It is unclear whether reduced plasma
pyridoxal 5'-phosphate (PLP) during
inflammation reflects an altered distribution or increased requirement of
vitamin B-6 that may impair overall
vitamin B-6 status in tissues. In plasma from 3035 patients undergoing coronary angiography for suspected
coronary heart disease, we investigated if plasma concentrations of any metabolites in the
kynurenine pathway, which depend on PLP as cofactor, may serve as metabolic marker(s) of
vitamin B-6 status. We also examined the association of
vitamin B-6 status with serum or plasma concentrations of several inflammatory markers. Among the kynurenines, only
3-hydroxykynurenine (HK) was inversely related to PLP and showed a positive relation to 4 investigated inflammatory markers. A segmented relationship was observed between PLP and HK, with a steep slope at PLP concentrations < 18.4 nmol/L, corresponding to the 5th percentile, and an almost zero slope at higher PLP concentrations. Low PLP and the steep PLP-HK slope were essentially confined to participants with 1 or more inflammatory markers in the upper tertile. Oral supplementation with
pyridoxine hydrochloride (40 mg/d) for 1 mo increased plasma PLP 8-fold, reduced the geometric mean (95% CI) of HK from 29.5 to 20.2 nmol/L (P < 0.001), and abolished the steep segment of the PLP-HK curve. The steep inverse relationship of plasma PLP with HK at low plasma PLP and the lowering of HK by
pyridoxine suggest plasma HK as a metabolic marker of
vitamin B-6 status. Thus, low plasma PLP during
inflammation may reflect impaired cellular
vitamin B-6 status, as indicated by the concurrent increase in plasma HK.