Diabetes Research Unit, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield.
Department of Oncology and Human Metabolism, University of Sheffield, Sheffield.
Diabet Med. 2019 Jan;36(1):44-51. doi: 10.1111/dme.13798. Epub 2018 Sep 20.
Recent studies have reported an association between low vitamin D levels and diabetic peripheral neuropathy. However, many of these did not differentiate between people with painful diabetic peripheral neuropathy and those with painless diabetic peripheral neuropathy, or assess major confounding factors including sunlight exposure and daily activity. Our study addressed these limitations and evaluated vitamin D levels in people with carefully phenotyped diabetic peripheral neuropathy and controls.
Forty-five white Europeans with Type 2 diabetes and 14 healthy volunteers underwent clinical and neurophysiological assessments. People with Type 2 diabetes were then divided into three groups (17 with painful diabetic peripheral neuropathy, 14 with painless diabetic peripheral neuropathy and 14 with no diabetic peripheral neuropathy). All had seasonal sunlight exposure and daily activity measured, underwent a lower limb skin biopsy and had 25-hydroxyvitamin D measured during the summer months, July to September.
After adjusting for age, BMI, activity score and sunlight exposure, 25-hydroxyvitamin D levels (nmol/l) (se) were significantly lower in people with painful diabetic peripheral neuropathy [painful diabetic peripheral neuropathy 34.9 (5.8), healthy volunteers 62.05 (6.7), no diabetic peripheral neuropathy 49.6 (6.1), painless diabetic peripheral neuropathy 53.1 (6.2); ANCOVAP = 0.03]. Direct logistic regression was used to assess the impact of seven independent variables on painful diabetic peripheral neuropathy. Vitamin D was the only independent variable to make a statistically significant contribution to the model with an inverted odds ratio of 1.11. Lower 25-hydroxyvitamin D levels also correlated with lower cold detection thresholds (r = 0.39, P = 0.02) and subepidermal nerve fibre densities (r = 0.42, P = 0.01).
We have demonstrated a significant difference in 25-hydroxyvitamin D levels in well-characterized people with painful diabetic peripheral neuropathy, while accounting for the main confounding factors. This suggests a possible role for vitamin D in the pathogenesis of painful diabetic peripheral neuropathy. Further prospective and intervention trials are required to prove causality between low vitamin D levels and painful diabetic peripheral neuropathy.
最近的研究报告称，维生素 D 水平低与糖尿病周围神经病变有关。然而，其中许多研究没有区分有痛性糖尿病周围神经病变和无痛性糖尿病周围神经病变患者，也没有评估包括阳光暴露和日常活动在内的主要混杂因素。我们的研究解决了这些局限性，并评估了经过精心表型分析的糖尿病周围神经病变患者和对照者的维生素 D 水平。
45 名白人欧洲 2 型糖尿病患者和 14 名健康志愿者接受了临床和神经生理学评估。然后，2 型糖尿病患者被分为三组（17 名有痛性糖尿病周围神经病变患者、14 名无痛性糖尿病周围神经病变患者和 14 名无糖尿病周围神经病变患者）。所有患者均测量了季节性阳光暴露和日常活动量，进行了下肢皮肤活检，并在 7 月至 9 月夏季测量了 25-羟维生素 D。
在调整年龄、BMI、活动评分和阳光暴露后，痛性糖尿病周围神经病变患者的 25-羟维生素 D 水平（nmol/L）[痛性糖尿病周围神经病变患者 34.9（5.8），健康志愿者 62.05（6.7），无糖尿病周围神经病变患者 49.6（6.1），无痛性糖尿病周围神经病变患者 53.1（6.2）；ANCOVAP=0.03]显著较低。直接逻辑回归用于评估七个独立变量对痛性糖尿病周围神经病变的影响。维生素 D 是唯一对模型有统计学意义贡献的独立变量，其比值比为 1.11。较低的 25-羟维生素 D 水平也与较低的冷觉阈值（r=0.39，P=0.02）和表皮下神经纤维密度（r=0.42，P=0.01）相关。
我们已经证明了在经过精心表型分析的痛性糖尿病周围神经病变患者中，25-羟维生素 D 水平存在显著差异，同时考虑了主要混杂因素。这表明维生素 D 可能在痛性糖尿病周围神经病变的发病机制中起作用。需要进一步的前瞻性和干预性试验来证明低维生素 D 水平与痛性糖尿病周围神经病变之间的因果关系。
