目的:以前的研究表明,左旋多巴治疗帕金森病(PD)可提高循环同型半胱氨酸水平,这与心血管和神经系统疾病的风险增加有关,或血栓形成。本试验旨在检查是否摄入维生素B12,叶酸,和维生素D3补充剂改善了同型半胱氨酸水平和生活质量(QoL)。
方法:在罗马尼亚的多个中心进行了一项干预性前瞻性试验。临床确定的PD参与者服用至少300毫克/天的左旋多巴超过1年,每天服用含有800UI维生素D3,1000微克叶酸的补充剂,和15微克的维生素B12.他们被随访6个月,他们的血清同型半胱氨酸,维生素B12,维生素D,在基线和治疗6个月时测量QoL评分。QoL是使用15D问卷测量的,评估流动性,愿景,听力,呼吸,睡觉,吃,演讲,排泄,平时的活动,心理功能,不适和症状,抑郁症,苦恼,活力,性活动。
结果:24名PD患者,平均年龄71±5.04岁(男性54.2%,女性45.8%)完成了研究。干预之后,演讲的平均得分,心理功能,不适和症状,抑郁症,QoL显著增加(均p<0.05)。此外,血清同型半胱氨酸和维生素D显著升高(分别为p<0.0001和p=0.025)。治疗6个月时维生素B12的变化无统计学意义(p=0.996)。在我们已经证明的高半胱氨酸变化中没有发现性别差异,维生素B12,维生素D,和QoL水平(全部p<0.05)。
结论:这项研究的结果表明,膳食中维生素B12、叶酸、和维生素D3显著降低PD患者的同型半胱氨酸维度,最终提高患者的QoL总分。随着时间的推移,我们已经成功地捕捉到了补充方案的潜在益处,并提供了对管理PD的更广泛影响的见解,重点是营养支持。
OBJECTIVE: Previous studies have shown that the levodopa treatment of Parkinson\'s disease (PD) elevates circulating homocysteine levels, which are associated with an increased risk of cardiovascular and neurological disorders, or thrombosis. The present trial aimed to examine whether the intake of vitamin B12, folic acid, and vitamin D3 supplements improved homocysteine level and quality of life (QoL).
METHODS: An interventional prospective trial was conducted in multiple centers across Romania. Participants with clinically established PD taking at least 300 mg/day of levodopa for more than 1 year received a daily tablet of a supplement containing 800 UI of vitamin D3, 1000 µg of folic acid, and 15 µg of vitamin B12. They were followed for 6 months and their serum homocysteine, vitamin B12, vitamin D, and QoL scores were measured at baseline and at 6 months of treatment. QoL was measured using a 15D questionnaire, which assesses mobility, vision, hearing, breathing, sleeping, eating, speech, excretion, usual activities, mental function, discomfort and symptoms, depression, distress, vitality, and sexual activity.
RESULTS: Twenty-four PD patients with a mean age of 71 ± 5.04 years (54.2% male and 45.8% female) finished the study. After the intervention, the mean score of speech, mental function, discomfort and symptoms, depression, and QoL significantly increased (p < 0.05 for all). Also, the serum homocysteine and vitamin D were significantly enhanced (p < 0.0001 and p = 0.025, respectively). Changes in vitamin B12 were not statistically significant at 6 months of treatment (p = 0.996). No gender differences were found among the changes that we have demonstrated for homocysteine, vitamin B12, vitamin D, and QoL levels (p < 0.05 for all).
CONCLUSIONS: The findings of this study showed that the dietary intake of vitamin B12, folic acid, and vitamin D3 remarkably decreased the dimensions of homocysteine and finally increased the total score of QoL in PD patients. We have successfully captured the potential benefits of the supplementation regimen over time and provided insights into the broader implications for managing PD with a focus on nutritional support.