11 May 2010

Vitiligo may offer natural defense against skin cancer

Results of a new study suggest that people with vitiligo may have natural protection against skin cancer, BBC News reports. A University of London study of 4,300 people identified a common gene mutation that both increases the chance of vitiligo and cuts cancer risk. The finding, reported in the New England Journal of Medicine, is based on genetic testing of 1,514 patients with vitiligo and 2,813 without. Researchers identified a total of seven genes that were linked to vitiligo. According to the study authors, about 70 percent of people in the general population have the gene combination that increases the risk of vitiligo while reducing the risk of malignant melanoma. Thirty percent have a different version that raises melanoma risk while lessening the chances of vitiligo. The study notes that while everyone has one of the two variants, neither guarantees that either vitiligo or melanoma will actually develop — just as neither guarantees protection.

09 May 2010

vitiligo and Vitamin D

According to the research I have done, it’s safe to say that Vitamin D plays a large role in vitiligo. This morning I came across a very interesting article in the Journal of Drugs in Dermatology from July, 2008. Have a read and tell me what you think Vitiligo: nonsurgical treatment options and the evidence behind their use Topical Vitamin D3 Analogs Topical treatment with vitamin D3 analogs, specifically calciprotriol and tacalcitol, gained consideration as possible treatments for vitiligo following reports of hyperpigmentation in psoriasis patients. (48) The exact mechanism by which vitamin D may be a useful treatment for vitiligo is unclear, but there are numerous possibilities. One possible aspect of vitamin D’s utility is believed to be through modulation of the immune system. This is based on the fact that immune cells, such as T cells, B cells, and macrophages, express vitamin D receptors. In addition, animal models of autoimmune disease have been shown to respond to vitamin D supplementation. Vitamin D suppresses T-cell activation and the expression of cytokines such as TNF-[alpha] and IFN-[gamma]. Vitamin D’s immune modulation has already proven to be useful in the treatment of psoriasis. Furthermore, keratinocytes, melanocytes, and fibroblasts also express vitamin D receptors, and vitamin D has been associated with the maturation and differentiation of melanocytes. (5) There has even been found a polymorphism of the vitamin D receptor gene, APAI, that was shown to be associated with vitiligo in a small inbred Romanian community. (49) The efficacy of topical vitamin D3 may also be due to its antioxidant properties, helping melanocytes respond to increased levels of reactive oxygen species found in keratinocytes and melanocytes from vitiligo lesions. Another mechanism may be through vitamin D’s ability to regulate calcium homeostasis. Oxidative stress from hydrogen peroxide has been shown to disrupt calcium homeostasis in vitiligo epidermis, and some believe that vitamin D may have the capacity to restore it. (5), (50) Investigations of the use of calciprotriol as a monotherapy have generally showed poor results. In 1 study, however, the combination of calciprotriol with corticosteroids indicated that it may hold promise. This study treated 12 patients with combination topical steroids and calciprotriol, and 83% responded to therapy with an average repigmentation of 95% of body surface area. Interestingly, 4 of the patients who responded had previously failed steroid monotherapy. (51) There have also been positive results in studies combining it with phototherapy. A placebo-controlled, double-blind study of 35 patients concluded that calciprotriol combined with PUVA resulted in significantly higher percentages of repigmentation. Sixty-three percent of the lesions treated with PUVA and calciprotriol achieved complete repigmentation as compared to only 15% when PUVA was used with a placebo. (52) Unfortunately, investigations of calciprotriol combined with NBUVB have had conflicting results. Some studies have found that calciprotriol potentiates the effects of NBUVB treatment, such as a recent prospective left, right comparison study of 28 patients by Goktas et al. (53) However, a more recent randomized comparative study of 40 patients concluded that topical calciprotriol did not significantly enhance the results of NBUVB. (54) In addition, Goldinger et al concluded in a single-blinded, right/left comparison that topical calciprotriol did not enhance the activity of treatment with a 308-nm excimer laser. (48) Adding to the confusion, other studies indicate that the related vitamin D analog tacalcitol has synergistic effects with both NBUVB and the 308-nm excimer laser. (55), (56) Despite some negative results, the use of vitamin D analogs is still being pursued. This is evidenced by a recent case report which described a pediatric patient who had failed steroid treatment, but was successfully treated with tacalcitol and 30 minutes of daily sunlight exposure. (57)