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血浆维生素 B12 水平、高剂量维生素 B12 治疗与痴呆风险。

Plasma Vitamin B12 Levels, High-Dose Vitamin B12 Treatment, and Risk of Dementia.

机构信息

Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.

Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.

出版信息

J Alzheimers Dis. 2021;79(4):1601-1612. doi: 10.3233/JAD-201096.

DOI:10.3233/JAD-201096
PMID:33459639
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7990402/
Abstract

BACKGROUND

It is controversial whether B12 deficiency causes dementia or B12 treatment can prevent dementia.

OBJECTIVE

To assess associations between low plasma (P-)B12 levels, B12 treatment, and risk of Alzheimer's disease (AD; primary outcome) and all-cause or vascular dementia (secondary outcomes).

METHODS

We conducted a population-based cohort study using Danish registry data to assess associations between low P-B12 levels, high-dose injection or oral B12 treatment, and risk of dementia (study period 2000-2013). The primary P-B12 cohort included patients with a first-time P-B12 measurement whose subsequent B12 treatment was recorded. The secondary B12 treatment cohort included patients with a first-time B12 prescription and P-B12 measurement within one year before this prescription. For both cohorts, patients with low P-B12 levels (<200 pmol/L) were propensity score-matched 1:1 with patients with normal levels (200-600 pmol/L). We used multivariable Cox regression to compute 0-15-year hazard ratios for dementia.

RESULTS

For low P-B12 and normal P-B12 level groups, we included 53,089 patients in the primary P-B12 cohort and 13,656 patients in the secondary B12 treatment cohort. In the P-B12 cohort, hazard ratios for AD centered around one, regardless of follow-up period or treatment during follow-up. In the B12 treatment cohort, risk of AD was unaffected by low pre-treatment P-B12 levels, follow-up period and type of B12 treatment. Findings were similar for all-cause and vascular dementia.

CONCLUSION

We found no associatio1n between low P-B12 levels and dementia. Associations were unaffected by B12 treatment. Results do not support routine screening for B12 deficiency in patients with suspected dementia.

摘要

背景

维生素 B12 缺乏是否会导致痴呆,以及 B12 治疗能否预防痴呆,这一直存在争议。

目的

评估低血浆(P-)B12 水平、B12 治疗与阿尔茨海默病(AD;主要结局)以及全因性或血管性痴呆(次要结局)风险之间的关联。

方法

我们开展了一项基于人群的队列研究,使用丹麦注册数据评估低 P-B12 水平、高剂量注射或口服 B12 治疗与痴呆风险之间的关联(研究期间为 2000-2013 年)。主要 P-B12 队列纳入了首次 P-B12 检测且随后记录有 B12 治疗的患者。次要 B12 治疗队列纳入了首次开具 B12 处方且在该处方前一年内进行过 P-B12 检测的患者。对于两个队列,低 P-B12 水平(<200 pmol/L)患者与正常水平(200-600 pmol/L)患者按倾向评分 1:1 匹配。我们使用多变量 Cox 回归计算痴呆的 0-15 年风险比。

结果

在主要 P-B12 队列和次要 B12 治疗队列中,低 P-B12 和正常 P-B12 水平组分别纳入了 53089 名患者和 13656 名患者。在 P-B12 队列中,无论随访时间或随访期间的治疗如何,AD 的风险比都接近 1。在 B12 治疗队列中,低治疗前 P-B12 水平、随访时间和 B12 治疗类型均不会影响 AD 的风险。全因性和血管性痴呆也有类似的发现。

结论

我们未发现低 P-B12 水平与痴呆之间存在关联。B12 治疗不会影响这种关联。结果不支持对疑似痴呆患者常规筛查 B12 缺乏症。

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