Original articleRepigmentation in vitiligo using the Janus kinase inhibitor tofacitinib may require concomitant light exposure
Section snippets
Methods
This study is a retrospective case series of 10 patients seen between July 2014 and January 2017. Medical records of patients with vitiligo, age 18 years and older, who were treated with tofacitinib for at least 3 months were reviewed. Clinical and demographic information, including biological sex, age, disease duration and course, medical history, family history, and prior treatments, were collected. Before initiation of tofacitinib therapy, all patients underwent baseline laboratory
Patient characteristics
All 10 patients in this case series were adults. Duration of disease ranged from 4 to 33 years (mean, 16.6; standard deviation, 8.8). Eight patients had generalized vitiligo and 2 patients had primarily acral involvement, with BSA 1% to 100%. Additional patient characteristics, together with previous treatments, are described in Table I.
Clinical response to treatment
Ten patients underwent treatment with tofacitinib, 5 to 10 mg daily or twice daily, for an average of 9.9 months (standard deviation, 4.1; range, 3-15). A mean
Discussion
The pathogenesis of vitiligo involves CD8+ T cell production of IFN-γ, which leads to CXCL9/CXCL10 expression by keratinocytes and further recruitment of CD8+ T cells, resulting in melanocyte destruction.7, 13, 14, 15, 16, 23 Originally, we hypothesized that inhibition of IFN-γ signaling using JAK inhibitors would lead to repigmentation, and the results in 2 patients19, 20 using 2 different oral JAK inhibitors, tofacitinib and ruxolitinib, supported this hypothesis. Recently, a case series
References (26)
- et al.
Vitiligo: a comprehensive overview. Part I. Introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology, and work-up
J Am Acad Dermatol
(2011) - et al.
The burden of vitiligo: patient characteristics associated with quality of life
J Am Acad Dermatol
(2009) - et al.
Psychological reaction to chronic skin disorders: a study of patients with vitiligo
Gen Hosp Psychiatry
(1979) - et al.
Combination therapy with 308-nm excimer laser, topical tacrolimus, and short-term systemic corticosteroids for segmental vitiligo: a retrospective study of 159 patients
J Am Acad Dermatol
(2015) - et al.
The Vitiligo Working Group recommendations for narrowband ultraviolet B light phototherapy treatment of vitiligo
J Am Acad Dermatol
(2017) Six decades of vitiligo genetics: genome-wide studies provide insights into autoimmune pathogenesis
J Invest Dermatol
(2012)- et al.
HLA-A2 restricted, melanocyte-specific CD8(+) T lymphocytes detected in vitiligo patients are related to disease activity and are predominantly directed against MelanA/MART1
J Invest Dermatol
(2001) - et al.
Rapid skin repigmentation on oral ruxolitinib in a patient with coexistent vitiligo and alopecia areata (AA)
J Am Acad Dermatol
(2016) - et al.
Confetti-like depigmentation: a potential sign of rapidly progressing vitiligo
J Am Acad Dermatol
(2015) - et al.
Keratinocyte-derived chemokines orchestrate T-cell positioning in the epidermis during vitiligo and may serve as biomarkers of disease
J Invest Dermatol
(2017)
Tofacitinib for the treatment of alopecia areata and variants in adolescents
J Am Acad Dermatol
Tofacitinib for the treatment of severe alopecia areata and variants: A study of 90 patients
J Am Acad Dermatol
Investigation of factors associated with health-related quality of life and psychological distress in vitiligo
J Dtsch Dermatol Ges
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Ms Liu and Mr Strassner contributed equally to this article.
Supported by National Center for Advancing Translational Sciences grant UL1-TR001453. Dr Harris is supported by National Institute of Arthritis and Musculoskeletal and Skin Diseases grant AR069114 and a Stiefel Scholar Award from the Dermatology Foundation. Dr King received funding support from The Ranjini and Ajay Poddar Resource Fund for Dermatologic Diseases Research.
Disclosure: Dr King has served on advisory boards or is a consultant for Aclaris Therapeutics, Concert Pharmaceuticals, Eli Lilly and Company, Pfizer, Regeneron Pharmaceuticals, and Roivant Sciences Ltd. Dr Harris has served on advisory boards, as a consultant, or as principal investigator on research agreements with Pfizer, AbbVie, Genzyme/Sanofi, Concert Pharmaceuticals, Stiefel/GSK, Mitsubishi Tanabe Pharma, Novartis, Aclaris Therapeutics, The Expert Institute, Celgene, Biologics MD, and Dermira. Ms Liu and Mr Strassner and Dr Refat have no conflicts of interest to declare.
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