Vitiligo Treatment and JAK Inhibitors: AAD President Susan Taylor, MD

A deeper understanding of vitiligo's autoimmune mechanisms has fundamentally transformed vitiligo care—reshaping how clinicians diagnose, counsel, and treat patients and expanding the therapeutic toolkit to include targeted topical and oral JAK inhibitors, explained Susan Taylor, MD, the Bernett Johnson Endowed Professor of Dermatology at the University of Pennsylvania, founder of the Skin of Color Society, and American Academy of Dermatology president (2025–2026).

At the Winter Clinical Miami meeting, Taylor presented on how Janus kinase (JAK) inhibition has been reshaping routine vitiligo care. After the meeting, she answered questions for The American Journal of Managed Care^® (AJMC^®) via email on how these insights are guiding individualized treatment selection. She also noted a sobering reality: despite these advances, insurance approval remains the most significant barrier preventing patients of color from accessing the therapies most likely to benefit them, but there aren’t any great answers on how to solve the problem yet.

AJMC: How has our evolving understanding of the Th1 pathway and JAK/STAT signal disruption fundamentally changed the way a "routine" vitiligo consultation looks today compared with 5 years ago?

Taylor: Our evolving understanding of the Th1 immune pathway and the role of JAK/STAT signaling in driving melanocyte destruction has reshaped what a routine vitiligo consultation looks like today compared with 5 years ago. At that time, the typical visit focused on confirming the diagnosis, assessing extent and activity, and then discussing our limited armamentarium of therapies such as topical and systemic corticosteroids or calcineurin inhibitors.

Today, at the consultation we can explain the autoimmune mechanism in simple terms like how interferon‑γ–driven Th1 leads to CXCL10‑mediated T‑cell recruitment and destruction of melanocytes and that JAK inhibitors can work to treat this!

AJMC: You highlighted phase 2 data for several oral JAK inhibitors, including upadacitinib, povorcitinib, and ritlecitinib. From a practice-efficiency standpoint, what are you looking for in a patient profile to determine if an oral or topical option makes the most sense?

Taylor: In regard to patient profile for selecting an oral or topical option, I am looking at 6 factors:

• Extent of disease: Patients with 10% or less vitiligo and particularly facial or limited lesions tend to benefit most from topical JAK ruxolitinib. Extensive or rapidly spreading disease is more appropriately treated with an oral JAK inhibitor.
• Pace of progression: If the vitiligo is active or accelerating, with new lesions, confetti depigmentation, or trichrome borders, an oral agent offers a more efficient way to quickly suppress the underlying inflammatory process. For stable disease, topical therapy may be sufficient.
• Anatomic considerations and practicality: Areas that are difficult to treat topically (scalp, hands/feet, large surface areas) often steer me toward an oral therapy.
• Psychosocial burden and patient preference
• Comorbidities and safety profile: For oral JAK inhibitors, we must carefully consider medical history, including infection risk, cardiovascular profile, and risk for thrombosis.
• Treatment goals and timeline: Patients with rapid widespread vitiligo or who have long histories of inadequate response to topicals would respond best to an oral JAK inhibitor.

AJMC: For patients with darker skin tones, there’s a greater psychosocial burden of vitiligo due to the stark contrast of depigmented areas. How should clinicians evolve their initial consultations?

Taylor: Since there is a greater psychosocial burden of vitiligo for these patients, a discussion of and screening for anxiety and depression should be done. Additionally, it is also helpful to discuss and provide guidance regarding effective methods of camouflage.