PORTLAND, ORE. – When given within an hour, a single dose of at least 100,000 IU vitamin D₃ rapidly attenuates sunburn, according to the results of a randomized, double-blind, placebo-controlled pilot study of 25 healthy adults.

This is the first in vivo study to evaluate whether vitamin D₃ can modulate acute inflammation in target tissues, Jeffrey F. Scott, MD, wrote in a poster presented at the annual meeting of the Society for Investigative Dermatology. The findings “have broad implications for the role of vitamin D in skin homeostasis, and suggest that oral vitamin D may be clinically therapeutic for its immunomodulatory properties,” he and his coauthors concluded.

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Study participants were exposed to ultraviolet radiation to induce experimental sunburn on the left arm. One hour later, they received either oral placebo or 50,000 IU, 100,000 IU, or 200,000 IU vitamin D₃. After 24 hours, recipients of the 100,000 IU and 200,000 IU doses had a marked, sustained reduction in skin redness compared with recipients of placebo or the 50,000 IU dose.

Higher doses of vitamin D₃ also produced significant decreases in skin levels of tumor necrosis factor–alpha (TNF-alpha) (P = .02) and inducible nitric oxide synthase (iNOS) (P = .04) compared with placebo, reported Dr. Scott, a resident in dermatology at University Hospitals Cleveland Medical Center.

Notably, 48 hours after sunburn, hematoxylin and eosin histology of punch biopsies showed that participants who received 200,000 IU vitamin D₃ had the least structural damage to the skin, while placebo recipients had the most damage. Expression profiling also linked vitamin D₃ treatment with upregulation of genes associated with skin barrier repair.

Studies continue to document diverse biologic effects of vitamin D, including “modulation of immune response, inflammatory disease, cardiovascular health, and carcinogenesis,” the researchers wrote. Vitamin D₃ also has been shown to suppress inflammatory mediators and induce autophagy, they added. Previously, their group showed that oral D₃ induced similar protective effects in a mouse model of chemical skin injury. Treatment inhibited proinflammatory cytokines and chemokines within the skin, including iNOS and TNF-alpha.

The current study also included a control phase in which participants underwent experimental sunburn on the right arm without any treatment. Forty-eight hours later, punch biopsies revealed high levels of iNOS and TNF-alpha, with increased expression of proinflammatory genes, the researchers wrote.

During the subsequent experimental phase, seven participants were assigned to receive placebo, and six were assigned to receive 50,000 IU, 100,000 IU, or 200,000 IU of vitamin D₃. After treatment, participants with the highest serum D₃ levels had significantly decreased skin redness compared with participants with lower serum D₃ levels (P less than .05). Higher vitamin D₃ serum levels were also associated with significant (P less than .05) upregulation of skin barrier repair genes and of arginase-1, a cytosolic enzyme that helps mediate anti-inflammatory activity.

“Arginase-1 may be a clinically useful tissue biomarker for monitoring the immunomodulatory effects of vitamin D₃ in humans,” the researchers concluded.

The National Institute of Arthritis Musculoskeletal and Skin Diseases and the National Institutes of Health supported the work. Dr. Scott had no relevant financial disclosures.

Mridu Singh, MD

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