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


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

In This Article

Oral Steroids and Other Immunosuppressants

Oral Steroid Minipulse Therapy

Studies on systemic steroids have been sparingly reported in the literature. Pulse therapy refers to the intermittent administration of large (suprapharmacological) doses to enhance the therapeutic effect and reduce the side-effects of a particular drug. Oral minipulse (OMP) of moderate doses of betamethasone/dexamethasone has been pioneered in India by Pasricha et al.[75] Systemic steroids can arrest the activity of the disease,[75–79] but are not effective in repigmenting stable vitiligo. Moreover side-effects associated with long-term use of daily systemic corticosteroids contraindicate their common use. In these first reported studies,[76,77] betamethasone or dexamethasone was given as a single oral dose of 5 mg on two consecutive days per week. In adult nonresponders to the standard dose of corticosteroids, the dose was increased to 7·5 mg daily and then reduced to 5 mg daily when disease progression was arrested. Within 1–3 months of treatment, 89% of patients with progressive disease stabilized, while within 2–4 months, repigmentation was observed in 80% of the patients. The area of repigmentation continued to progress as treatment continued, although none of the patients achieved complete repigmentation. Radakovic-Fijan et al.[77] used dexamethasone minipulses of 10 mg daily on two consecutive days per week up to 24 weeks. Disease activity was arrested in 88% of patients with progressive disease after 18·2 weeks of treatment. Side-effects (weight gain, insomnia, agitation, acne, menstrual disturbances and hypertrichosis) were observed in 69% of patients. Overall, OMP with either betamethasone or dexamethasone can arrest, without inducing repigmentation, the progression of vitiligo. During fast-spreading vitiligo, phototherapy is usually commenced after this intervention. However, there are no randomized clinical trials (RCTs) confirming that either speed or magnitude of response to phototherapy and photochemotherapy might be potentiated by concomitant administration of OMP.

Other Immunosuppressants and Biologics

Immunosuppressants other than oral steroids have been evaluated in a limited number of studies. Anecdotal reports also exist on the off-label use of some immunomodulating biologics in vitiligo.

Cyclophosphamide. Cyclophosphamide (2 × 50 mg daily) was assessed in a small case study of 33 patients. In 29 patients, some repigmentation was seen including acral sites.[80] Side-effects included hair loss, cytopenia and nausea. Quality of life was not recorded and further details of this case study are not available.

Ciclosporin. Systemic ciclosporin (6 mg kg−1 daily) was tested in six patients.[81] Little or no repigmentation was seen in five out of six patients after several months of therapy. Detailed information on the treated patients is not available. The most prominent side-effects were renal dysfunction and hypertension.

Antitumour Necrosis Factor-α. A case study assessed the therapeutic potential of etanercept in a small open-label pilot study of four patients with progressive NSV.[82] Etanercept 50 mg was given weekly for 12 weeks, followed by 25 mg weekly for a further 4 weeks. Although tolerability was good, none of the patients had a repigmentation response. In another case report,[83] a patient with ankylosing spondylitis and progressive NSV was treated with infliximab (350 mg infliximab intravenously in weeks 0, 2 and 6, and then every other week for 10 months). After 6 months, spreading of vitiligo stopped and partial or complete repigmentation occurred on several spots. However, NSV may be induced by anti-TNF-α agents.[84]