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Oral Vitamin D Increases Cathelicidin in Lesional Skin


 

KYOTO, JAPAN — Supplementation with oral vitamin D boosted chronically low levels of the antimicrobial peptide cathelicidin in the lesional skin of atopic dermatitis patients in a controlled trial, reported Dr. Tissa R. Hata.

These promising results of an initial 28-patient, 3-week, proof-of-concept study provide the rationale for larger and longer clinical trials testing the hypothesis that oral vitamin D supplementation will reduce the susceptibility of atopic dermatitis patients to recurrent skin infections, added Dr. Hata of the University of California, San Diego, at an international investigative dermatology meeting.

The expression of cathelicidin is abnormally low in the lesional skin of atopic dermatitis patients, she said. It is also known, based upon in vitro studies, that toll-like receptor stimulation of human macrophages induces expression of the vitamin D receptor as well as an enzyme, CYP27B1, which converts 25-hydroxycholecalciferol into immunologically active 1,25-dihydroxycholecalciferol, which then induces expression of cathelicidin in myeloid dendritic cells and keratinocytes. Dr. Hata and coworkers decided to see if this was also true in vivo.

She reported on 14 atopic dermatitis patients and 14 healthy controls who took 4,000 IU of oral vitamin D daily for 21 days. Two-millimeter punch biopsies were obtained before and after treatment.

After 3 weeks of vitamin D supplementation, cathelicidin expression in the lesional skin of atopic dermatitis patients increased significantly from a median baseline 2.7 relative copy units to 21.8 relative copy units.

Supplementation with oral vitamin D appeared to boost cathelicidin production in atopic lesional skin only. There was no significant change in cathelicidin levels in the control subjects' skin, nor in the nonlesional skin of atopic dermatitis patients, Dr. Hata noted at the meeting of the European Society for Dermatological Research, the Japanese Society for Investigative Dermatology, and the Society for Investigative Dermatology.

Her study builds upon the work of Dr. Robert L. Modlin and coworkers at the University of California, Los Angeles, who 2 years ago in a landmark study elucidated the physiologic mechanism for vitamin D's antimicrobial and immunologic effects.

The UCLA study (Science 2006;311:1770–3) triggered ongoing intense worldwide dermatologic research into the role of vitamin D in various inflammatory skin diseases. It also helped turn the role of vitamin D deficiency in a variety of diseases into a hot topic among the general public.

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