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(Stroke. 2004;35:12.)
© 2004 American Heart Association, Inc.

Original Contributions

Inflammation, Homocysteine, and Vitamin B6 Status After Ischemic Stroke

P.J. Kelly, MB, MS, MRCPI; J.P. Kistler, MD; V.E. Shih, MD; R. Mandell, BA; N. Atassi, MD; M. Barron, BS; H. Lee, PhD; S. Silveira, BA K.L. Furie, MD, MPH

From the Stroke Service (P.J.K., J.P.K., N.A., M.B., S.S., K.L.F.) and Amino Acid Laboratory (V.E.S., R.M.), Department of Neurology, and Biostatistics Center (H.L.), Massachusetts General Hospital and Harvard Medical School, Boston, Mass.

Correspondence and reprint requests to Dr P.J. Kelly, Stroke Service, Department of Neurology, VBK 802, Massachusetts General Hospital, Fruit St, Boston, MA 02114. E-mail pjkelly{at}partners.org

Background and Purpose— Epidemiological studies have described an association between low vitamin B6 (measured as pyridoxal 5'-phosphate [PLP]) and ischemic stroke, independent of homocysteine (tHcy). We investigated B6 status, tHcy, and inflammation (measured by C-reactive protein [CRP]) in patients with stroke and controls.

Methods— Consecutive cases with new ischemic stroke were compared with matched controls. Fasting tHcy, PLP, and CRP were measured.

Results— The adjusted odds ratio of low PLP in the highest compared with the lowest CRP quartile was 16.6 (2, 139.9, P=0.01). Age, CRP, supplemental vitamin use, and albumin were independent predictors of PLP (P<0.05 for all). No relationship was observed between CRP and tHcy.

Conclusion— The relationship between inflammation and low B6 status may partially explain the findings of previous epidemiological studies.

Key Words: homocyst(e)ine • inflammation • nutrition • pyridoxine • stroke

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