Component

Plasma pyridoxal 5-prime-phosphate concentration

Independently recorded entity or measured process. Linked claims specify compartment, assay and experimental scope.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. All 14 hypophosphatasia patients had elevated plasma PLP; the mean was 1174 nM versus 57 nM in controls.

    Tissue-nonspecific alkaline phosphatase ALPL / TNAP → Plasma pyridoxal 5-prime-phosphate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    ALPL links mineralization biology with B6 handling; this result alone does not imply calcium causes B6 deficiency.
    experimental_model
    Fourteen hypophosphatasia patients compared with 38 controls; urinary catabolite studied in four affected children.
    exposure
    Endogenous ALPL enzyme deficiency; ordinary dietary B6 in urinary subset.
    limitations
    Small heterogeneous disease cohort; concentrations are not diagnostic thresholds for general nutrition.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    A high B6-related blood measurement can reflect faulty processing rather than extra intake.
    primary_references
    [b6-whyte1985] Markedly increased circulating pyridoxal-5'-phosphate levels in hypophosphatasia. Alkaline phosphatase acts in vitamin B6 metabolism (1985). https://pubmed.ncbi.nlm.nih.gov/4031070/ DOI: 10.1172/jci112031
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1608–1619

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fourteen hypophosphatasia patients compared with 38 controls; urinary catabolite studied in four affected children. · source_derived_draft · unverified_draft

    ### b6-hpp-high-plasma-plp All 14 hypophosphatasia patients had elevated plasma PLP; the mean was 1174 nM versus 57 nM in controls. Condition category: machinery_impairment nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A high B6-related blood measurement can reflect faulty processing rather than extra intake. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Fourteen hypophosphatasia patients compared with 38 controls; urinary catabolite studied in four affected children. limitations: Small heterogeneous disease cohort; concentrations are not diagnostic thresholds for general nutrition. exposure: Endogenous ALPL enzyme deficiency; ordinary dietary B6 in urinary subset. cross_nutrient: ALPL links mineralization biology with B6 handling; this result alone does not imply calcium causes B6 deficiency. [b6-whyte1985] Markedly increased circulating pyridoxal-5'-phosphate levels in hypophosphatasia. Alkaline phosphatase acts in vitamin B6 metabolism (1985). https://pubmed.ncbi.nlm.nih.gov/4031070/ DOI: 10.1172/jci112031
    Complete structured claim and evidence

  2. RA patients had lower plasma PLP than controls but no significant difference in erythrocyte PLP, AST activation coefficient or urinary 4-pyridoxic acid.

    Rheumatoid arthritis disease activity → Plasma pyridoxal 5-prime-phosphate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    experimental_model
    Human cross-sectional comparison: 33 RA patients, 17 healthy controls; separate pair-fed rat adjuvant-arthritis experiment.
    exposure
    Human observational samples; rats studied at peak day 21 and chronic day 42 inflammation. Human arm shares recruitment program with supplementation study.
    limitations
    Cross-sectional association; disease, treatment and nutrition are not fully separable. Shared recruitment with related 2005 trial.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    A low blood-plasma result did not mean that every measured B6 compartment was low.
    primary_references
    [b6-chiang2005-inflammation] Inflammation causes tissue-specific depletion of vitamin B6 (2005). https://pubmed.ncbi.nlm.nih.gov/16277678/ DOI: 10.1186/ar1821
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1523–1533

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cross-sectional comparison: 33 RA patients, 17 healthy controls; separate pair-fed rat adjuvant-arthritis experiment. · source_derived_draft · unverified_draft

    ### b6-ra-plasma-redcell-divergence RA patients had lower plasma PLP than controls but no significant difference in erythrocyte PLP, AST activation coefficient or urinary 4-pyridoxic acid. Condition category: biomarker_context nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low blood-plasma result did not mean that every measured B6 compartment was low. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Human cross-sectional comparison: 33 RA patients, 17 healthy controls; separate pair-fed rat adjuvant-arthritis experiment. limitations: Cross-sectional association; disease, treatment and nutrition are not fully separable. Shared recruitment with related 2005 trial. exposure: Human observational samples; rats studied at peak day 21 and chronic day 42 inflammation. Human arm shares recruitment program with supplementation study. [b6-chiang2005-inflammation] Inflammation causes tissue-specific depletion of vitamin B6 (2005). https://pubmed.ncbi.nlm.nih.gov/16277678/ DOI: 10.1186/ar1821
    Complete structured claim and evidence

  3. Supplementation improved plasma and erythrocyte PLP compared with placebo.

    Pyridoxine → Plasma pyridoxal 5-prime-phosphate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    experimental_model
    Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation.
    exposure
    Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation.
    limitations
    Selected low-PLP RA patients; blood response is not direct all-organ cofactor measurement.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    The measured B6 pools responded to added pyridoxine.
    primary_references
    [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1461–1471

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. · source_derived_draft · unverified_draft

    ### b6-ra-vitamer-response Supplementation improved plasma and erythrocyte PLP compared with placebo. Condition category: biomarker_context nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured B6 pools responded to added pyridoxine. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. limitations: Selected low-PLP RA patients; blood response is not direct all-organ cofactor measurement. exposure: Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation. [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    Complete structured claim and evidence

  4. During TNF-inhibitor therapy, disease-activity changes correlated with PLP and HK: XA changes; good responders showed a 31% PLP increase.

    Rheumatoid arthritis disease activity → Plasma pyridoxal 5-prime-phosphate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    experimental_model
    Longitudinal 106 RA patients beginning TNF-inhibitor therapy, assessed at baseline and three months.
    exposure
    Clinical TNF inhibitors; not randomized B6 supplementation.
    limitations
    Observational treatment-response association; cannot show B6 caused improvement. The 11% HK: XA decrease in good responders was not statistically significant (P=0.1).
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    B6 markers changed while inflammation was being treated, without a B6 intervention.
    primary_references
    [b6-sande2019] Vitamin B-6 Status Correlates with Disease Activity in Rheumatoid Arthritis Patients During Treatment with TNFα Inhibitors (2019). https://pubmed.ncbi.nlm.nih.gov/31050750/ DOI: 10.1093/jn/nxz001
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1547–1557

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Longitudinal 106 RA patients beginning TNF-inhibitor therapy, assessed at baseline and three months. · source_derived_draft · unverified_draft

    ### b6-tnf-treatment-marker-change During TNF-inhibitor therapy, disease-activity changes correlated with PLP and HK: XA changes; good responders showed a 31% PLP increase. Condition category: biomarker_context nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: B6 markers changed while inflammation was being treated, without a B6 intervention. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Longitudinal 106 RA patients beginning TNF-inhibitor therapy, assessed at baseline and three months. limitations: Observational treatment-response association; cannot show B6 caused improvement. The 11% HK: XA decrease in good responders was not statistically significant (P=0.1). exposure: Clinical TNF inhibitors; not randomized B6 supplementation. [b6-sande2019] Vitamin B-6 Status Correlates with Disease Activity in Rheumatoid Arthritis Patients During Treatment with TNFα Inhibitors (2019). https://pubmed.ncbi.nlm.nih.gov/31050750/ DOI: 10.1093/jn/nxz001
    Complete structured claim and evidence

  5. Thirty-five of 66 alcoholic subjects selected for normal liver function and haematology had plasma PLP below 5 ng/ml, the lowest value found in 94 controls.

    Habitual alcohol consumption → Plasma pyridoxal 5-prime-phosphate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/4359937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08", "start_char": 0, "end_char": 1650, "text_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08"}
    experimental_model
    Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays
    exposure
    Chronic alcohol abuse; acetaldehyde and ethanol applied to erythrocytes
    limitations
    Selecting subjects without abnormal liver function isolates the vitamin effect from liver disease. The phosphatase mechanism is shown in erythrocytes, not liver.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Human
    plain_language
    More than half had less of the active vitamin than any healthy control, with healthy livers.
    primary_references
    [alcohol-p4359937] Vitamin B6 metabolism in chronic alcohol abuse. Pyridoxal phosphate levels in plasma and the effects of acetaldehyde on pyridoxal phosphate synthesis and degradation in human erythrocytes. (1974). https://pubmed.ncbi.nlm.nih.gov/4359937/ DOI: 10.1172/jci107607
    tissue_or_cell_type
    Plasma and erythrocytes
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 631–642

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays · source_derived_draft · unverified_draft

    ### alcohol-low-plp-prevalence Thirty-five of 66 alcoholic subjects selected for normal liver function and haematology had plasma PLP below 5 ng/ml, the lowest value found in 94 controls. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: More than half had less of the active vitamin than any healthy control, with healthy livers. organism: Human tissue_or_cell_type: Plasma and erythrocytes experimental_model: Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays limitations: Selecting subjects without abnormal liver function isolates the vitamin effect from liver disease. The phosphatase mechanism is shown in erythrocytes, not liver. exposure: Chronic alcohol abuse; acetaldehyde and ethanol applied to erythrocytes evidence_span: {"source_cache": "artifacts/alcohol-research/4359937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08", "start_char": 0, "end_char": 1650, "text_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08"} [alcohol-p4359937] Vitamin B6 metabolism in chronic alcohol abuse. Pyridoxal phosphate levels in plasma and the effects of acetaldehyde on pyridoxal phosphate synthesis and degradation in human erythrocytes. (1974). https://pubmed.ncbi.nlm.nih.gov/4359937/ DOI: 10.1172/jci107607
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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