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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #203716
Title: Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis

Author
item CHIANG, EN-PEI - NAT'L CHUNG-HSING UNIV
item Selhub, Jacob
item BAGLEY, PAMELA - TUFTS UNIVERSITY
item Dallal, Gerald
item ROUBENOFF, RONENN - TUFTS UNIVERSITY

Submitted to: Arthritis Research & Therapy
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/14/2005
Publication Date: 10/14/2005
Citation: Chiang, E.I., Selhub, J., Bagley, P.J., Dallal, G., Roubenoff, R. 2005. Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis. Arthritis Research & Therapy. 133(4):1056-1059.

Interpretive Summary: People who suffer from Rheumatoid arthritis have been found to have a low level of vitamin B6 in their plasma. This low level of vitamin B6 appears to be connected with the severity of pain, disease and others. In the present study we gave patients with Rheumatoid arthritis vitamin B6 to determine if this supplementation would improve the conditions of these patients. We found that vitamin B6 increases the amount of vitamin in the blood but had no effect on the symptoms of the disease. The meaning of this relationship between B6 and disease remains to be investigated.

Technical 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)-alpha 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-alpha 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 (alpha-EAST), net homocysteine increase in response to a methionine load test (delta-tHcy), 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-alpha 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 alpha-EAST, 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 delta-tHcy. 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.