This case-control study of 100 cases and 100 controls in The First Afﬁliated Hospital of Xinjiang Medical University from January 2019 to December 2019,provides compelling evidence that vitamin D deficiency of PD patients is 17.13 times that in controls of similar ages with-out PD. Individuals with levels in the lowest quartile of 25(OH)D values had the highest prevalence of PD(p =0.026,OR=11.786,95%CI,1.342-103.51)compared with individuals with values in the highest quartile.To the best of our knowledge, this is the first study to investigate the relation between the deficiency of the 25(OH)D and PD in Xinjiang of China.
Several studies have reported an association of PD with lower plasma 25(OH)D concentrations[16-18]. Ding et al study shows that there was vitamin D deficiency in 17.6% of cases (68/388) compared with 9.3% of controls (26/283; p =0.002). After adjusting for for age, sex, race, and vitamin D supplementation,deficiency of total 25(OH)D remained enriched in PD with p =0.03. Wang et al study shows that Vitamin D deficiency (total 25 (OH) D <20 ng / mL) was significantly correlated with PD (P <0.0001).The lowest quartile of 25(OH)D values had the highest prevalence of PD with an OR = 2.66, P <0.0001 (95 %% CI, 1.746-4.03) compared with individuals with values in the highest quartile.Our study also draws results consistent with the above studies，in our case-control study, cases are 11.786 times as likely as controls to be in the lowest quartile compared with the highest quartile.
Suzuki et al conducted a randomized, double-blind, placebo-controlled vitamin D intervention trial,the results showed that vitamin D significantly inhibited the deterioration of the Hoehn-Yahr staging score of PD patients compared with placebo. [difference between groups: P = 0.005; mean±SD change within vitamin D3 group: +0.02 ±0.62 (P = 0.79); change within placebo group: +0.33±0.70 (P = 0.0006)]. It is suggested that vitamin D has a delaying effect on the severity of disease in PD patients, and does not cause adverse reactions such as hypercalcemia.
In our study, it was verified that there is a certain correlation between VD and H-Y classification.Especially for patients who does not yet exist with motor dysfunction (HY grade <3),There was a significant negative correlation between serum VD concentration and H-Y grade.Therefore, it can be inferred that VD can be used as an index to predict the severity of PD before PD sports injury.The lower the serum VD concentration in PD patients, the more likely to be exercise impairment.
Sleemana et alstudy result showed that mean serum 25(OH)D concentrations were lower in PD than control participants at baseline (44.1±21.7 vs. 52.2±22.1 nmol/L, p<0.05) and 18 months (44.2±23.6 vs. 55.7±28.8 nmol/L, p<0.05). There was a small but significant association between vitamin D status at baseline and disease motor severity at 36 months.
Our study is consistent with previous study results, and there is a certain correlation between VD and disease course.Especially for patients with a long course of disease (course> 6 months), the course of disease is significantly negatively correlated with serum VD concentration. With the extension of the course of disease, the value of VD in the serum of PD patients will decrease accordingly.
A prospective studyshowed that there are no support to the hypothesis that vitamin D may reduce the risk of PD.In other words, supplementing VD before the disease cannot reduce the incidence of PD. Meamar et al  study confirmed that supplementing VD during PD cannot delay the development of the disease.Previous reports indicate that there is a significant difference in the biochemical levels of bone metabolism between PD cases and the control group, this may be due to the impact of PD, not the direct role of PD pathogenesis.
Scherzer et al  study pointed out that vitamin D has been produced in rats to improve the toxicity induced by 6-hydroxydopamine.Our study also shows that there is a certain correlation between VD and H-Y classification, but the correlation is not significant (R 2 = 0.4). Studies have shown that there is a certain polymorphism of VDR in the central nervous system, and this polymorphism affects the impact of VD on its downstream response. However, it is not sufficient to explain the problem only by genetic polymorphism, so further research is needed to confirm it.
There are several limitations in our study.First,our study was conducted on patients and controls in the First Affiliated Hospital of Xinjiang Medical University, not the general Chinese population. The population and ethnic composition of this region and the differences in life are large. It is necessary to evaluate the population lacking vitamin D in other regions of China.Second,because of the relationship between detection methods, our study failed to detect the association between vitamin D from different sources and PD, only to show the correlation between serum VD concentration and PD disease progression, which needs further exploration in the next study.Three,our study is a case-control study and lacks longitudinal clinical evaluation, including multiple vitamin D measurements that fail to assess the relationship between vitamin D status (and its changes over time) and disease progression. In order to provide valuable information, the time window is essential for adequate exposure of vitamin D to prevent or delay the onset of PD. It is necessary to study the longitudinal cohort at different periods to provide valuable information.