Wang Liyong, Evatt Marian L, Maldonado Lizmarie G, Perry William R, Ritchie James C, Beecham Gary W, Martin Eden R, Haines Jonathan L, Pericak-Vance Margaret A, Vance Jeffery M, Scott William K
John P. Hussman Institute for Human Genomics, University of Miami, Miller School of Medicine, Miami, Florida, USA; Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami, Miller School of Medicine, Miami, Florida, USA.
Mov Disord. 2015 Apr;30(4):560-6. doi: 10.1002/mds.26117. Epub 2014 Dec 27.
An inverse association between Parkinson disease (PD) and total vitamin D levels has been reported, but whether vitamin D from different sources, that is, 25(OH)D2 (from diet and supplements) and 25(OH)D3 (mainly from sunlight exposure), all contribute to the association is unknown. Plasma total 25(OH)D, 25(OH)D2, and 25(OH)D3 levels were measured by liquid chromatography-tandem mass spectrometry in PD patients (n = 478) and controls (n = 431). Total 25(OH)D was categorized by clinical insufficiency or deficiency; 25(OH)D2 and 25(OH)D3 were analyzed in quartiles. Vitamin D deficiency (total 25[OH]D < 20 ng/mL) and vitamin D insufficiency (total 25[OH]D < 30 ng/mL) are associated with PD risk (odds ratio [OR] = 2.6 [deficiency] and 2.1 [insufficiency]; P < 0.0001), adjusting for age, sex, and sampling season. Both 25(OH)D2 and 25(OH)D3 levels are inversely associated with PD (P(trend) < 0.0001). The association between 25(OH)D2 and PD risk is largely confined to individuals with low 25(OH)D3 levels (P(trend) = 0.0008 and 0.12 in individuals with 25[OH]D3 < 20 ng/mL and 25[OH]D3 ≥ 20 ng/mL, respectively). Our data confirm the association between vitamin D deficiency and PD, and for the first time demonstrate an inverse association of 25(OH)D2 with PD. Given that 25(OH)D2 concentration is independent of sunlight exposure, this new finding suggests that the inverse association between vitamin D levels and PD is not simply attributable to lack of sunlight exposure in PD patients with impaired mobility. The current study, however, cannot exclude the possibility that gastrointestinal dysfunction, a non-motor PD symptom, contributes to the lower vitamin D2 levels in PD patients.
已有报道称帕金森病（PD）与总维生素D水平呈负相关，但来自不同来源的维生素D，即25（OH）D2（来自饮食和补充剂）和25（OH）D3（主要来自阳光照射）是否都与这种相关性有关尚不清楚。采用液相色谱-串联质谱法测定了478例PD患者和431例对照者的血浆总25（OH）D、25（OH）D2和25（OH）D3水平。总25（OH）D根据临床不足或缺乏进行分类；25（OH）D2和25（OH）D3按四分位数进行分析。维生素D缺乏（总25[OH]D＜20 ng/mL）和维生素D不足（总25[OH]D＜30 ng/mL）与PD风险相关（优势比[OR]分别为2.6[缺乏]和2.1[不足]；P＜0.0001），并对年龄、性别和采样季节进行了校正。25（OH）D2和25（OH）D3水平均与PD呈负相关（P趋势＜0.0001）。25（OH）D2与PD风险之间的关联主要局限于25（OH）D3水平较低的个体（25[OH]D3＜20 ng/mL和25[OH]D3≥20 ng/mL的个体中，P趋势分别为0.0008和0.12）。我们的数据证实了维生素D缺乏与PD之间的关联，并首次证明了25（OH）D2与PD呈负相关。鉴于25（OH）D2浓度与阳光照射无关，这一新发现表明维生素D水平与PD之间的负相关并非仅仅归因于行动不便的PD患者缺乏阳光照射。然而，目前的研究不能排除胃肠道功能障碍（一种非运动性PD症状）导致PD患者维生素D2水平较低的可能性。
