TY - JOUR
T1 - Therapeutic management of vitiligo
AU - Bleuel, Rachela
AU - Eberlein, Bernadette
N1 - Publisher Copyright:
© 2018 Deutsche Dermatologische Gesellschaft (DDG). Published by John Wiley & Sons Ltd.
PY - 2018/11
Y1 - 2018/11
N2 - Affecting 0.5 % of the world's population, vitiligo is an acquired skin disorder that poses major challenges in terms of dermatological care. Characterized by patchy depigmentation, the disease is frequently associated with cosmetic disfigurement and considerable psychological distress. The primary pathophysiological causes for the loss of functional melanocytes are thought to include genetic predisposition, autoimmune mechanisms, and oxidative stress. The present article highlights treatment recommendations contained in the European guidelines as well as those provided by recent reviews on vitiligo. Current therapeutic options are based on three approaches: (1) Regulation of the autoimmune response using topical and systemic immunomodulatory agents (corticosteroids and calcineurin inhibitors); (2) decrease in oxidative stress in melanocytes by means of topical and systemic antioxidants; and (3) activation of melanocyte regeneration using phototherapy (UVB in particular) and transplantation of pigment cells. In addition, patients should be educated in techniques for cosmetic camouflage. Following successful repigmentation, application of calcineurin inhibitors is recommended to prevent recurrences. Combination therapies of the aforementioned approaches are generally considered to be more successful than monotherapies. Early initiation of treatment is associated with a more favorable prognosis. Using the above treatment options, it may be possible to halt disease progression, stabilize depigmented lesions, and achieve repigmentation. Only in exceptional cases should permanent depigmentation be considered as a possible option. New insights into the pathogenesis of vitiligo will likely give rise to novel therapeutic approaches.
AB - Affecting 0.5 % of the world's population, vitiligo is an acquired skin disorder that poses major challenges in terms of dermatological care. Characterized by patchy depigmentation, the disease is frequently associated with cosmetic disfigurement and considerable psychological distress. The primary pathophysiological causes for the loss of functional melanocytes are thought to include genetic predisposition, autoimmune mechanisms, and oxidative stress. The present article highlights treatment recommendations contained in the European guidelines as well as those provided by recent reviews on vitiligo. Current therapeutic options are based on three approaches: (1) Regulation of the autoimmune response using topical and systemic immunomodulatory agents (corticosteroids and calcineurin inhibitors); (2) decrease in oxidative stress in melanocytes by means of topical and systemic antioxidants; and (3) activation of melanocyte regeneration using phototherapy (UVB in particular) and transplantation of pigment cells. In addition, patients should be educated in techniques for cosmetic camouflage. Following successful repigmentation, application of calcineurin inhibitors is recommended to prevent recurrences. Combination therapies of the aforementioned approaches are generally considered to be more successful than monotherapies. Early initiation of treatment is associated with a more favorable prognosis. Using the above treatment options, it may be possible to halt disease progression, stabilize depigmented lesions, and achieve repigmentation. Only in exceptional cases should permanent depigmentation be considered as a possible option. New insights into the pathogenesis of vitiligo will likely give rise to novel therapeutic approaches.
UR - http://www.scopus.com/inward/record.url?scp=85055256878&partnerID=8YFLogxK
U2 - 10.1111/ddg.13680
DO - 10.1111/ddg.13680
M3 - Review article
C2 - 30335222
AN - SCOPUS:85055256878
SN - 1610-0379
VL - 16
SP - 1309
EP - 1313
JO - JDDG - Journal of the German Society of Dermatology
JF - JDDG - Journal of the German Society of Dermatology
IS - 11
ER -