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. Impaired 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.
Highlights
Patients with rheumatoid arthritis have reduced circulating levels of vitamin B6 compared to healthy subjects [1,2,3]
Abnormal vitamin B6 status in rheumatoid arthritis has been associated with spontaneous tumor necrosis factor (TNF)-α production [1] and markers of inflammation, including C-reactive protein (CRP) and erythrocyte sedimentation rate [5]
We previously reported that patients with rheumatoid arthritis have mild but significantly elevated ∆total homocysteine (tHcy) in response to methionine load compared to age- and gender-matched healthy controls [2,16]
Summary
Patients with rheumatoid arthritis have reduced circulating levels of vitamin B6 compared to healthy subjects [1,2,3]. We have demonstrated that low plasma pyridoxal 5'-phosphate levels reflect the impaired functional vitamin B6 status in these patients. 4-PA = 4-pyridoxic acid; αEAST = erythrocyte aspartate aminotransferase activity coefficient; CRP = C-reactive protein; ∆tHcy = net homocysteine increase in response to a methionine load test; EAST = erythrocyte aspartate aminotransferase; ESR = erythrocyte sedimentation rate; GCRC = General Clinical Research Center; NEMC = New England Medical Center; PBMC = peripheral blood mononuclear cells; tHcy = plasma total homocysteine; TNF = tumor necrosis factor; XA = 24 h urinary xanthurenic acid excretion in response to a tryptophan load test. Abnormal vitamin B6 status in rheumatoid arthritis has been associated with spontaneous tumor necrosis factor (TNF)-α production [1] and markers of inflammation, including C-reactive protein (CRP) and erythrocyte sedimentation rate [5]. We recently showed that adjuvant arthritis caused tissue-specific depletion of vitamin B6 in rats [6], suggesting that the impaired vitamin B6 metabolism in patients with rheumatoid arthritis result from inflammation, and these patients may have higher requirements for vitamin B6 than those in a normal healthy population
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