Overview of Vitiligo

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EP: 1.Overview of Vitiligo

EP: 2.Real-World Impact of Vitiligo

EP: 3.Role of HCPs in the Management of Vitiligo

EP: 4.Approaching the Treatment of Vitiligo

EP: 5.Differences in Treatment Response to Vitiligo Therapy

EP: 6.Emerging Agents for the Treatment of Vitiligo

EP: 7.Clinical Pearls for the Management of Vitiligo

Amit G. Pandya, MD, FAAD: Vitiligo is a skin disorder in which patients lose pigment in their skin due to a lack of melanocytes. Its prevalence is about 1% of the population worldwide. There have been many discoveries in determining the pathogenesis of vitiligo in the last 10 years. It turns out that melanocytes are the start of the pathogenesis of vitiligo. Melanocytes are inherently unstable because they produce a large amount of melanin, which causes the unfolded protein response and many reactive oxygen species to be produced within melanocytes. That stress on the melanocyte causes the secretion of various mediators that stimulate the innate immune system and the local area. Other things can add to this stress and increase reactive oxygen species, such as trauma, UV [ultraviolet] light, and chemicals. There is this response by the melanocytes and the surrounding area that causes the activation of local natural killer cells and especially the dendritic cells in the immune system. These dendritic cells then migrate to the local draining lymph nodes, and they present these melanocytic antigens to naive T cells. This causes the production of many autoreactive, melanocyte-specific, cytotoxic, CD8-positive T cells, an army of these, which are then released into the circulation. These are the cells that subsequently cause the adaptive immune response that causes widespread vitiligo. Now, the patient tends to develop vitiligo in many areas of the body, and it can occur due to trauma and other forms of stress, but it often occurs in places for which we don’t see a reason. These cytotoxic T cells come out of the bloodstream, crawl into the epidermis, find the melanocytes, secrete various enzymes, and kill the melanocytes, and then we see areas of depigmentation in the skin.

When you treat a patient with vitiligo, the most important thing is to ensure you have the right diagnosis, as there are several conditions that are on the differential diagnosis of vitiligo. You must ensure they don’t have things like tinea versicolor, which is a cutaneous infection caused by a yeast-like organism. Some patients have nevus depigmentosus, which is usually a single lesion, but sometimes more, where there is an area of hypopigmentation that occurs early in life in children, but once it appears it doesn’t spread. Nevus depigmentosus tends to have more irregular edges as opposed to vitiligo, which has smooth edges. Another condition is idiopathic guttate hypomelanosis, which is caused by what we think is chronic sun damage and senescent melanocytes, and leaves areas with what looks like depigmentation, especially on the arms and legs. They tend to be less than 6 mm in diameter, and they don’t spread beyond that in size. There are other conditions, such as pityriasis alba, in which inflammatory cells, perhaps from eczema, cause melanocytes to temporarily reduce production of melanin, which then looks like a lighter area of the skin. Patients come in often with these disorders concerned that they might be vitiligo, and it’s up to us to look at the pattern, size, distribution, and sometimes do a biopsy or a scraping to determine the correct diagnosis and rule out other diseases before we make the diagnosis of vitiligo.

Transcript Edited for Clarity