Chiang En-Pei I, Selhub Jacob, Bagley Pamela J, Dallal Gerard, Roubenoff Ronenn
Department of Food Science and Biotechnology, National Chung-Hsing University, 250 Kuo-Kuang Road, Taichung, Taiwan 402, Republic of China.
Arthritis Res Ther. 2005;7(6):R1404-11. doi: 10.1186/ar1839. Epub 2005 Oct 14.
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 (alphaEAST), net homocysteine increase in response to a methionine load test (DeltatHcy), 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 alphaEAST, 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 DeltatHcy. 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.
类风湿关节炎患者的维生素B6水平无论在数量上还是功能上都低于正常水平。类风湿关节炎患者维生素B6状态异常与自发性肿瘤坏死因子（TNF）-α产生以及炎症标志物有关，包括C反应蛋白和红细胞沉降率。维生素B6状态受损可能是炎症的结果，并且这些患者可能对维生素B6有更高的需求。本研究的目的是确定连续30天每天补充50毫克吡哆醇是否可以纠正类风湿关节炎患者维生素B6状态的静态和/或功能异常，并进一步研究补充吡哆醇是否对关节炎的促炎细胞因子TNF-α或IL-6产生有任何影响。这是一项双盲、安慰剂对照研究，涉及血浆5'-磷酸吡哆醛低于弗雷明汉心脏队列研究第25百分位数的类风湿关节炎患者。通过血浆和红细胞5'-磷酸吡哆醛浓度、红细胞天冬氨酸转氨酶活性系数（αEAST）、蛋氨酸负荷试验后同型半胱氨酸净增加量（ΔtHcy）以及色氨酸负荷试验后24小时尿黄尿酸（XA）排泄量来评估维生素B6状态。测量尿4-吡哆酸（4-PA）以检查吡哆醇治疗对这些患者维生素B6排泄的影响。还检查了补充前后促炎细胞因子（TNF-α和IL-6）产生、C反应蛋白水平和红细胞沉降率。补充吡哆醇显著改善了血浆和红细胞5'-磷酸吡哆醛浓度、红细胞αEAST、尿4-PA和XA排泄。无论基线B6水平如何，这些改善都是明显的。补充吡哆醇还显示出蛋氨酸负荷后ΔtHcy有降低的趋势（p<0.09）。补充并未影响促炎细胞因子的产生。虽然补充吡哆醇并未抑制类风湿关节炎患者促炎细胞因子的产生，但类风湿关节炎患者中未达最佳水平的维生素B6状态可通过连续30天补充50毫克吡哆醇得到纠正。本研究数据表明，类风湿关节炎患者对维生素B6的需求可能高于正常健康人群。
