Bimatoprost 0.03% Solution for the Treatment of Nonfacial Vitiligo

June 2016 | Volume 15 | Issue 6 | Original Article | 703 | Copyright © 2016

Pearl E. Grimes MD

The Vitiligo & Pigmentation Institute of Southern California, Los Angeles, CA

Abstract

BACKGROUND: Topical prostaglandin E2 has shown efficacy in patients with localized, stable vitiligo. Bimatoprost is a synthetic prostamide (prostaglandin-ethanolamides) F2a analog. Bimatoprost 0.03% ophthalmic solution showed efficacy in the treatment of vitiligo in one small study.
OBJECTIVE: To assess the efficacy and safety of bimatoprost 0.03% alone and in combination with a topical steroid (mometasone) compared with mometasone alone in patients with nonsegmental vitiligo on nonfacial areas in a proof-of-concept study.
METHODS: This randomized, double-blind, controlled study was conducted over a 20-week treatment period. Patients were randomized to 1 of 3 treatment groups: bimatoprost monotherapy (n=11), bimatoprost plus mometasone (n=10), and mometasone plus placebo (n=11). The primary outcome was global response at week 20, based on an investigator’s assessment of improvement score of at least 5 (at least 50%–75% improvement from baseline) on an 8-point scale (0=worse; 7=cleared). Other outcomes included global response at other visits, response by anatomic site, change from baseline lesion severity (overall and by site), and safety.
RESULTS: Because of a lack of response observed for the primary end point, a post hoc analysis with a less stringent definition of response (score of ≥4 [25%–50% improvement]) was conducted. In this analysis, 46% of the bimatoprost plus mometasone group responded overall compared with 18% in the bimatoprost monotherapy group, and no patients in the mometasone plus placebo group. Greater response rates were observed in both bimatoprost groups compared with the mometasone plus placebo group starting at week 12. There were no differences among groups in signs and symptoms of irritation.
CONCLUSIONS: Bimatoprost alone or with mometasone provided greater repigmentation than treatment with mometasone alone. Larger studies that also assess facial lesions are warranted.

J Drugs Dermatol. 2016;15(6):703-710.

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INTRODUCTION

Vitiligo, characterized by patches of depigmented skin, is a common acquired disease affecting up to 2% of the population worldwide.1 The white macules and patches are cosmetically disfiguring and often cause significant psychological trauma.2-4 Vitiligo can be precipitated by multiple factors,5-7 and numerous etiologies have been proposed for the pathogenesis of vitiligo, including genetic, neural, biochemical, melanocyte self-destruction, viral, and autoimmune mechanisms.7-11 However, indirect and direct evidence support an immune-mediated pathogenesis of this disease.12,13 Recent studies suggest a Th1 interferon γ-mediated destruction of melanocytes, promulgated by the chemokine CXCL10.14,15

Vitiligo can negatively impact the quality of life of those affected with the disease.2 Stigmatization, avoidance of social situations, anxiousness, and a sense of helplessness have been reported in patients with vitiligo.2,12 Topical corticosteroids (eg, mometasone furoate cream 0.1% [hereafter referred to as mometasone]; Schering Corporation, Heist-op-den-Berg, Belgium) are currently the standard of care for vitiligo, owing to evidence from clinical trials showing their short-term benefit.16,17 Other medical therapies include systemic corticosteroids, calcineurin inhibitors, calcipotriol, narrow band UVB (NB-UVB) phototherapy, and targeted phototherapy.18 However, none of these treatments provide optimal outcomes.

Prostaglandins, such as topical prostaglandin E2 (PGE2), have shown efficacy in patients with localized, stable vitiligo; repigmentation with PGE2 was observed in 71% of patients in one study.19 This effect may be attributed to the ability of PGE2 to stimulate human melanocyte dendricity.20 Studies have shown that the release of prostaglandins (mainly PGE2 and PGF2α) in response to exposure of the skin to ultraviolet rays (UVR) causes an increase in the size of melanocytes, the number of active melanocytes, and the number of melanosomes transferred to keratinocytes.21,22

Bimatoprost is a synthetic prostamide (prostaglandin-ethanolamides) F2α analog.23 In the US, bimatoprost 0.01% ophthalmic solution (Lumigan; Allergan plc, Dublin, Ireland) is approved for treatment of glaucoma and elevated intraocular pressure, and bimatoprost 0.03% (Latisse, Allergan plc) is approved for the treatment of eyelash hypotrichosis.24,25 In patients undergoing treatment with bimatoprost, cases of skin hyperpigmentation

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