and complex. Two European groups have
recently demonstrated that a C(-260)
T polymorphism in the
promoter of the CD14 lipopolysaccharide receptor may be a risk
factor for coronary artery disease (CAD). The T allele of
this polymorphism reportedly increases the expression of CD14 and
may be involved in atherogenesis. In the present study we
investigated a possible association between the C(-260)
T
polymorphism in the CD14 promoter and the occurrence of
symptomatic ischemic cerebrovascular disease
(CVD).
MethodsGenotype frequencies of the C(-260)
T
polymorphism in the CD14 promoter were determined in 235 patients
with CVD, as confirmed by brain CT and/or MRI, and 309 age- and
sex-matched control subjects.
ResultsThe distribution of genotypes was as follows: CVD
patients, T/T 24.3%,
C/T 53.2%, and
C/C 22.6%; controls,
T/T 26.9%,
C/T 50.2%, and
C/C 23.0%. There was no significant
difference between the CD14 promoter genotypes of the CVD
patients and the controls (
2=0.601,
P=0.741). We also measured the concentration of serum
soluble CD14 and the density of membranous CD14 on monocytes in the CVD
patients, but the polymorphism was not associated with either the
concentration of soluble CD14 or the density of membranous CD14
(P=0.358, P=0.238, respectively).
ConclusionsOur results indicate that the C(-260)
T
polymorphism in the CD14 promoter is not associated with an
increased risk for CVD.
Key Words: lipopolysaccharides polymorphism (genetics) risk factors stroke
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