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CLINUVEL Vitiligo Communiqué

19 December 2018

 

As a depigmentation disorder (hypomelanosis), vitiligo is the most well-known of all leucodermatoses (“white skin”) whereby other variants of loss of skin pigmentation – temporary or permanent – are described as albinism, piebaldism, pityriasis alba, tuberous sclerosis, idiopathic guttate hypomelanosis and tinea versicolor.

The precise mechanism which leads to generalised loss of skin pigmentation is still unknown. Patients with immunological disorders do have a higher prevalence of vitiligo. That is not to say that vitiligo patients necessarily suffer from immune disorders, since many of these patients have no other underlying disease. At the current state of clinical practice it is believed that in vitiligo pigment cells (melanocytes) become dysregulated and susceptible to intracellular oxidative stress, and therefore lose the ability to produce melanin (pigment) due to increased activity of antigen-specific T-cells (immune cells). It is thought that the intracellular pathways through protein expressions and signalling via IFN-γ-STAT1-CXCL10 are part of the primary inflammatory pathway responsible for both progression and maintenance of the condition.

 

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Figure 1: Melanocyte and signalling pathways – including CD9+ T-cells attacking the cell