Background: Vitiligo is an acquired dermatological condition that is characterized by depigmentation of patches of skin. It is relatively common, occuring in about 0.38-0.50% of the general population, and can engender significant cosmetic disfigurement and psychological sequelae in the affected individual. Recent studies demonstrate that topical tacrolimus (Protopic; Astellas, Markham, ON, Canada) is efficacious in the treatment of vitiligo. We propose that the successful treatment of vitiligo with topical tacrolimus involves the unique immunosuppressive actions of the T lymphocyte T-helper (Th) 2 cytokine, interleukin (IL)-10.
Objectives: We aimed to monitor clinical changes in lesions of vitiligo treated with topical tacrolimus 0.1% ointment and quantify IL-10 cytokine levels in nonvitiliginous skin, as well as lesions of vitiligo before and following topical tacrolimus therapy.
Methods: Clinical evaluation of lesions of vitiligo on the basis of surface area and follicular repigmentation under Wood's lamp was performed in 20 enrolled adult patients. Biopsy specimens were obtained from nonvitiliginous skin, as well as lesions of vitiligo before and following topical tacrolimus therapy. Specimens were processed and analysed for expression of IL-10 using the method of enzyme-linked immunosorbent assay.
Results: A statistically significant mean +/- SEM decrease in vitiligo lesion size of 41.0 +/- 5.2% was observed following 3 months of treatment. A pattern of follicular repigmentation was noted by the third month of treatment for all patients completing the study. In addition, there was a statistically significant difference between IL-10 expression in vitiligo lesions following treatment for 3 months with topical tacrolimus compared with untreated vitiligo lesions (P = 0.017) and normal skin (P = 0.004).
Conclusions: These results confirm that topical tacrolimus is an effective treatment for vitiligo. We propose that topical tacrolimus increases IL-10 expression in vitiligo lesions, and thereby inhibits melanocyte destruction triggered by unchecked Th1 pathways in vitiligo.