Format

Send to

Choose Destination
Indian J Dermatol Venereol Leprol. 2013 Nov-Dec;79(6):750-8. doi: 10.4103/0378-6323.120720.

The role of vitamin D in melanogenesis with an emphasis on vitiligo.

Author information

1
Department of Dermatology; Vitiligo Research Chair, College of Medicine, King Saud University, Riyadh, Saudi Arabia.

Abstract

Vitiligo is a common pigmentary disorder caused by the destruction of functional melanocytes. Vitamin D is an essential hormone synthesized in the skin and is responsible for skin pigmentation. Low levels of vitamin D have been observed in vitiligo patients and in patients with other autoimmune diseases. Therefore, the relationship between vitamin D and vitiligo needs to be investigated more thoroughly. We reviewed the literature to date regarding the role of vitamin D in skin pigmentation. Our review revealed that vitamin D deficiency has been identified in many conditions, including premature and dysmature birth, pigmented skin, obesity, advanced age, and malabsorption. Vitamin D increases melanogenesis and the tyrosinase content of cultured human melanocytes by its antiapoptotic effect. However, a few growth-inhibitory effects on melanocytes were also reported. Vitamin D regulates calcium and bone metabolism, controls cell proliferation and differentiation, and exerts immunoregulatory activities. Vitamin D exerts its effect via a nuclear hormone receptor for vitamin D. The topical application of vitamin D increased the number of L-3,4-dihydroxyphenylalanine-positive melanocytes. The topical application of vitamin D yields significant results when used in combination with phototherapy and ultraviolet exposure to treat vitiligo in humans. Vitamin D decreases the expression of various cytokines that cause vitiligo. In conclusion, application of vitamin D might help in preventing destruction of melanocytes thus causing vitiligo and other autoimmune disorders. The association between low vitamin D levels and the occurrence of vitiligo and other forms of autoimmunity is to be further evaluated.

PMID:
24177606
DOI:
10.4103/0378-6323.120720
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Medknow Publications and Media Pvt Ltd
Loading ...
Support Center