Editors' ChoiceDERMATOLOGY

A vitamin to D-crease sunburn

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Science Translational Medicine  14 Jun 2017:
Vol. 9, Issue 394, eaan5233
DOI: 10.1126/scitranslmed.aan5233


High doses of oral vitamin D3 attenuate skin inflammation following experimentally induced sun damage.

Summer is upon us; so what to do if you forget to reapply your sunscreen? To avoid a nasty sunburn, Scott et al. suggest we could reach for vitamin D rather than aloe vera. Produced in the skin following ultraviolet (UV) light exposure and then hydoxylated to its active form in the liver and kidney, vitamin D has long been recognized as critical for calcium homeostasis and bone health. Although recently touted to reduce cancer risk, cardiovascular disease, and susceptibility to infections and autoimmunity, there is as yet insufficient evidence to recommend dietary supplementation for any of these extra-skeletal indications.

Scott et al. report a randomized, double-blinded pilot study designed to test whether vitamin D attenuates skin inflammation following UV-induced injury— i.e., sunburn. Twenty healthy adult subjects received either placebo or one of three oral vitamin D3 doses 1 hour after controlled exposure to UV light. Compared with placebo and lower doses tested, 200,000 IU of vitamin D3 reduced visible redness and histologic evidence of structural skin damage assessed at 48 hours. These protective effects were associated with dose-dependent reductions in skin expression of tumor necrosis factor–α and inducible nitric oxide synthase (iNOS), two key mediators of UV-induced inflammation. Unsupervised hierarchical clustering based on results of whole-skin microarray revealed a subset of subjects with a gene signature characterized by reduced expression of proinflammatory mediators and skin barrier repair pathways. These “vitamin D responders,” most of whom had received high-dose vitamin D3, also had less skin redness and higher serum levels of 25-hydroxylated vitamin D post-intervention.

These intriguing results suggest that a single high-dose of oral vitamin D mitigates inflammatory sequelae of UV-induced skin injury. Although the authors note that arginase-1, which has the capacity to reduce iNOS, was up-regulated in skin macrophages of “vitamin D responders,” the mechanisms for vitamin D-associated protection from skin inflammation remain unknown. Assuming these findings are replicated in a larger study, we also need to understand whether high-dose vitamin D could increase mutation rates by uncoupling UV injury from immune-mediated tissue repair and removal of damaged keratinocytes. For now, this dermatologist will keep her sunscreen close by.

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