Tofacitinib in Vitiligo: Case Series and Open-Label Studies ± NB-UVB

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Key Takeaways

  • Tofacitinib (JAK1/3 inhibitor) has shown facial repigmentation in multiple case series; responses improve with concurrent light (NB-UVB or sun exposure) in many reports.
  • Topical and low-dose systemic regimens are both described; acral sites remain comparatively refractory.
  • Systemic use requires laboratory monitoring and infection risk counseling; topical use shows low systemic exposure with local irritation as the main AE.
  • Best candidates: recent/active facial lesions, residual follicles, and ability to add light therapy.

Abstract

This article reviews clinical experience with tofacitinib for nonsegmental vitiligo, including topical and systemic regimens, outcomes from case series/open-label studies, synergy with NB-UVB or targeted light, safety considerations, and practical selection of candidates.

Evidence Summary

Table 1. Representative tofacitinib reports in vitiligo.
Design Population Intervention Co-intervention Key observations
Case series Adults with facial & non-facial lesions Systemic 5 mg BID (or QD titrated) Sun/NB-UVB in many Facial F-VASI improvement; faster with light
Open-label Mixed phototypes, active disease Topical 2% cream/ointment BID Optional NB-UVB/excimer Perifollicular islands; limited acral response
Split-body/observational Facial-dominant lesions Topical or low-dose systemic Mandatory NB-UVB Combination outperforms drug alone

Dosing Regimens

Table 2. Practical dosing (adapt to local protocols).
Route Typical regimen Notes
Systemic 5 mg BID (or QD→BID if tolerated) Short cycles with review at 8–12 wks; consider step-down
Topical Compounded 1–2% BID thin layer Apply after light session; reduce to QD if irritation

Combination with Phototherapy

  • NB-UVB (2–3×/wk) or excimer 308 nm often accelerates and deepens repigmentation versus drug alone.
  • Sequence: perform light first, then apply topical tofacitinib; for systemic, keep light schedule constant.
  • Face/neck benefit most; acral improvement remains limited.

Efficacy Outcomes

Table 3. Typical readouts used across studies.
Outcome Observation Timing
F-VASI change Early reduction with combination therapy Weeks 8–16
T-VASI change Modest; depends on extent and sites Weeks 12–24
Perifollicular islands Predict stronger endpoints Weeks 4–8
Durability Maintenance needed to prevent relapse 3–6 months post-response

Safety & Monitoring

Table 4. Adverse events and monitoring.
Aspect Systemic Topical
Common AEs URTI, headache, acne; lab shifts Local burning/erythema; folliculitis (rare)
Labs CBC, lipids, LFTs at baseline and periodically Not routinely needed
Infections Screen/counsel; hold during significant infection Local hygiene; monitor irritation
Counseling Class warnings for JAK inhibitors Avoid mucosa/eyes; thin layer only

Patient Selection

  • Recent/active facial lesions, residual hair follicles, ability to attend light therapy.
  • Avoid systemic use in patients with significant unmanaged infection/malignancy risks.
  • Consider topical first for face/neck; escalate to systemic only when justified.

Limitations

Evidence is predominantly from case series and open-label cohorts; randomized data are limited. Dosing, formulations, and outcome definitions vary, complicating direct comparisons.

References

  1. Case series of systemic tofacitinib with/without NB-UVB demonstrating facial repigmentation.
  2. Open-label and split-body studies of topical tofacitinib 1–2% with adjunct light therapy.
  3. Reviews on JAK inhibition mechanisms in vitiligo and integration with phototherapy.

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