25-hydroxyvitamin D status is associated with chronic cerebral small vessel disease

Pil-Wook Chung1, Kwang-Yeol Park2, Jeong-Min Kim1

  • 1From the Department of Neurology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea (P.-W.C., Y.B.K., H.-S.M.); Department of Neurology (K.-Y.P., J.-M.K., D.-W.S., M.-S.P., S.-W.A., H.-W.S.) and Division of Endocrinology, Department of Internal Medicine (Y.J.C.), Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea; and Department of Neurology, Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea (S.-Y.H.).

Stroke
|November 27, 2014
PubMed

Insights

Low levels of 25-hydroxyvitamin D (25(OH)D) are linked to markers of cerebral small vessel disease, including lacunes, white matter hyperintensity, and microbleeds. These findings suggest vitamin D may play a role in preventing small vessel disease.

Area of Science:

  • Neurology
  • Endocrinology
  • Radiology

Background:

  • Cerebral small vessel disease (SVD) is a major cause of stroke and cognitive impairment.
  • Neuroimaging techniques reveal key SVD markers such as lacunes, white matter hyperintensity, and cerebral microbleeds (CMB).
  • The role of vitamin D in cerebrovascular health is an emerging area of research.

Purpose of the Study:

  • To investigate the association between 25-hydroxyvitamin D (25(OH)D) levels and neuroimaging indicators of SVD.
  • To determine if 25(OH)D deficiency is linked to specific SVD markers like lacunes, white matter hyperintensity, and CMB.

Main Methods:

  • A cohort of 759 patients with acute ischemic stroke or transient ischemic attack was analyzed.
  • Magnetic resonance imaging (MRI) was used to assess lacunes, white matter hyperintensity, and CMB.
  • Linear and logistic regression models were employed to test the association between 25(OH)D levels and SVD markers.

Main Results:

  • Lower 25(OH)D levels were significantly associated with an increased presence of lacunes, severe white matter hyperintensity, and deep CMB.
  • Vitamin D deficiency (≤25 nmol/L) showed a strong association with all assessed SVD markers.
  • These associations persisted after multivariable adjustment and in subgroups of previously healthy individuals.

Conclusions:

  • 25-hydroxyvitamin D is inversely associated with key neuroimaging markers of cerebral small vessel disease.
  • The findings suggest a potential link between vitamin D status and SVD.
  • Future clinical trials should explore the efficacy of 25(OH)D supplementation in preventing SVD progression.
Abstract

Keywords:
vitamin D