Addition of oral minipulse dexamethasone to narrowband ultraviolet B phototherapy and topical steroids helps arrest disease activity in patients with vitiligo

Dear Editor, Vitiligo is a common autoimmune disease. It affects 0·5–1% of the world's population and has significant effects on quality of life.1 Unfortunately, there are currently no treatments approved by the U.S. Food and Drug Administration to induce repigmentation of affected areas.2 3 Rapidly progressive disease has been shown to respond to systemic corticosteroids; however, this treatment is associated with a high incidence of side‐effects when given continuously.4,5,6 For this reason, minipulse dosing of systemic steroids has been used to treat vitiligo and has fewer side‐effects.7 8 Few controlled studies have been performed using this treatment. We conducted a retrospective cohort study of patients presenting to the pigmentary disorders clinic at the University of Texas Southwestern Medical Center with active nonsegmental vitiligo from January 2014 to December 2016. Disease activity was defined as the presence of confetti‐like depigmentation, trichrome lesions or Koebner phenomenon on exam, or new lesions documented by photography in the past 3 months. Patients who had received oral minipulse dexamethasone 4 mg on two consecutive days per week, narrowband ultraviolet B (NB‐UVB), and clobetasol cream 0·05% four times daily, five consecutive days per week were assigned to group A. NB‐UVB was given three times weekly starting at a dose of 200 mJ and increasing by 10–15% per session as tolerated. Patients who had either refused or had a contraindication to systemic steroids were treated with a similar regimen of NB‐UVB and topical clobetasol alone and were assigned to group B. Patients who discontinued therapy and those who were not compliant with treatment were excluded. Disease arrest was defined as the absence of signs of disease activity (confetti‐like, trichrome or new lesions or Koebner phenomenon) and/or stability or improvement of lesions at follow‐up. Degree of repigmentation was assessed through analysis of photographs by a blinded investigator obtained at regularly scheduled clinic visits. Repigmentation was assessed as poor (< 25% improvement), moderate (25–50%), good (51–75%) or excellent (> 75%). Body surface area (BSA) involvement and development of adverse effects during treatment were also noted at each visit. In total 25 patients were assigned to group A and 15 patients to group B. The mean ages were 40 ± 11·8 and 45 ± 18·4 years, respectively. The baseline percentage BSA was higher in group A than in group B (P = 0·02). No difference in compliance was observed between the two groups. Disease arrest was achieved in 23 of 25 patients (92%) in group A, compared with only eight of 15 (53%) in group B. The results at the first follow‐up evaluation are shown in Table 1. The mean time to disease arrest was slightly lower in group A than in group B (3·6 vs. 3·9 months, respectively). Only two patients in group A still had confetti‐like lesions at the last follow‐up visit, compared with six patients in group B. Both groups showed a decrease in mean BSA involvement, with group A decreasing from 16 ± 17·1% to 11 ± 12·1% at the first follow‐up visit and group B from 5 ± 4·6% to 3 ± 3·9% (P < 0·001). Repigmentation of the face/neck and trunk in both groups was similar, with the majority of patients achieving moderate repigmentation at 3 months. However, patients in group A had greater repigmentation on the extremities than group B. Seven patients (28%) in group A developed side‐effects, including insomnia (16%), weight gain > 4·5 kg (8%) and steroid‐induced acne (4%). Only four patients (16%) had to discontinue treatment due to side‐effects. One patient in group B had temporary phototoxicity, which resolved with dose adjustment. Results at the first follow‐up evaluation Group B received narrowband ultraviolet B and clobetasol; group A in addition received oral minipulse therapy with dexamethasone. BSA, body surface area. aFisher's exact test, bt‐test, cPearson χ2‐test. Results at the first follow‐up evaluation Group B received narrowband ultraviolet B and clobetasol; group A in addition received oral minipulse therapy with dexamethasone. BSA, body surface area. aFisher's exact test, bt‐test, cPearson χ2‐test. After discontinuation of systemic steroids, patients in group A continued treatment with NB‐UVB and topical clobetasol. The majority of patients (67%) remained stable at the time of this second evaluation (mean 11·4 ± 1·6 months). Of the eight patients in whom disease activity had recurred, seven admitted to noncompliance with NB‐UVB and clobetasol. Therefore, compliance with treatment during the first year appeared to be important in maintaining disease stability (Fisher's exact test, P < 0·001). At the second evaluation, an additional decrease in BSA involvement was noted from 11 ± 12·1% to 6 ± 7·4% (P < 0·001). Repigmentation was good to excellent in the majority of patients on the face/neck and trunk, occurring in 72% and 62%, respectively. On the extremities, 46% of patients achieved good‐to‐excellent repigmentation. This was a small retrospective study, which suggests that the addition of oral minipulse dexamethasone may be effective in halting disease progression. Overall 92% of patients treated with the combination of dexamethasone, NB‐UVB and clobetasol had achieved disease arrest, compared with 53% of those on NB‐UVB and clobetasol alone. The majority (71%) of the patients had no side effects. Four patients had to discontinue the oral dexamethasone due to insomnia and weight gain. Compliance with phototherapy and topical clobetasol after discontinuation of systemic steroids is important to avoid recurrence of disease activity. Potential limitations to this study include the small sample size, retrospective nature and difference in baseline BSA involvement between the two groups. Further studies are needed to identify the optimal candidates for oral minipulse systemic steroid therapy.