(Circulation. 2001;103:2788.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, Mass (S.F., P.F.J., I.H.R., J.S.); and Boston University School of Medicine and the National Heart, Lung, and Blood Institutes Framingham Heart Study, Framingham, Mass (P.W.F.W.).
Correspondence to Jacob Selhub, PhD, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, 711 Washington St, Boston, MA 02111. E-mail jselhub{at}hnrc.tufts.edu
BackgroundLower vitamin B6 concentrations are reported to confer an increased and independent risk for cardiovascular disease (CVD). The mechanism underlying this relationship, however, remains to be defined. Other diseases, such as rheumatoid arthritis, are associated with reduced vitamin B6 levels. Despite a clear distinction in pathophysiology, inflammatory reaction may be the major link between these diseases. We hypothesized a relationship between pyridoxal 5'-phosphate (PLP), the active form of vitamin B6, and the marker of inflammation C-reactive protein (CRP). We also evaluated whether total plasma homocysteine (tHcy), a well-defined risk factor for CVD and a major determinant of plasma PLP levels, had a possible role as a mediator of this hypothesized relationship.
Methods and
ResultsData from 891 participants from the
population-based Framingham Heart Study cohort were analyzed.
Subjects were divided into 2 groups according to normal or elevated CRP
values: group 1, CRP <6 mg/L; group 2, CRP
6 mg/L. Plasma PLP levels
were substantially lower in group 2 than in group 1 (mean values in
group 2, 36.5 nmol/L versus 55.8 nmol/L in group 1,
P<0.001). In a multiple
logistic regression model adjusted for tHcy, the association of PLP
with CRP remained highly significant
(P=0.003).
ConclusionsLow plasma PLP is associated with higher CRP levels independently of tHcy. This observation may reflect a vitamin B6 utilization in the presence of an underlying inflammatory process and represent a possible mechanism to explain the decreased vitamin B6 levels in CVD.
Key Words: atherosclerosis risk factors homocysteine vitamins inflammation
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