KMCRIC

Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease.

Suzuki M, Yoshioka M, Hashimoto M, Murakami M, Noya M, Takahashi D, Urashima M.

Am J Clin Nutr.

2013

97(5)

1004-1013.

10.3945/ajcn.112.051664.

23485413

http://www.ncbi.nlm.nih.gov/pubmed/23485413

Aged
Blood Pressure
Body Mass Index
Calcium, Dietary/blood
Cholecalciferol/administration & dosage*
Cholecalciferol/blood
Dietary Supplements*
Disease Progression
Double-Blind Method
Endpoint Determination
Female
Follow-Up Studies
Genotype
Humans
Male
Middle Aged
Parathyroid Hormone/blood
Parkinson Disease/drug therapy*
Parkinson Disease/genetics
Questionnaires
Receptors, Calcitriol/genetics
Receptors, Calcitriol/metabolism

KMCRIC 비평 보기 +

BACKGROUND: In our previous study, higher serum 25-hydroxyvitamin D [25(OH)D] concentrations and the vitamin D receptor (VDR) FokI CC genotype were associated with milder Parkinson disease (PD). OBJECTIVE: We evaluated whether vitamin D3 supplementation inhibits the progression of PD on the basis of patient VDR subgroups. DESIGN: Patients with PD (n = 114) were randomly assigned to receive vitamin D3 supplements (n = 56; 1200 IU/d) or a placebo (n = 58) for 12 mo in a double-blind setting. Outcomes were clinical changes from baseline and the percentage of patients who showed no worsening of the modified Hoehn and Yahr (HY) stage and Unified Parkinson's Disease Rating Scale (UPDRS). RESULTS: Compared with the placebo, vitamin D3 significantly prevented the deterioration of the HY stage in patients [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)]. Interaction analyses showed that VDR FokI genotypes modified the effect of vitamin D3 on changes in the HY stage (P-interaction = 0.045), UPDRS total (P-interaction = 0.039), and UPDRS part II (P-interaction = 0.021). Compared with the placebo, vitamin D3 significantly prevented deterioration of the HY stage in patients with FokI TT [difference between groups: P = 0.009; change within vitamin D3 group: -0.38 ± 0.48 (P = 0.91); change within placebo group, +0.63 ± 0.77 (P = 0.009)] and FokI CT [difference between groups: P = 0.020; change within vitamin D3 group: ±0.00 ± 0.60 (P = 0.78); change within placebo group: +0.37 ± 0.74 (P = 0.014)] but not FokI CC. Similar trends were observed in UPDRS total and part II. CONCLUSION: Vitamin D3 supplementation may stabilize PD for a short period in patients with FokI TT or CT genotypes without triggering hypercalcemia, although this effect may be nonspecific for PD. This trial was registered at UMIN Clinical Trials Registry as UMIN000001841.

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