Abstract

Plasma concentrations of most vitamins decrease as part of the systemic inflammatory response (SIR). Thus low plasma values do not necessarily indicate deficiency. Vitamin B6 status is usually assessed by measurement of pyridoxal phosphate (PLP) in plasma, although vitamin concentrations in blood cells tend to be better markers of cellular stores. In health, plasma PLP appears to be determined primarily by intake, its binding to albumin, and its hydrolysis by alkaline phosphatase (ALP). To examine, using invitro studies, the effect of albumin concentration and ALP activity on PLP concentration in plasma and red blood cells of healthy subjects (HS) and critically ill patients (CI). Heparin and EDTA (ALP inhibited) whole blood samples from HS (n=8) and CI (n=26) were incubated with PLP. Concentration of PLP in plasma and red cells was measured. Albumin and ALP levels were determined in plasma. In PLP incubated heparin samples, there was a strong direct relationship between albumin in the concentration range 10-44g/L and increase in plasma PLP concentration (rs=0.93, P<0.001) and an inverse relationship with increase in red cell PLP concentration (rs=-0.90, P<0.001). In contrast, ALP activity was inversely associated with increase in plasma PLP concentration (rs=-0.42; P=0.013) and directly associated with red cell PLP concentration (rs=0.49; P=0.003). Plasma albumin concentration and to a lesser extent ALP activity influences PLP concentration in plasma and red cells. In conditions associated with low albumin (e.g. SIR) or altered ALP activity, red cell PLP measurements are more likely to be reliable than plasma measurements in differentiating true from apparent vitamin B6 deficiency and to guide vitamin B6 supplementation.

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