The relationship between plasma albumin, alkaline phosphatase and pyridoxal phosphate concentrations in plasma and red cells: Implications for assessing vitamin B6 status

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 ce...

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Published inClinical nutrition (Edinburgh, Scotland) Vol. 39; no. 9; pp. 2824 - 2831
Main Authors Talwar, Dinesh, Catchpole, Anthony, Wadsworth, John M., Toole, Barry J., McMillan, Donald C.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.09.2020
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ISSN0261-5614
1532-1983
1532-1983
DOI10.1016/j.clnu.2019.12.012

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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 in vitro 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 10–44 g/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.
AbstractList 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 in vitro 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 10–44 g/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.
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).BACKGROUNDPlasma 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 in vitro 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).OBJECTIVETo examine, using in vitro 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.DESIGNHeparin 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 10-44 g/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).RESULTSIn PLP incubated heparin samples, there was a strong direct relationship between albumin in the concentration range 10-44 g/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.CONCLUSIONSPlasma 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.
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 in vitro 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 10–44 g/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.
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 in vitro 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 10-44 g/L and increase in plasma PLP concentration (r  = 0.93, P < 0.001) and an inverse relationship with increase in red cell PLP concentration (r  = -0.90, P < 0.001). In contrast, ALP activity was inversely associated with increase in plasma PLP concentration (r  = -0.42; P = 0.013) and directly associated with red cell PLP concentration (r  = 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.
Author McMillan, Donald C.
Toole, Barry J.
Catchpole, Anthony
Wadsworth, John M.
Talwar, Dinesh
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Issue 9
Keywords Pyridoxal phosphate
Albumin
Plasma
Alkaline phosphatase
Red cell
Vitamin B6 status
Language English
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Snippet Plasma concentrations of most vitamins decrease as part of the systemic inflammatory response (SIR). Thus low plasma values do not necessarily indicate...
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StartPage 2824
SubjectTerms Albumin
albumins
Alkaline phosphatase
blood plasma
blood sampling
EDTA (chelating agent)
erythrocytes
heparin
hydrolysis
in vitro studies
inflammation
patients
Plasma
Pyridoxal phosphate
pyridoxine
Red cell
Vitamin B6 status
Title The relationship between plasma albumin, alkaline phosphatase and pyridoxal phosphate concentrations in plasma and red cells: Implications for assessing vitamin B6 status
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0261561419331814
https://dx.doi.org/10.1016/j.clnu.2019.12.012
https://www.ncbi.nlm.nih.gov/pubmed/31883613
https://www.proquest.com/docview/2331430048
https://www.proquest.com/docview/2400444904
Volume 39
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