VITILIGO: EPIDEMIOLOGY, DIFFERENTIAL DIAGNOSIS AND ETIOLOGY

By: Sandeep Dhand

Vitiligo is a depigmenting disorder characterized by the development of white patches in various distributions, which are due to the loss of melanocytes from the epidermis.

Alikhan provided statistical data on the treatments and symptoms of vitiligo patients. In his studies he states cases have been reported as early as 6 weeks after birth.

This article mentions one study found progression in 88.8% of patients, more so with positive family histories, NSV, a longer duration, Koebner phenomenon, and mucous membrane involvement.

The link with AI thyroid disorders (hypothyroidism and hyperthyroidism) is the most well established. They may be present in as many as 24% of pediatric vitiligo patients. One study identified thyroid disease in 18.5% of 15,126 vitiligo patients.

The current thought is that vitiligo represents a group of heterogeneous pathophysiologic disorders with a similar phenotype

Among vitiligo patients, 20% report thyroid disease (an 8-fold increase over the general population), particularly hypothyroidism.

The Oxidative stress hypothesis states it is unclear why both lesional and nonlesional skin from vitiligo patients has abnormally low levels of catalase enzyme, which correlates with high H2O2 levels throughout the epidermis.

-Kingo aimed to analyze changes in expression of genes involved in skin pigmentation .

With quantitative RT-PCR they measured the mRNA expression levels of eight genes from the melanocortin system and two enzymes involved in melanogenesis.

Expression of melanocortin receptors was increased in unaffected skin of vitiligo patients compared to healthy subjects.

The differences were statistically significant in the cases of MC1R (melanocortin receptor 1) and MC4R (melanocortin receptor 4).

The purpose of Park’s study was to use UV-B radiation exclusively on vitiligo patches of individuals affected by SV.

BIOSKIN can produce a focused beam of UV-B (microphoto-therapy) on vitiligo patches only.

In Park’s studies it is suggested that the sera of vitiligo patients have autoantibodies mostly directed to the 65-kDa melanocyte surface antigen and that this antigen may play a role in the development or improvement of vitiligo.

It has been shown that concentrations of a-MSH are reduced in the epidermis of vitiligo patients which could contribute to the pathogenesis of vitiligo.

a-MSH immunoreactivity originates, possibly in the pituitary but also other tissues, e.g., the skin.

Lower plasma a-MSH levels might represent an immuno-endocrine condition with higher susceptibility for the development of autoimmune depigmentation.

In conclusion, it is suggested that the sera of vitiligo patients have autoantibodies mostly directed to the 65-kDa melanocyte surface antigen and that this antigen may play a role in the development or improvement of vitiligo.

CITATIONS Alikhan, A. (2011). Vitiligo: A comprehensive overview: Part I.

Introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology, and work-up. Journal of the American Academy of Dermatology, 65(3), 473- 491.

Kingo, K. (2007). Gene expression analysis of melanocortin system in vitiligo. Journal of dermatological science, 48(2), 113-122.

Lotti, T M. (1999). UV-B radiation microphototherapy. An elective treatment for segmental vitiligo. Journal of the European Academy of Dermatology and Venereology, 13(2), 102-108.

Pichler, R. (2006). Vitiligo patients present lower plasma levels of α-melanotropin immunoreactivities. Neuropeptides, 40(3), 177-

184. Park, Y. (1996). Identification of autoantibody to melanocytes and

characterization of vitiligo antigen in vitiligo patients. Journal of dermatological science, 11(2), 111-121.

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