Vitiligo: An Update on Pathophysiology and Treatment Options

Reinhart Speeckaert; Nanja van Geel

Disclosures

Am J Clin Dermatol. 2017;18(6):733-744. 

In This Article

Pathophysiology of Segmental Vitiligo

Distribution Pattern Pointing to Somatic Mosaicism

Segmental vitiligo has clear differences compared with its non-segmental counterpart. In segmental vitiligo, only melanocytes residing in a particular area seem to be susceptible. For many years, the literature has described segmental vitiligo to follow a dermatomal distribution. This led to the hypothesis that neural mechanisms could play a role. Several reports pointing to increased neuropeptide release (e.g., neuropeptide Y) have been published.[51] However, neuropeptides could also be considered as a bystander effect of inflammation. Additionally, the observation that segmental vitiligo more often does not follow a dermatomal distribution illustrates that neural mechanisms are probably not the primary cause. Comparison of the distribution pattern of segmental vitiligo with other unilateral skin disorders revealed that segmental vitiligo has a unique distribution pattern with the most overlap with segmental lentiginosis.[52] Currently, somatic mosaicism is the most plausible theory, although this hypothesis has not yet been confirmed on a genetic level.

Role of Immunity

In 2010, a patient with segmental vitiligo with a recent onset vitiligo was investigated. Perilesional biopsies showed an inflammatory infiltrate and perilesional lymphocyte isolation confirmed the presence of anti-Mart-1- and gp100-specific cytotoxic T cells.[53] More recently, the presence of inflammatory cells was observed in 39/50 (78%) of recently evolving segmental vitiligo lesions, suggesting that immune-mediated mechanisms may indeed play a role.[54]

Although no definitive statements are currently possible, segmental vitiligo could represent a somatic mosaicism of melanocytes, leading to a localized and self-limiting inflammatory response.[55] This subsequently results in the loss of melanocytes in a localized area. This mechanism would be similar to other presumably mosaic skin diseases such as lichen striatus.

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