Vitiligo: The comprehensive overview of epidemiology, treatment, for segmental vitiligo

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Journal of Writing in the Sciences

May 2012, Pages 1-12

Research Review

Vitiligo: The comprehensive overview of epidemiology, treatment, for segmental vitiligo.

Sandeep K. Dhand

Department of School of Natural Sciences, University of California Merced, U.S.A.

Writing 116, Professor Shirley Khalert


Abstract: Vitiligo is a common skin disorder that results in depigmentation. With the appropriate management, many patients can minimize disease progression, attain repigmentation, and achieve cosmetically pleasing results (Felsten 1-2). Patients with vitiligo have circulating antibodies to melanocytes (Park 1). The purpose of this research review was to understand the overview of vililitgo in epidemiology, differential diagnosis, etiology, studying UV-B radiation against generalized vitiligo along with other new advanced treatments such as BIOSKIN, ELSIA, and their success rate.



Vitiligo: A comprehensive overview : Part I. Introduction, epidemiology, quality of life, diagnosis, differential diagnosis,

associations, histopathology, etiology, and work-up.

The prevalence of the disease is around 1% in the United States and in Europe, but ranges from less than 0.1% to greater than 8% worldwide (1). Half of all patients develop the disease before 20 years of age (1). Onset at an advanced age occurs but is unusual, and should raise concerns about associated diseases, such as thyroid dysfunction, rheumatoid arthritis, diabetes mellitus, and alopecia areata. Generalized vitiligo is the most common clinical presentation and often involves the face and acral regions (1). The course of the disease is unpredictable and the response to treatment varies.

Its prevalence appears to be equal between men and women, and there is no difference in rates of occurrence according to skin type or race. It appears to be transmitted genetically in a polygenic/multifactorial manner. The actual pathogenesis is under debate and has been attributed to autoimmune (AI) causes, oxidative stress, and/or sympathetic neurogenic disturbance [1,5,6] (1). Vitiligo is generally slowly progressive, either by centrifugal expansion of current lesions and/or the appearance of new lesions. 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 (1). A significantly higher incidence of koebnerization and disease progression is seen in NSV (nonsegmetal vitiligo) (1).

Chemical leukoderma and occupational vitiligo initially present with contact depigmentation but may later spread to other areas (Picture 1). With a Wood's lamp, the contrast between lesional and normal skin is less marked than in vitiligo (1).

(Picture 1)

Vitiligo may be associated with many primarily AI disorders. The link with AI thyroid disorders (hypothyroidism and hyperthyroidism) is the most well established[1,5,6] (1). They may present in as many as 24% of pediatric vitiligo patients (1). One study identified thyroid disease in 18.5% of 15,126 vitiligo patients (1). A higher incidence of thyroid microsomal antibody is found in vitiligo patients and their family members. Conversely, vitiligo is more common in those with AI thyroid disorders. Patients with generalized vitiligo, especially when familial, are more likely to have AI disorders than those with segmental vitiligo. A controlled study of 226 vitiligo patients found an increased incidence of antinuclear (12.4%), antimicrosomal (7.1%), and anti–smooth muscle antibodies (25.7%) (1).Up to 20% of patients with vitiligo have hearing loss, which is caused by functional disorders of intermediate cells (melanocytes) of the stria vascularis (1). Ocular abnormalities present in up to 40% include choroidal anomalies, uveitis, iritis, and some degree of fundal pigment disturbance (1). Image 2 shows the difference between a healthy, and vitiligo affected skin.

(Image 2)

  1. As opposed to the normal number seen in unaffected skin. B) Also, there is notable patchy loss of melanin pigment in vitiligo. A) whereas normal skin B) shows homogenous distribution of melanin granules in the lower epidermis.

It remains unclear what causes damage to melanocytes and their subsequent disappearance in affected skin. There are several pathophysiologic theories; the most prominent are autoimmune, neurohumoral, and autocytotoxic (1). The current thought is that vitiligo represents a group of heterogeneous pathophysiologic disorders[1,4,5] with a similar phenotype (1). Autoimmune mechanisms likely underlie generalized vitiligo. The frequency of vitiligo among first-degree relatives in white, Indo-Pakistani, and Hispanic populations is 7.1%, 6.1%, and 4.8%, respectively, compared to an estimated worldwide frequency of 0.14% to 2% (1).

Monozygotic twins with identical DNA have only a 23% concordance in developing vitiligo, suggesting a significant nongenetic component. Among vitiligo patients, 20% report thyroid disease (an 8-fold increase over the general population), particularly hypothyroidism (1).The autoimmune hypothesis states that there is substantial evidence for the immune-mediated destruction of melanocytes[1,3] (1). Melanoma patients who develop hypopigmentation have a better prognosis, indicating that a common immune response to melanocytes is responsible for both hypopigmentation and tumor control (1).The peripheral blood of vitiligo patients shows high frequencies of Melan-A specific CD8+ T cells with cutaneous lymphocyte antigen, and their number may correlate with disease extent (1). 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 (1).

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