Abstract: Previously we observed strong and consistent associations
between vitamin B6 status and several indicators of inflammation in patients with
rheumatoid arthritis. Clinical indicators, including the disability score, the length
of morning stiffness, and the degree of pain, and biochemical markers, including the
erythrocyte sedimen... read moretation rate and C-reactive protein levels, were found to be
inversely correlated with circulating vitamin B6 levels. Such strong associations
imply that impaired vitamin B6 status in these patients results from inflammation. In
the present study we examined whether inflammation directly alters vitamin B6 tissue
contents and its excretion in vivo. A cross-sectional case-controlled human clinical
trial was performed in parallel with experiments in an animal model of inflammation.
Plasma and erythrocyte and pyridoxal 5'-phosphate concentrations, urinary 4-pyridoxic
acid excretion, and the activity coefficient of erythrocyte aspartate
aminotransferase were compared between patients and healthy subjects. Adjuvant
arthritis was induced in rats for investigating hepatic and muscle contents as well
as the urinary excretion of vitamin B6 during acute and chronic inflammation.
Patients with rheumatoid arthritis had low plasma pyridoxal 5'-phosphate compared
with healthy control subjects, but normal erythrocyte pyridoxal 5'-phosphate and
urinary 4-pyridoxic acid excretion. Adjuvant arthritis in rats did not affect
4-pyridoxic acid excretion or muscle storage of pyridoxal 5'-phosphate, but it
resulted in significantly lower pyridoxal 5'-phosphate levels in circulation and in
liver during inflammation. Inflammation induced a tissue-specific depletion of
vitamin B6. The low plasma pyridoxal 5'-phosphate levels seen in inflammation are
unlikely to be due to insufficient intake or excessive vitamin B6 excretion. Possible
causes of decreased levels of vitamin B6 are discussed.