Current and emerging therapy for the management of vitiligo

Vitiligo is an acquired cutaneous disorder of pigmentation, with an incidence of 0.5% to 2% worldwide. There are three major hypotheses for the pathogenesis of vitiligo that are not exclusive of each other: biochemical/cytotoxic, neural and autoimmune. Recent data provide strong evidence supporting an autoimmune pathogenesis of vitiligo. As vitiligo can have a major effect on quality of life, treatment can be considered and should preferably begin early when the disease is active. Current treatment modalities are directed towards stopping progression of the disease and achieving repigmentation. Therapies include corticosteroids, topical immunomodulators, photo(chemo)therapy, surgery, combination therapies and depigmentation of normally pigmented skin. Topical class 3 corticosteroids can be used for localized vitiligo. The use of topical immunomodulators (TIMs) in vitiligo seems to be equally effective as topical steroids, especially when used in the face and neck region. In photo(chemo)therapy, narrowband ultraviolet-B therapy (NB-UVB) seems to be superior to psoralen ultraviolet-A therapy (PUVA) and broadband UVB. In surgical techniques, split-thickness grafting and epidermal blister grafting were shown to be effective methods, although the non-cultured epidermal suspension technique has many advantages and seems to be a promising development. Depigmentation therapy can be considered if vitiligo affects more than 60% to 80% of the body. Complementary therapies such as Polypodium leucotomos show promising results in combination with UVB therapy. No causative treatment for vitiligo is currently available. More randomized controlled trials on the treatment of vitiligo are necessary

Variant of TYR and Autoimmunity Susceptibility Loci in Generalized Vitiligo.

BACKGROUND Generalized vitiligo is an autoimmune disease characterized by melanocyte loss, which results in patchy depigmentation of skin and hair, and is associated with an elevated risk of other autoimmune diseases. METHODS To identify generalized vitiligo susceptibility loci, we conducted a genomewide association study. We genotyped 579,146 single-nucleotide polymorphisms (SNPs) in 1514 patients with generalized vitiligo who were of European-derived white (CEU) ancestry and compared the genotypes with publicly available control genotypes from 2813 CEU persons. We then tested 50 SNPs in two replication sets, one comprising 677 independent CEU patients and 1106 CEU controls and the other comprising 183 CEU simplex trios with generalized vitiligo and 332 CEU multiplex families. RESULTS We detected significant associations between generalized vitiligo and SNPs at several loci previously associated with other autoimmune diseases. These included genes encoding major-histocompatibility-complex class I molecules (P=9.05×10−23) and class II molecules (P=4.50×10−34), PTPN22 (P=1.31×10−7), LPP (P=1.01×10−11), IL2RA (P=2.78×10−9), UBASH3A (P=1.26×10−9), and C1QTNF6 (P=2.21×10−16). We also detected associations between generalized vitiligo and SNPs in two additional immune-related loci, RERE (P=7.07×10−15) and GZMB (P=3.44×10−8), and in a locus containing TYR (P=1.60×10−18), encoding tyrosinase. CONCLUSIONS We observed associations between generalized vitiligo and markers implicating multiple genes, some associated with other autoimmune diseases and one (TYR) that may mediate target-cell specificity and indicate a mutually exclusive relationship between susceptibility to vitiligo and susceptibility to melanoma

Common variants in FOXP1 are associated with generalized vitiligo

In a recent genome-wide association study of generalized vitiligo, we identified ten confirmed susceptibility loci. By testing additional loci that showed suggestive association in the genome-wide study, using two replication cohorts of European descent, we observed replicated association of generalized vitiligo with variants at 3p13 encompassing FOXP1 (rs17008723, combined P = 1.04 × 10−8) and with variants at 6q27 encompassing CCR6 (rs6902119, combined P = 3.94 × 10−7)

Current and emerging therapy for the management of vitiligo

Alicia Cecile Borderé, Jo Lambert, Nanny van GeelUniversity Hospital of Ghent, Department of Dermatology, Ghent, BelgiumAbstract: Vitiligo is an acquired cutaneous disorder of pigmentation, with an incidence of 0.5% to 2% worldwide. There are three major hypotheses for the pathogenesis of vitiligo that are not exclusive of each other: biochemical/cytotoxic, neural and autoimmune. Recent data provide strong evidence supporting an autoimmune pathogenesis of vitiligo. As vitiligo can have a major effect on quality of life, treatment can be considered and should preferably begin early when the disease is active. Current treatment modalities are directed towards stopping progression of the disease and achieving repigmentation. Therapies include corticosteroids, topical immunomodulators, photo(chemo)therapy, surgery, combination therapies and depigmentation of normally pigmented skin. Topical class 3 corticosteroids can be used for localized vitiligo. The use of topical immunomodulators (TIMs) in vitiligo seems to be equally effective as topical steroids, especially when used in the face and neck region. In photo(chemo)therapy, narrowband ultraviolet-B therapy (NB-UVB) seems to be superior to psoralen ultraviolet-A therapy (PUVA) and broadband UVB. In surgical techniques, split-thickness grafting and epidermal blister grafting were shown to be effective methods, although the non-cultured epidermal suspension technique has many advantages and seems to be a promising development. Depigmentation therapy can be considered if vitiligo affects more than 60% to 80% of the body. Complementary therapies such as Polypodium leucotomos show promising results in combination with UVB therapy. No causative treatment for vitiligo is currently available. More randomized controlled trials on the treatment of vitiligo are necessary.Keywords: vitiligo, non-surgical treatment, surgical treatmen