Systemic and topical psoralens with subsequent long-wave UV-A exposure (PUVA) is the most common treatment prescribed. Support groups and other adjuncts to therapy may be very beneficial and should always be offered to the patient. 4 However, the disease is cosmetically disfiguring and may produce profound adverse psychological effects because it can lower self-esteem and interfere with interpersonal relationships. ![]() 3 For this reason, most clinicians surveyed do not offer therapy to their patients with vitiligo. Even among patients who respond to treatment there is a high potential for relapse. Patients have numerous treatment options available, but none is universally effective. It is believed that the normal defense mechanisms of melanocytes against oxidative stress and melanin precursors are defective in vitiligo melanocytes. The autocytotoxicity theory postulates that melanocytes are destroyed either by themselves through self-generation of melanin precursors (or metabolites) or by keratinocytes, which release chemicals that generate oxidative stresses. 2 Vitiligo has been associated with antibody-mediated autoimmune diseases such as thyroid disease, pernicious anemia, diabetes mellitus, Addison disease, alopecia areata, and myasthenia gravis. The existence of antimelanocyte surface antigen antibodies has been demonstrated, and the severity of vitiligo has proven to be related to the amount of antibodies present. 1, 2 The autoimmune theory speculates that patients with vitiligo form autoantibodies against melanocytes. 1 Two of the major theories of the pathogenesis of vitiligo are the autoimmune theory and the autocytotoxicity theory. Although the disease can occur at any age, 50% of patients acquire it before age 20 years. Vitiligo is an acquired, idiopathic disorder characterized by depigmented macules that result from damage to and destruction of melanocytes. None of the patients had any local adverse effects, including pruritus or erythema. All 3 patients have maintained repigmentation after 6 to 9 months of follow-up, even with discontinuation of treatment. Patient 3 demonstrated good facial repigmentation in 4 weeks and complete repigmentation in 2 months. His repigmentation persisted 9 months later. He was completely repigmented in 2 months, at which time he showed no Wood light enhancement. Patient 2 ( Figure 2) began to show repigmentation at 6 weeks. ![]() The patient in case 1 developed noticeable follicular repigmentation after 3 weeks of therapy and had complete repigmentation in 4 months ( Figure 1). ![]() ![]() They were instructed to apply sunscreens of sun protection factor 30 or higher at all other times. Patients were allowed unprotected (no sunscreen) natural sunlight exposure at midday: 5 minutes in the summer and 10 minutes in fall, winter, and spring. Patients were instructed to apply the medication to the affected areas twice daily on dry skin.
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