Diphenylcyclopropenone-Induced Vitiligo in a Patient with Alopecia Universalis
A 52-year-old, diabetic, white male presented with an 18-year history of generalized hair loss. The patient was diagnosed as having AU. Upon examination, there was a universal loss of hair on the whole scalp, the face, the eyebrows and eyelashes, the arms, the axilla, the moustache and the beard areas. Dermoscopy did not show any cicatrization, but extensive areas of yellow dots and small areas with black dots and fine, small exclamation-mark hairs were noticed. There were no signs of regrowth in any of the affected areas. Nails and mucous membranes were normal. He had a positive family history of alopecia areata, but no family or personal history of vitiligo. Laboratory investigations showed an elevation of antithyroid peroxidase and antinuclear antibody (1:160) speckled pattern. Antiparietal cell antibody and anti-intrinsic-factor antibody were negative. Thyroid function test, homocysteine and vitamin B12 showed normal levels. Before attending our OPD clinic, the patient underwent topical and intralesional steroid therapies at another hospital without improvement. In January 2011, we decided to initiate DCP therapy on the scalp only. Following the classic sensitization regimen, we started with one 2% application, followed by 0.0001% after 2 weeks, and then a weekly dose escalation guided by the appearance of erythema and the contact dermatitis reaction. The scalp showed erythema and crusts formation during therapy with no signs of hair regrowth. In July 2011, after 6 months of therapy and when we had reached a concentration of 0.01%, the patient presented with multiple white patches on the occipital and parietal areas of the scalp, diagnosed clinically and by Wood's light examination as vitiligo (fig. ). We discontinued DCP and from July 2011 to April 2012, we administered a combined therapy of monochromic excimer laser radiation (308 nm; XTRAC, Photomedex, USA) in 3 sessions weekly (total dose 18.3 J/cm2) combined with topical pimecrolimus 1% cream twice daily. Depigmented areas showed a mild improvement, but this combined therapy had no effect on hair regrowth. The patient discontinued both lines of treatment. In September 2012, we started a low-pulse prednisone therapy, administering 80 mg prednisone per day on weekends (2 days of therapy and 5 days off treatment) for 4 months (until January 2013). In conjunction with prednisone, we prescribed topical prostaglandin E2 solution (Latisse: bimatoprost 0.03%) for the eyebrows and eyelashes. The hair regrowth was significant. After years, he at last achieved hair regrowth on his scalp, even though the vertex showed a moderate, androgenic, permanent loss of hair. His eyebrows recovered, but his eyelashes showed no response. He also experienced considerable though incomplete repigmentation of areas of skin with vitiligo. Oral pulse prednisone therapy was tapered and then discontinued after 4 months. Potent topical clobetasone propionate 0.05% ointment was applied once daily to the scalp in addition to topical pimecrolimus 1% cream twice daily to the moustache and beard areas. Topical prostaglandin E2 solution was continued for the eyebrows and eyelashes. The topical therapies were continued for the next 16 weeks (until May 2013). The improvement was satisfactory for the patient, although tiny residual patches of colocalized alopecia and vitiligo can still be seen on the vertex and occipital areas (fig. ). Regrowth of his facial hair is almost complete, especially his moustache. There has been no relapse and hair growth has continued. A maintenance therapy consisting of a topical weekend application of local agents is being continued with no intention of interruption. A spontaneous regression of both conditions cannot be ruled out.