Guidelines for the Management of Vitiligo

The European Dermatology Forum Consensus

A. Taieb; A. Alomar; M. Böhm; M.L. Dell'Anna; A. De Pase; V. Eleftheriadou; K. Ezzedine; Y. Gauthier; D.J. Gawkrodger; T. Jouary; G. Leone; S. Moretti; L. Nieuweboer-Krobotova; M.J. Olsson; D. Parsad; T. Passeron; A. Tanew; W. van der Veen; N. van Geel; M. Whitton; A. Wolkerstorfer; M. Picardo

Disclosures

The British Journal of Dermatology. 2013;168(1):5-19. 

In This Article

Conclusions

Given the importance of charlatanism in the vitiligo field, counselling patients to avoid some therapies of dubious efficacy is a major step. As stated in the Cochrane review on vitligo,[6] there are many limitations to deriving a valuable algorithm of treatment for all patients with vitiligo based on RCTs. Firstly, RCTs are rare and often lacking important methodological steps or details. Secondly, studies have often been conducted in heterogeneous groups in terms of duration or progression, and mixing localized, segmental and nonsegmental forms. Thirdly, there are many confounding factors (light exposure in long-term interventions, nutritional intake for antioxidants, or awareness on limitation of the Koebner phenomenon).

Nevertheless, a stepwise treatment approach divided by type of vitiligo and extent, which needs modulation by visibility, age and coping is outlined in Table 4 and the algorithm in Figure 1. A zero line is always possible, meaning no treatment if the disease is not bothering the patient. The environmental factors (occupation, Koebner phenomenon, sustained stress or anxiety) should always be discussed. For SV, triggering neurogenic factors are usually envisaged but good studies are lacking to prove this point. This stepwise approach should be considered as a proposal based mostly on evidence-based medicine data. However, there is much room for modulation and innovation based on this scheme.[119]

Figure 1.

The algorithms represent a handy support for the management of patients with nonsegmental vitiligo (NSV) (a) or segmental vitiligo (SV) (b) during the clinical routine. CS, corticosteroid; KP, Koebner phenomenon; TIM, topical immunomodulating macrolactams; NB-UVB, narrowband ultraviolet B; MEL, monochromatic excimer lamp; w/o, without.

The polygenic and multifactorial background in vitiligo should be reflected in more personalized approaches in the future.[119] An early therapeutic intervention before the appearance of leucotrichia is recommended. Cutaneous inflammation may be a shared feature in all cases. Accordingly, a more aggressive anti-inflammatory therapy, including methotrexate, would probably be helpful. If the initial step preceding inflammation comes from a local predisposition of melanocytes to attach poorly to the basement membrane, there are possible targets to improve adhesion mechanisms. The issue of self-renewal ('stemness') aptitude of melanocytes has been raised especially for SV,[119] which clearly benefits from autologous grafting. If impairment of melanocyte survival mechanisms are a cause, growth factor supplementation, such as melanocyte-stimulating hormone (MSH) analogues[120,121] could be used. Improving the antioxidant status of the epidermis has been attempted, but more powerful tools using gene transfer might be used in the future.[122]

When melanocyte loss has been stopped, therapy needs to address repigmentation. New repigmenting therapies are emerging such as helium–neon (He–Ne) lasers and prostaglandin E2.[123,124] Recent development in the field of melanocyte precursors are promising. If we can better stimulate the migration of those cells towards the epidermis and understand why they usually stop migrating when becoming pigmented, a major step would be achieved. Newer technologies derived from progenitors or reprogrammed skin cells[125] will probably further increase the possibility of surgical intervention.

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