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Repigmentation in vitiligo using the Janus kinase inhibitor tofacitinib may require concomitant light exposure - 14/09/17

Doi : 10.1016/j.jaad.2017.05.043 
Lucy Y. Liu, BA a, James P. Strassner, BS b, Maggi A. Refat, MD b, John E. Harris, MD, PhD b, , Brett A. King, MD, PhD c,
c Department of Dermatology, New Haven, Connecticut 
a Yale University School of Medicine, New Haven, Connecticut 
b Department of Dermatology, University of Massachusetts Medical School, Worcester, Massachusetts 

Correspondence to: John E. Harris, MD, PhD, Department of Dermatology, University of Massachusetts Medical School, 364 Plantation St, LRB 325, MA 01605.Department of Dermatology, University of Massachusetts Medical School364 Plantation St, LRB 325MA01605∗∗Brett A. King, MD, PhD, Department of Dermatology, Yale University School of Medicine, PO Box 208059, New Haven, CT 06520.Department of Dermatology, Yale University School of MedicinePO Box 208059New HavenCT06520

Abstract

Background

Vitiligo is an autoimmune disease in which cutaneous depigmentation occurs. Existing therapies are often inadequate. Prior reports have shown benefit of the Janus kinase (JAK) inhibitors.

Objective

To evaluate the efficacy of the JAK 1/3 inhibitor tofacitinib in the treatment of vitiligo.

Method

This is a retrospective case series of 10 consecutive patients with vitiligo treated with tofacitinib. Severity of disease was assessed by body surface area of depigmentation.

Results

Ten consecutive patients were treated with tofacitinib. Five patients achieved some repigmentation at sites of either sunlight exposure or low-dose narrowband ultraviolet B phototherapy. Suction blister sampling revealed that the autoimmune response was inhibited during treatment in both responding and nonresponding lesions, suggesting that light rather than immunosuppression was primarily required for melanocyte regeneration.

Limitations

Limitations include the small size of the study population, retrospective nature of the study, and lack of a control group.

Conclusion

Treatment of vitiligo with JAK inhibitors appears to require light exposure. In contrast to treatment with phototherapy alone, repigmentation during treatment with JAK inhibitors may require only low-level light. Maintenance of repigmentation may be achieved with JAK inhibitor monotherapy. These results support a model wherein JAK inhibitors suppress T cell mediators of vitiligo and light exposure is necessary for stimulation of melanocyte regeneration.

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Key words : JAK, Janus kinase, narrowband ultraviolet B, nbUVB, phototherapy, ruxolitinib, tofacitinib, vitiligo

Abbreviations used : BSA, CXCL9, ELISA, IFN-γ, JAK, nbUVB, PBMCs


Plan


 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.
 Reprints not available from the authors.


© 2017  American Academy of Dermatology, Inc.. Publié par Elsevier Masson SAS. Tous droits réservés.
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Vol 77 - N° 4

P. 675 - octobre 2017 Retour au numéro
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