Tovar A R, Gómez E, Bourges H, Ortíz V, Kraus A, Torres N
Department of Physiology of Nutrition, Instituto Nacional de Ciencias Médicas y Nutricion, México, México.
Eur J Clin Nutr. 2002 Nov;56(11):1087-93. doi: 10.1038/sj.ejcn.1601450.
There is evidence that pyridoxine deficiency may alter the immune response. It is not known whether a deficiency of this vitamin is evident in subjects with primary Sjögren's syndrome (SS).
We studied whether subjects with primary SS showed a biochemical deficiency of pyridoxine, and if it is associated with abnormal production of interleukin-2 from lymphocytes stimulated in vitro with phytohemagglutinin (PHA).
Two studies were conducted, (i) biochemical and nutritional assessments were performed in a cross-over study in subjects with primary SS, who were supplemented with 25 mg/day of pyridoxine or placebo for 3 months. After 1 month washout, they were supplemented for 3 months with placebo, (ii) patients with SS and matched controls received pyridoxine or placebo for 45 days, and a blood sample was obtained to study IL-2 production and expression in T-lymphocytes stimulated with PHA.
Subjects with primary SS showed limited dietary intake of pyridoxine and biochemical deficiency of this vitamin assessed through the activation coefficient of the erythrocyte aspartate aminotransferase. The biochemical deficiency did not affect production nor mRNA expression of IL-2 from T-lymphocytes stimulated in vitro with PHA compared with the control group. Supplementation of subjects with primary SS with 25 mg/day with pyridoxine for 45 days did not produce any significant change as compared to those patients supplemented with placebo.
Subjects with primary SS showed biochemical deficiency of pyridoxine, possibly due to limited intake of this vitamin which was corrected by supplementation with pyridoxine. However, IL-2 production and mRNA expression from stimulated lymphocytes were unaffected by supplementation, probably because the deficiency was not severe enough to affect the immune system.
This work was supported by the National Council of Science and Technology (CONACYT), Mexico, grant no. 212226-5-0902PM.
有证据表明维生素B6缺乏可能会改变免疫反应。目前尚不清楚原发性干燥综合征（SS）患者是否存在这种维生素缺乏的情况。
我们研究了原发性SS患者是否存在维生素B6的生化缺乏，以及这是否与体外经植物血凝素（PHA）刺激的淋巴细胞白细胞介素-2的异常产生有关。
进行了两项研究，（i）在一项交叉研究中，对原发性SS患者进行生化和营养评估，这些患者每天补充25毫克维生素B6或安慰剂，为期3个月。经过1个月的洗脱期后，他们接受3个月的安慰剂补充，（ii）SS患者和匹配的对照组接受45天的维生素B6或安慰剂治疗，并采集血样以研究经PHA刺激的T淋巴细胞中白细胞介素-2的产生和表达。
原发性SS患者通过红细胞天冬氨酸转氨酶激活系数评估显示维生素B6的饮食摄入量有限且存在生化缺乏。与对照组相比，这种生化缺乏并不影响体外经PHA刺激的T淋巴细胞中白细胞介素-2的产生或mRNA表达。原发性SS患者每天补充25毫克维生素B6，持续45天，与补充安慰剂的患者相比，未产生任何显著变化。
原发性SS患者存在维生素B6的生化缺乏，可能是由于这种维生素的摄入量有限，补充维生素B6可纠正这一情况。然而，补充维生素对刺激淋巴细胞产生的白细胞介素-2和mRNA表达没有影响，可能是因为缺乏程度不够严重，不足以影响免疫系统。
这项工作得到了墨西哥国家科学技术委员会（CONACYT）的支持，资助号为212226-5-0902PM。
