Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis.
Chiang, En-Pei I.
Selhub, Jacob.
Bagley, Pamela J.
Dallal, Gerard.
Roubenoff, Ronenn.
2005
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Abstract: Patients with rheumatoid arthritis have subnormal vitamin B6
status, both quantitatively and functionally. Abnormal vitamin B6 status in
rheumatoid arthritis has been associated with spontaneous tumor necrosis factor
(TNF)-α production and markers of inflammation, including C-reactive protein and
erythrocyte sedimentation rate. ... read moreImpaired vitamin B6 status could be a result of
inflammation, and these patients may have higher demand for vitamin B6. The aim of
this study was to determine if daily supplementation with 50 mg of pyridoxine for 30
days can correct the static and/or the functional abnormalities of vitamin B6 status
seen in patients with rheumatoid arthritis, and further investigate if pyridoxine
supplementation has any effects on the pro-inflammatory cytokine TNF-α or IL-6
production of arthritis. This was a double-blinded, placebo-controlled study
involving patients with rheumatoid arthritis with plasma pyridoxal 5'-phosphate below
the 25th percentile of the Framingham Heart Cohort Study. Vitamin B6 status was
assessed via plasma and erythrocyte pyridoxal 5'-phosphate concentrations, the
erythrocyte aspartate aminotransferase activity coefficient (αEAST), net homocysteine
increase in response to a methionine load test (ΔtHcy), and 24 h urinary xanthurenic
acid (XA) excretion in response to a tryptophan load test. Urinary 4-pyridoxic acid
(4-PA) was measured to examine the impact of pyridoxine treatment on vitamin B6
excretion in these patients. Pro-inflammatory cytokine (TNF-α and IL-6) production,
C-reactive protein levels and the erythrocyte sedimentation rate before and after
supplementation were also examined. Pyridoxine supplementation significantly improved
plasma and erythrocyte pyridoxal 5'-phosphate concentrations, erythrocyte αEAST,
urinary 4-PA, and XA excretion. These improvements were apparent regardless of
baseline B6 levels. Pyridoxine supplementation also showed a trend (p < 0.09)
towards a reduction in post-methionine load ΔtHcy. Supplementation did not affect
pro-inflammatory cytokine production. Although pyridoxine supplementation did not
suppress pro-inflammatory cytokine production in patients with rheumatoid arthritis,
the suboptimal vitamin B6 status seen in rheumatoid arthritis can be corrected by 50
mg pyridoxine supplementation for 30 days. Data from the present study suggest that
patients with rheumatoid arthritis may have higher requirements for vitamin B6 than
those in a normal healthy population.
Keywords: 4-pyridoxic acid, erythrocyte aspartate aminotransferase activity coefficient, C-reactive protein, net homocysteine increase in response to a methionine load test, erythrocyte aspartate aminotransferase, erythrocyte sedimentation rate, General Clinical Research Center, New England Medical Center, peripheral blood mononuclear cells, plasma total homocysteine, tumor necrosis factor, 24 h urinary xanthurenic acid excretion in response to a tryptophan load test.
Springer Open.read less - Chiang, En-Pei, Jacob Selhub, Pamela J. Bagley, Gerard Dallal, and Ronenn Roubenoff. "Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis." Arthritis Research & Therapy 7, no. 6 (12, 2005): 1-8.
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