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DR AMIT G PANDYA (Orcid ID : 0000-0002-3916-2651)

Accepted Article
Article type : Research Letter

Addition of oral mini pulse dexamethasone to NBUVB phototherapy and topical steroids helps arrest

disease activity in patients with vitiligo

A. Tovar-Garza,1 J.A. Hinojosa,1 L.S. Hynan,2,3 A.G. Pandya1


1
Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, Texas
2
Departments of Clinical Sciences (Biostatistics) and 3Psychiatry, University of Texas Southwestern

Medical Center, Dallas, Texas

Corresponding author: Amit G. Pandya, M.D.

Email: amit.pandya@utsouthwestern.edu

This article has no funding source.

Conflicts of interest: The authors have no conflicts of interest to disclose.

Dear Editor,

Vitiligo is a common autoimmune disease affecting 0.5-1% of the world’s population with

significant effects on quality of life.1 Unfortunately, there are currently no FDA-approved treatments 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, mini-pulse dosing of systemic steroids has been used to
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treat vitiligo and has fewer side effects.7, 8 Few controlled studies have been performed using this
Accepted Article
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 non-segmental vitiligo from

January 2014 to December 2016. Disease activity was defined as the presence of confetti-like

depigmentation, trichrome lesions, Koebner phenomenon on exam or new lesions documented by

photography in the past 3 months. Patients who received oral mini pulse dexamethasone 4 mg on 2

consecutive days a week, narrow-band UVB (NBUVB) and clobetasol cream 0.05% QD five consecutive

days per week were assigned into Group A. NBUVB was given 3 times weekly starting at a dose of 200 mj

and increasing by 10-15% per session as tolerated. Patients who either refused or had a contraindication

to systemic steroids were treated with a similar regimen of NB-UVB and topical clobetasol alone and

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, Koebner lesions, new lesions) 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 as poor (<25% improvement), moderate (25-

50% improvement), good (51-75% improvement) or excellent (>75% improvement). Body surface area

(BSA) involvement and development of adverse effects during treatment were also noted at each visit.

A total of 25 patients were assigned to Group A and 15 patients to group B. The mean age in

years was 40 ±11.8 and 45 ±18.4, respectively. Baseline percentage BSA was higher in group A compared

to group B (p=0.02). No difference in compliance was observed between the two groups.

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Disease arrest was achieved in 23/25 (92%) in group A compared to only 8/15 (53%) in group B.
Accepted Article
Results at first follow-up evaluation are shown in Table 1. Mean time to disease arrest was slightly lower

in group A vs. group B (3.6 months vs. 3.9 months, respectively). Only 2 patients in group A still had

confetti-like lesions at the last follow-up visit compared to 6 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, while in group B it decreased from 5 ±4.6 to 3 ±3.9 (p<0.0001). Repigmentation of the

face/neck and trunk in both groups was similar, the majority achieving moderate repigmentation at 3

months. However, patients on group A had greater repigmentation on the extremities compared to

group B. Seven (28%) patients in Group A developed side effects, including insomnia (16%), weight gain

>10lbs (8%) and steroid induced acne (4%). Only 4 (16%) patients had to discontinue treatment due to

side effects. One patient in Group B had temporary phototoxicity which resolved with dose adjustment.

After discontinuation of systemic steroids, patients in Group A continued treatment with NBUVB

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 non-compliance with NBUVB and clobetasol. Therefore, compliance with treatment during

the first year appeared to be important in maintaining disease stability (Fisher’s exact test, p<0.0001). At

this second evaluation, an additional decrease in BSA involvement was noted from 11 ±12.1 to 6 ±7.4

(p<0.0001). Repigmentation was good to excellent in the majority of patients on the face/neck and

trunk, which was 72% and 62% respectively. On the extremities, 46% of patients achieved good to

excellent repigmentation.

This was a small retrospective study which suggests the addition of oral mini pulse

dexamethasone may be effective in halting disease progression. 92% of patients treated with the

combination of dexamethasone, NBUVB and clobetasol had achieved disease arrest compared to 53% of

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those on NBUVB and clobetasol alone. Mild side effects were present in 16% of patients and resolved
Accepted Article
with discontinuation of treatment. 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 a small sample size, retrospective nature and difference at baseline BSA

involvement between the two groups. Further studies are needed to identify the optimal candidates for

oral mini pulse systemic steroid therapy.

References

1. Ezzedine K, Eleftheriadou V, Whitton M, van Geel N. Vitiligo. Lancet. 2015;386(9988):74-84.

2. Rodrigues M, Ezzedine K, Hamzavi I, Pandya AG, Harris JE, Vitiligo Working Group. Current and

emerging treatments for vitiligo. Journal of the American Academy of Dermatology.

2017;77(1):17-29.

3. Nordlund JJ. The Medical Treatment of Vitiligo: An Historical Review. Dermatologic Clinics.

2017;35(2):107-16.

4. Seiter S, Ugurel S, Tilgen W, Reinhold U. Use of high-dose methylprednisolone pulse therapy in

patients with progressive and stable vitiligo. International journal of dermatology.

2000;39(8):624-7.

5. Rath N, Kar HK, Sabhnani S. An open labeled, comparative clinical study on efficacy and

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UVB phototherapy in progressive vitiligo. Indian Journal of Dermatology, Venereology, and

Leprology. 2008;74(4):357.

6. Kanwar AJ, Mahajan R, Parsad D. Low-dose oral mini-pulse dexamethasone therapy in

progressive unstable vitiligo. Journal of cutaneous medicine and surgery. 2013;17(4):259-68.

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7. Singh H, Kumaran MS, Bains A, Parsad D. A randomized comparative study of oral corticosteroid
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minipulse and low-dose oral methotrexate in the treatment of unstable vitiligo. Dermatology.

2015;231(3):286-90.

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treatment for vitiligo. Journal of the American Academy of Dermatology. 2001;44(5):814-7.

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Table 1. Results at first follow-up evaluation
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Group A Group B p-value

Arrest of disease activity 23 (92%) 8 (53%) 0.008**

Mean follow-up visit in 3.6 (2 to 6) 3.9 (3 to 6) 0.118***

months (range)

Signs of disease activity

after treatment

Confetti-like lesions 2 (8%) 6 (40%)

Trichrome vitiligo 0 (0%) 2 (13%)

Koebner phenomenon 0 (0%) 1 (7%)

New lesions 0 (0%) 2 (13%)

Total 2 11 0.008**

Moderate repigmentation

Face/neck 13 (60%) 8 (62%) 0.296*

Trunk 12 (57%) 5 (50%) 0.257*

Extremities 12 (48%) 6 (42%) 0.826*

Mean BSA involvement 11 (±12.1) 3 (±3.9) 0.0001***

Note: *Pearson chi-square, ** Fisher’s exact test, ***t-test

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