Vitiligo is an idiopathic acquired depigmentation disorder that shows a localized or generalized distribution. Although vitiligo is not life-threatening, its effects may be psychologically and cosmetically devastating, especially in dark skin. The treatment for vitiligo includes systemic and topical corticosteroids, topical immune modulators such as tacrolimus, and phototherapy. Among them, phototherapy has been used for many years and has been reported to be an effective and safe therapeutic option.1 The effect of phototherapy depends on lesional location, while face and neck lesions generally show good response, acral areas are resistant to phototherapy.2
Lesions on the wrists, hands, ankles, and feet constitute acral vitiligo. Acral lesions and lesions over joints are resistant to medical treatment, and their response to surgical management is often disappointing.3 Few reasons for resistance of the acral areas were suggested. The well-known theory is the relatively lower density or absence of pilosebaceous follicles; the reservoirs from which the melanocytes migrate. Relatively less melanocyte density, as well as higher chances of koebnerization (appearance of new lesions at blistered sites) over these friction and injury prone anatomical sites, were other suggestions.4
Phototherapy is quite effective in the treatment of vitiligo as 50–75% re-pigmentation can be routinely expected in vitiligo of recent onset.5 Phototherapy using oral psoralens and ultraviolet A (UVA) (320–400 nm) has been used for a very long time.6 Topical psoralen plus ultraviolet A (topical PUVA) is a good therapeutic approach for localized vitiligo in adults and children over 2 years old and may provide a wider margin of safety because of a lesser cumulative UVA dose and negligible systemic absorption of psoralen. Topical PUVA has to be carried out cautiously to avoid phototoxicity and koebnerization.7 Narrowband ultraviolet B (NB-UVB) phototherapy remains to be an effective and safe therapeutic option in vitiligo.8 However, reported side effects with NB-UVB phototherapy include: erythema, pruritis, and xerosis.9
Long-wave ultraviolet A1 (UVA1) (340–400 nm) therapy with low dose 10–30 Joules (J)/centimeter2 (cm2), medium-dose (40–70 J/cm2) and high dose (up to 130 J/cm2) has been available since 1981.10 UVA1 penetrates deeper than UVA2 (320–340 nm) and thus is able to reach deep dermal components of the skin.11 UVA1 phototherapy has overlapping biological effects with NB-UVB and is relatively free of side effects associated with other phototherapy regimens. UVA1 phototherapy has been successfully used in the treatment of inflammatory skin diseases such as atopic dermatitis, localized scleroderma, and granuloma annulare. Response to UVA1 phototherapy seems to be dose dependent, 8 so further studies using higher doses of UVA1 are certainly needed to either confirm or negate this assumption.
Therefore, we aimed by this study to evaluate the effect of medium dose UVA1 phototherapy (40 J -70 J) in the treatment of acral vitiligo and comparing it with topical PUVA in the treatment of this resistant type of vitiligo.