INTRODUCTION
Hypopigmentation and depigmentation of the skin can be caused by multiple disorders. These include seborrheic dermatitis, mycosis fungoides, tinea versicolor, pityriasis alba, nevus depigmentosus, leprosy, and vitiligo (Figure 1).1,2 The most common cause of depigmentation worldwide is vitiligo. This disorder affects 1-2% of the world’s population and can be seen in all races.3 Vitiligo can have a significant impact on the quality of life of affected individuals.4 Although the disease course is often unpredictable, a few clinical signs that indicate increased disease activity have been identified. Confetti-like lesions, trichome lesions, and evidence of the Koebner phenomenon all indicate the need for immediate treatment (Figure 2).5,6 Vitiligo is caused by a disorder in the immune system in which CD8+ cytotoxic T cells attack melanocytes in the epidermis causing apoptosis and subsequent depigmentation.3 Although there are no current biomarkers to measure activity of vitiligo, certain clinical findings have a bearing on prognosis and likelihood of repigmentation. Patients who tend to respond well to treatment include younger patients, darker skin types, a short history of disease (<2 years), and those with depigmentation of the face, ears, neck, axillae, and other hair bearing areas with pigmented hairs. Features that characterize a poor prognosis include older patients, lighter skin types, long history of disease or rapidly spreading disease, and involvement of the scalp, lips, hands, elbows, genitalia, feet, or knees. Additionally, evidence of leukotrichia within depigmented lesions is a sign of poor prognosis (Figure 3).Treatment options for vitiligo include psychological counseling, topical therapy, systemic therapy, phototherapy, surgical therapy, and depigmentation.7 The current mainstay of treatment is phototherapy although treatment courses are often prolonged, lasting 6-18 months.7 Narrow band-UVB, PUVA, PUVASOL, UVA, sunlight, and solarium therapy can all be utilized based on treatment availability. However, the most successful phototherapy type remains NBUVB, which is effective due to its immunosuppressive effects and ability to induce melanocyte differentiation and melanin production.7,8 Studies have shown that home phototherapy is more efficient and cost effective than in-office phototherapy.9 In patients with the signs of active disease discussed above, a short course of an oral corticosteroid, such as dexamethasone, may be warranted.7,10 Due to their
