Skip to main content
NCBI home page
Wiley Open Access Collection logoLink to Wiley Open Access Collection
. 2024 Oct 23;38(1):e13209. doi: 10.1111/pcmr.13209

Low‐Dose Baricitinib Plus Narrow‐Band Ultraviolet B for the Treatment of Progressive Non‐Segmental Vitiligo: A Prospective, Controlled, Open‐Label Study

Zhonghui Hu 1,2, Lu Lu 1, Jindi Feng 1, Hongbin Song 1, Shiyu Zhang 1, Lu Yang 1, Yuehua Liu 1,✉, Tao Wang 1,✉
PMCID: PMC11681843  PMID: 39441554

ABSTRACT

Vitiligo is a chronic autoimmune disease, and current treatments for vitiligo have limited efficacy. Janus kinase (JAK) inhibitors could offer new therapeutic options. To evaluate the efficacy and safety of baricitinib, an oral JAK1/2 inhibitor, combined with narrow‐band ultraviolet B (NB‐UVB) in vitiligo treatment. This prospective, controlled, open‐label study included adults with progressive non‐segmental vitiligo (NSV). Patients were assigned to combination therapy with baricitinib 2 mg daily and NB‐UVB three times a week or NB‐UVB alone three times a week (control). The primary endpoint was the proportion of patients achieving 50% or greater improvement from baseline in the total Vitiligo Area Scoring Index (T‐VASI50) at week 16. Of the 33 patients (mean age, 34.1 years; 27.3% women) who completed the study, 12 of 17 (70.6%) patients in the combination group and 2 of 16 (12.5%) in the control group had a T‐VASI50 response at week 16 (relative risk [RR] = 5.6; 95% CI = 1.5–21.4; p = 0.001). Adverse events were minor, including erythema, mild blister after phototherapy and acne. Combination therapy with low‐dose baricitinib and NB‐UVB was effective and well tolerated in adults with progressive NSV.

Keywords: JAK inhibitors, phototherapy, vitiligo

graphic file with name PCMR-38-0-g003.jpg

Summary.

  • Baricitinib, a JAK1/2 inhibitor, can reduce abnormal autoimmune reactions by inhibiting the JAK/STAT pathway, and NB‐UVB can promote melanocyte regeneration in vitiligo.

  • The combination of baricitinib 2 mg/day and NB‐UVB was beneficial and well tolerated in progressive non‐segmental vitiligo, supporting further investigations of JAK inhibitors and combination regimens.

1. Introduction

Vitiligo is a chronic autoimmune disease characterized by depigmented patches of skin affecting 0.5%–2% of the global population (Frisoli, Essien, and Harris 2020; Cunningham and Rosmarin 2023). Vitiligo has a significant and broad effect on psychosocial well‐being, and it often co‐exists with other autoimmune comorbidities (Ezzedine et al. 2021; Hu and Wang 2023). However, current treatment options are limited, and their efficacy has been unsatisfactory.

In vitiligo, interferon‐γ (IFN‐γ) plays an important role in signaling via the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, resulting in the expression of C‐X‐C motif chemokine ligand 10 and the recruitment of CD8+ T cells that destroy melanocytes (Katz and Harris 2021; Diotallevi et al. 2023). Therefore, JAK inhibitors could be promising treatments, and a cream formulation of ruxolitinib (an inhibitor of JAK1 and JAK2) was the first medicine approved by the Food and Drug Administration (FDA) for vitiligo (Rosmarin et al. 2022, 2020). Nevertheless, topical ointments are not suitable for patients with widespread lesions, indicating that the oral JAK1/2 inhibitor baricitinib could be more convenient and efficient (Ezzedine et al. 2023; Song et al. 2022). Baricitinib has been approved for the treatment of refractory alopecia areata at a daily dose of 2 or 4 mg (King et al. 2022). Given the safety of JAK inhibitors, we used a daily dose of 2 mg for this study.

Narrow‐band ultraviolet B (NB‐UVB) is a well‐established effective phototherapy for vitiligo that promotes the regeneration of melanocytes. However, phototherapy alone or early phototherapy might increase the risk of progression and the therapeutic effect of NB‐UVB could be enhanced by adding a JAK inhibitor (Craiglow and King 2015; Anbar et al. 2017). In this study, the combination of baricitinib and NB‐UVB was used to treat patients with progressive non‐segmental vitiligo (NSV) for 16 weeks, with NB‐UVB alone serving as a control, to investigate the efficacy and safety of this combination therapy.

2. Methods

2.1. Study Design and Participants

This non‐randomized controlled open‐label study was conducted at Peking Union Medical College Hospital. The study was registered to www.Chictr.org.cn under the identification number ChiCTR2300072713.

The inclusion criteria were as follows: (1) definitive diagnosis of progressive NSV based on standard guidelines proposed by the British Association of Dermatologists (Eleftheriadou et al. 2022); (2) age of 18–60 years; (3) no receipt of systemic treatments or phototherapy in the prior 4 weeks; and (4) provided informed and agreed to participate in this study. Patients who fulfilled at least one of the following criteria were excluded from the analysis: (1) other types of vitiligo, including segmental vitiligo; (2) dermatologic diseases confounding vitiligo assessment; (3) photosensitivity diseases; (4) cardiovascular diseases; (5) infection, such as active tuberculosis, hepatitis B virus infection, HIV infection, or other types of infection; (6) liver or kidney dysfunction; (7) thromboembolic risk factors or coagulation function abnormalities; and (8) unwilling to attend follow‐up visits. Patients meeting the inclusion criteria were informed about current therapy options and selected the suitable treatment regimen according to their personal willingness and clinical status. Physicians responsible for the treatment and participants were aware of the interventions, while only physicians analyzing the data were blinded.

Before treatment, all patients underwent routine blood and urine examinations, liver and kidney function tests, blood lipid and electrolyte tests, examinations of coagulation profiles, T cell‐enzyme‐linked immunospot assays, tests for syphilis, hepatitis B, and HIV, electrocardiography, and chest X‐ray along with clinical evaluations of vitiligo, including photographs. Disease extent was assessed by Vitiligo Area Scoring Index (VASI) (Rosmarin et al. 2022; Hamzavi et al. 2004) and Vitiligo Extent Score (VES) (van Geel et al. 2016). Disease activity was assessed by Vitiligo Disease Activity Index (VIDA) score (Njoo et al. 1999).

VASI was determined by the body surface area (BSA) of vitiligo lesions by the Palmar Method (Rosmarin et al. 2022; Hamzavi et al. 2004). The body is divided into the following six separate and mutually exclusive sites: (1) face/neck, (2) hands, (3) upper extremities (excluding hands), (4) trunk, (5) lower extremities (excluding feet), and (6) feet. BSA should be estimated to the nearest 0.1%. The approximate size of the participant's entire palmar surface (i.e., the palm plus five digits) should be considered as 1% BSA, and the approximate size of the participant's thumb should be considered as 0.1% BSA. The degree of depigmentation was estimated to the nearest percentage (0% [no depigmentation present], 10%, 25%, 50%, 75%, 90%, or 100% [no pigment present]). The facial and total VASI (F‐VASI and T‐VASI, respectively) were then calculated by multiplying the values assessed for the vitiligo involvement by the percentage of affected skin for facial site or all body regions and summing the values of all sites together (possible range, 0–3 and 0–100, respectively). T‐VASI included facial and nonfacial areas. The facial and total VES (F‐VES and T‐VES, respectively) were calculated at www.vitiligo‐calculator.com.

VIDA score was assessed by the duration of disease progression, which defined as Grade 4 (≤ 6 weeks), Grade 3 (6 weeks–3 months), Grade 2 (3–6 months), and Grade 1 (6–12 months). All assessment scores were independently calculated and averaged by two experienced physicians.

Patients in the combination group received baricitinib 2 mg/day (Eli Lilly and Company, Indianapolis, IN, USA) combined with NB‐UVB three times a week. Control patients only received NB‐UVB three times a week without any oral medications. NB‐UVB was administered using an ultraviolet phototherapy instrument (Waldmann, UV7001K, Villingen‐Schwenningen, Germany) and performed as recommended by the Vitiligo Working Group consensus guidelines (Mohammad et al. 2017).

Patients were reviewed in the clinic every 4 weeks to record lesion changes and adverse events. Moreover, routine examinations of blood and urine, liver and kidney function, blood lipids and electrolytes, coagulation profiles and electrocardiography were performed for patients in combination group at the same time.

The final protocol, any amendments, and informed consent documentation were approved by the Institutional Review Board of Peking Union Medical College Hospital (I‐22PJ132). The study was conducted in accordance with the Declaration of Helsinki, and all patients provided written informed consent.

2.2. Outcomes

The primary endpoint was the proportion of patients achieving 50% or greater improvement from baseline in the T‐VASI (T‐VASI50) at week 16.

Key secondary endpoints included the proportion of patients achieving 75% or greater improvement from baseline in F‐VASI (F‐VASI75) at week 16 and the mean percentage change from baseline in T‐VASI, F‐VASI and T‐VES, F‐VES. Other secondary endpoints included the percentage of patients having a facial or total Physician's Global Vitiligo Assessment (F‐PhGVA and T‐PhGVA, respectively; ranges, 0–4 on a Likert scale) of clear or almost clear (scores of 0 or 1; PhGVA response) (Rosmarin et al. 2022), and the safety and side effect profile based on the monitoring of adverse events and laboratory data. The PhGVA score was defined as 0 (Clear, No signs of vitiligo), 1 (Almost clear, Only specks of depigmentation present), 2 (Mild disease, Pigmented and depigmented areas are equal), 3 (Moderate disease, More or complete depigmentation (may include < 30% hair whitening)), and 4 (Severe disease, Complete depigmentation plus > 30% hair whitening).

2.3. Sample Size Calculation

The sample size was calculated using PASS sample size calculation software. T‐VASI was considered in the sample size calculation. According to our previous study of the effectiveness of tofacitinib combined with NB‐UVB for vitiligo treatment, the T‐VASI50 response rate at week 16 was 93.3% in the combination group, versus 10.5% in the control group (Song et al. 2022). Combined with our pre‐experimental results, we expected T‐VASI50 response rates at week 16 of 12% and 65% in the control and combination groups, respectively. With a type I error rate of α = 0.05 and a power of 90% (1 − β), the sample size was estimated as 16 patients for each group. Considering potential loss and withdrawal (10%), 18 patients were needed for each group. Therefore, 36 patients were recruited in the study.

2.4. Statistical Analysis

Normally and abnormally distributed continuous variables were expressed as the mean ± standard deviation and median (interquartile range), respectively. Categorical variables were expressed as number (percentage). Continuous variables were compared between the combination and control groups by a t‐test or the Mann–Whitney U test. Fisher's exact test was used to compare the proportional composition between two or more categorical variables. Data were coded and analyzed using IBM SPSS ver. 27.0 (IBM Corp., Armonk, NY, USA). p < 0.05 was considered statistically significant.

3. Results

3.1. Patient Characteristics

Between February 2022 to June 2023, 40 patients were enrolled in our study and screened for eligibility. After excluding four patients, 36 patients were assigned to receive baricitinib 2 mg/day combined with NB‐UVB three times a week (n = 18) or only NB‐UVB three times a week (n = 18). Finally, 17 patients in the combination group and 16 patients in the control group completed the 16‐week study (Figure 1). The patients' mean age, sex distribution, disease duration, VASI, VES, and VIDA score at the onset of treatment are listed in Table 1. The distribution of baseline characteristics was similar between the groups.

FIGURE 1.

FIGURE 1

Open in a new tab

Study flow chart.

TABLE 1.

Baseline characteristics of patients.

Control group Combination group
Age‐yr 36.6 ± 9.4 31.8 ± 7.2
Male sex‐no. (%) 10 (62.5) 14 (82.4)
T‐VASI 8.6 (4.9, 28.7) 10.3 (5.7, 20.6)
F‐VASI 0.5 ± 0.3 0.3 ± 0.3
VASI—trunk 5.5 (3.0, 14.0) 6.0 (2.5, 10.0)
VASI—nonacral extremities 3.2 (1.0, 28.0) 4.0 (2.0, 12.0)
VASI—acral regions 1.6 ± 1.0 1.0 ± 1.1
T‐VES 8.5 (4.7, 28.4) 10.0 (5.4, 20.2)
F‐VES 0.5 ± 0.3 0.3 ± 0.4
VES—trunk 5.4 (3.0, 11.9) 5.7 (2.0, 10.2)
VES—nonacral 3.3 (1.1, 26.3) 4.4 (2.7, 9.3)
VES—acral regions 1.6 ± 1.0 0.9 ± 0.8
Duration of disease‐years 10.0 ± 6.0 11.3 ± 7.6
VIDA score 3 (2.0, 4.0) 3 (2.0, 4.0)
Other disorders‐–no. (%)
Hashimotos thyroiditis 0 1 (5.9)
Chronic urticaria 0 2 (11.8)
Rheumatoid arthritis 1 (6.2) 0
Open in a new tab

Note: Normally or abnormally distributed continuous variables are expressed as mean ± standard deviation or median (interquartile range), as appropriate.

Abbreviations: F‐VASI, facial Vitiligo Area Scoring Index; F‐VES, facial Vitiligo Extent Score; T‐VASI, total Vitiligo Area Scoring Index; T‐VES, total Vitiligo Extent Score; VIDA, Vitiligo Disease Activity.

3.2. Efficacy

3.2.1. Primary Endpoint: T‐VASI Response at Week 16

In total, 12 of 17 (70.6%) patients in the combination group and 2 of 16 (12.5%) patients in the control group had a T‐VASI50 response at week 16 (relative risk [RR] = 5.6, 95% confidence interval [CI] = 1.5–21.4, p < 0.001; Figure 2A ).

FIGURE 2.

FIGURE 2

Open in a new tab

Efficacy of treatment regimens in the combination group and the control group: (A) T‐VASI50 response; (B) F‐VASI75 response; (C) T‐VASI percentage change from baseline; (D) F‐VASI percentage change from baseline. CI, confidence interval; F‐VASI, facial Vitiligo Area Scoring Index; F‐VASI75, ≥ 75% improvement in F‐VASI from baseline; T‐VASI, total Vitiligo Area Scoring Index; T‐VASI50, ≥ 50% improvement in T‐VASI from baseline. *p < 0.05, **p < 0.01, ***p < 0.001.

3.2.2. Secondary Endpoints

At week 16, an F‐VASI75 response was observed in 14 of 15 (93.3%) patients in the combination group, compared with 5 of 11 (45.5%) patients in the control group (RR = 2.1; 95% CI = 1.1–4.0; p = 0.021; Figure 2B).

The mean percentage changes from baseline in T‐VASI (Figure 2C), F‐VASI (Figure 2D) T‐VES (Figure S2A) and F‐VES (Figure S2B) displayed clear separation between the combination and control groups as early as week 4 (T‐VASI: −13.5% vs. 4.7%, p < 0.001; F‐VASI: −30.9% vs. −1.1%, p < 0.001; T‐VES: −14.4% vs. 5.0%, p < 0.001; F‐VES: −34.2% vs. −0.5%, p = 0.003). Further improvements in T‐VASI and F‐VASI occurred in weeks 8 (T‐VASI: −31.7% vs. −11.9%, p < 0.001; F‐VASI: −58.9% vs. −15.3%, p < 0.001; T‐VES: −31.9% vs. −11.8%, p < 0.001; F‐VES: −64.1% vs. −12.8%, p < 0.001), week 12 (T‐VASI: −50.1% vs. −22.9%, p = 0.002; F‐VASI: −85.8% vs. −52.9%, p = 0.016; T‐VES: −50.9 vs. −22.8%, p < 0.001; F‐VES: −85.0% vs. −52.9%, p = 0.019) and week 16 (T‐VASI: −65.3% vs. −28.1%, p < 0.001, F‐VASI: −93.4% vs. −63.6%, p < 0.01; T‐VES, −65.8% vs. −27.6%, p < 0.001; F‐VES, −91.8% vs. −64.0%, p = 0.015) (Figures 2C,D and 3, Figure S2A,B).

FIGURE 3.

FIGURE 3

Open in a new tab

Representative clinical images of patients in the combination group. The area of vitiligo lesions was significantly reduced in the combination group. The greatest improvement was recorded for the face, followed by the trunk and non‐acral extremities, and the most refractory area was the acral region.

Even in areas that were difficult to treat relative to the face, such as the trunk, non‐acral extremities, and acral regions, patients in the combination group had numerically greater improvements from baseline in VASI and VES, and separation between the groups was observed in week 4 (Figures S1A–C and S2C–E ). Baseline VASI and VES in the trunk, non‐acral extremities, and acral regions were generally similar between the groups (Table 1). However, in the combination group, the greatest improvement was recorded for the face, followed by the trunk and non‐acral extremities, and the most refractory area was the acral region (Figures S1D and S2F).

At week 16, 7 of 17 (41.2%) patients in the combination group and 1 of 16 (6.3%) patients in the control group had a T‐PhGVA response (RR = 6.6, 95% CI = 0.9–47.8, p = 0.039; Figure S3A ). F‐PhGVA response was observed in 13 of 15 (86.7%) patients in the combination group, compared with 5 of 11 (45.5%) patients in the control group (RR = 1.9; 95% CI = 1.0–3.8; p = 0.038; Figure S3B). The T‐PhGVA and F‐PhGVA category are presented in Figure S3C,D.

3.3. Safety

In the combination group, two patients developed erythema, mild blister, and burning pain after phototherapy, and two other patients developed acne on the upper chest and back (Figure S4). In the control group, two patients experienced burns, erythema, and mild blister after phototherapy. All adverse events were mild, and no patient required treatment discontinuation. No patients developed skin cancer from phototherapy. Furthermore, there were no clinically relevant changes in hematological or chemical laboratory parameters in the combination group.

4. Discussion

This prospective controlled study evaluated the efficacy and safety of the combination of baricitinib 2 mg/day and NB‐UVB in patients with active NSV. The proportion of patients with T‐VASI50 and F‐VASI75 responses in week 16 was significantly greater in the combination group than in the control group. The endpoints were taken from another study that utilized 75% facial repigmentation and 50% non‐facial repigmentation as indicators of treatment success (Narayan et al. 2021).

In view of increased knowledge regarding IFN‐γ/JAK/STAT pathway involvement in the pathogenesis of vitiligo, oral and topical JAK inhibitors have been proved successful in clinical trials (Cunningham and Rosmarin 2023; Rosmarin et al. 2022; Ezzedine et al. 2023; Song et al. 2022; Fang et al. 2022). Ruxolitinib, a JAK1/2 inhibitor, was the first FDA‐approved treatment for patients with NSV affecting less than 10% BSA. Compared with topical preparations, the oral JAK1/2 inhibitor baricitinib has a wider distribution and stronger immunosuppressive effect, making it more suitable for patients with extensive lesions and resistance to treatment. Several case series and case reports described the effectiveness of baricitinib in vitiligo (Dong et al. 2022; Mumford, Gibson, and Chong 2020). Two recent single‐arm studies on novel oral JAK1 inhibitors have also demonstrated favorable results in the treatment of refractory vitiligo. One study involved the administration of upadacitinib alone, while the other assessed the combination of abrocitinib with NB‐UVB (Su et al. 2023; Xu et al. 2024). However, JAK inhibitors recently received additional warning labels from the FDA because of their increased risks of major adverse cardiovascular events, malignancy, venous thromboembolism, and mortality (Elmariah, Smith, and Merola 2022). A dose‐dependent risk was observed in patients who received baricitinib (4 mg daily as opposed to 2 mg daily or placebo) for rheumatoid arthritis (Taylor et al. 2019). Therefore, we chose a low‐dose regimen (2 mg daily).

NB‐UVB is considered an important part of the current standard of care for widespread vitiligo because of its efficacy and favorable side effect profile (Mohammad et al. 2017; Nicolaidou et al. 2007). Recent studies observed better repigmentation in sunlight‐exposed lesions than in unexposed lesions in patients treated with oral and topical JAK inhibitors (Ciechanowicz et al. 2019; Rothstein et al. 2017). A pilot study of 2% tofacitinib cream with NB‐UVB for the treatment of facial vitiligo observed a synergistic relationship (McKesey and Pandya 2019). In the current study, the combination of baricitinib and NB‐UVB also produced “one plus one greater than two” results. The difference in outcomes versus the control was evident as early as week 4, and this improvement continued through week 16, revealing an earlier onset of action than other studies with JAK inhibitors alone (Rosmarin et al. 2022; Ezzedine et al. 2023). It is noteworthy that seven people in the control group experienced progression in week 4, whereas no progression was noted in the combination group. The NB‐UVB phototherapy lasted only 16 weeks, so some patients in the control group may not have received adequate treatment doses to achieve repigmentation. Therefore, patients with NB‐UVB combined with baricitinib could achieve earlier repigmentation than patients with phototherapy alone.

The goals of vitiligo treatment are to slow disease progression, induce repigmentation, and prevent relapses. As such, baricitinib could suppress the autoimmune response and provide a favorable environment for melanocytes to regeneration, at the meantime, phototherapy could stimulate melanocytes migration from hair follicle bulges to the epidermis. This additive effect of baricitinib and phototherapy might explain the better outcomes observed in combination group than phototherapy alone. However, the role of combination therapy in preventing relapse requires longer follow‐up.

In the combination group, we further compared the repigmentation profile in different regions. Compatible with the findings for previous vitiligo treatments, repigmentation most commonly occurred in the face, whereas acral regions were the most resistant. The same repigmentation phenomenon was also observed in two studies involving the treatment of vitiligo with oral upadacitinib and abrocitinib (Su et al. 2023; Xu et al. 2024). This might be attributable to the lower density of hair follicles at acral sites and the greater exposure of the face to the sun (Esmat et al. 2012).

The incidence of adverse events associated with phototherapy was similar between the combination and control groups. In the combination group, acne might be a side effect relevant to baricitinib. Right now the pathogenesis of acne in this situation is unclear. No adverse events led to treatment termination in the study. These observations illustrated that the combination of baricitinib and NB‐UVB is well tolerated during vitiligo treatment. However, patients taking baricitinib should have regular relevant laboratory tests or electrocardiograms, and patients on long‐term phototherapy should have regular skin examinations due to the potential increased long‐term risk for skin cancer.

The limitations of this study included its small sample size, non‐randomized open‐label design, which might lead to selection bias, and the short treatment period. There was no assessment of quality of life during the study, and this should be addressed in future analyses. Additionally, future research should include the evaluation of clinical signs of active disease, such as confetti‐like depigmentations, Koebner phenomenon, and hypochromic areas/borders, to assess how these signs affect treatment efficacy (van Geel et al. 2019). Our research was a pilot study to explore the efficacy and safety of only low‐dose baricitinib in combination with NB‐UVB. However, the long‐term efficacy and safety of higher doses, such as 4 mg/day, and long‐term comparisons of efficacy and safety at different doses still need further clinical trials to confirm.

5. Conclusion

In conclusion, this prospective controlled study suggests that low‐dose baricitinib in combination with NB‐UVB is a valuable and well‐tolerated treatment for active NSV. Large‐scale, long‐term, randomized, controlled studies should be conducted in the future to further explore the efficacy and safety of oral JAK inhibitors combined with phototherapy in patients with vitiligo.

Author Contributions

Zhonghui Hu performed the data analysis and wrote the manuscript. Hongbin Song performed the data analysis. Lu Lu, Jindi Feng, Shiyu Zhang, Lu Yang performed the data collection. Yuehua Liu and Tao Wang performed the supervision and revised the manuscript.

Ethics Statement

Reviewed and approved by the Institutional Review Board of Peking Union Medical College Hospital (I‐22PJ132).

Consent

Consent for the publication of recognizable patient photographs or other identifiable material was obtained by the authors and included at the time of article submission to the journal stating that all patients gave consent with the understanding that this information may be publicly available.

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Figure S1‐S4

PCMR-38-0-s001.docx (3.6MB, docx)

Funding: This work was supported by National High Level Hospital Clinical Research Funding (2022‐PUMCH‐B‐092).

Contributor Information

Yuehua Liu, Email: yuehualiu63@163.com.

Tao Wang, Email: wangtaopumch@126.com.

Data Availability Statement

The data underlying this article cannot be shared publicly due to the privacy of individuals that participated in the study. The data will be shared on reasonable request to the corresponding author.

References

  1. Anbar, T. , Abdel‐Rahman A., Hegazy R., El‐Khayyat M., and Ragaie M.. 2017. “Simultaneous Improvement and Worsening of Vitiligo Lesions During the Course of NB‐UVB Phototherapy; Vitiligo May Not Act as One Unit.” Dermatologic Therapy 30, no. 1: e12420. [DOI] [PubMed] [Google Scholar]
  2. Ciechanowicz, P. , Rakowska A., Sikora M., and Rudnicka L.. 2019. “JAK‐Inhibitors in Dermatology: Current Evidence and Future Applications.” Journal of Dermatological Treatment 30, no. 7: 648–658. [DOI] [PubMed] [Google Scholar]
  3. Craiglow, B. G. , and King B. A.. 2015. “Tofacitinib Citrate for the Treatment of Vitiligo: A Pathogenesis‐Directed Therapy.” JAMA Dermatology 151, no. 10: 1110–1112. [DOI] [PubMed] [Google Scholar]
  4. Cunningham, K. N. , and Rosmarin D.. 2023. “Vitiligo Treatments: Review of Current Therapeutic Modalities and JAK Inhibitors.” American Journal of Clinical Dermatology 24, no. 2: 165–186. [DOI] [PubMed] [Google Scholar]
  5. Diotallevi, F. , Gioacchini H., De Simoni E., et al. 2023. “Vitiligo, From Pathogenesis to Therapeutic Advances: State of the Art.” International Journal of Molecular Sciences 24, no. 5: 4910. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Dong, J. , Huang X., Ma L. P., et al. 2022. “Baricitinib Is Effective in Treating Progressing Vitiligo In Vivo and In Vitro.” Dose‐Response 20, no. 2: 15593258221105370. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Eleftheriadou, V. , Atkar R., Batchelor J., et al. 2022. “British Association of Dermatologists Guidelines for the Management of People With Vitiligo 2021.” British Journal of Dermatology 186, no. 1: 18–29. [DOI] [PubMed] [Google Scholar]
  8. Elmariah, S. B. , Smith J. S., and Merola J. F.. 2022. “JAK in the [Black] Box: A Dermatology Perspective on Systemic JAK Inhibitor Safety.” American Journal of Clinical Dermatology 23, no. 4: 427–431. [DOI] [PubMed] [Google Scholar]
  9. Esmat, S. M. , El‐Tawdy A. M., Hafez G. A., et al. 2012. “Acral Lesions of Vitiligo: Why are They Resistant to Photochemotherapy?” Journal of the European Academy of Dermatology and Venereology 26, no. 9: 1097–1104. [DOI] [PubMed] [Google Scholar]
  10. Ezzedine, K. , Eleftheriadou V., Jones H., et al. 2021. “Psychosocial Effects of Vitiligo: A Systematic Literature Review.” American Journal of Clinical Dermatology 22, no. 6: 757–774. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Ezzedine, K. , Peeva E., Yamaguchi Y., et al. 2023. “Efficacy and Safety of Oral Ritlecitinib for the Treatment of Active Nonsegmental Vitiligo: A Randomized Phase 2b Clinical Trial.” Journal of the American Academy of Dermatology 88, no. 2: 395–403. [DOI] [PubMed] [Google Scholar]
  12. Fang, W. C. , Lin S. Y., Huang S. M., and Lan C. E.. 2022. “Low‐Dose Tofacitinib With 308‐nm Excimer Therapy Successfully Induced Repigmentation in Patients With Refractory Vitiligo.” Clinical and Experimental Dermatology 47, no. 4: 782–783. [DOI] [PubMed] [Google Scholar]
  13. Frisoli, M. L. , Essien K., and Harris J. E.. 2020. “Vitiligo: Mechanisms of Pathogenesis and Treatment.” Annual Review of Immunology 38: 621–648. [DOI] [PubMed] [Google Scholar]
  14. Hamzavi, I. , Jain H., McLean D., Shapiro J., Zeng H., and Lui H.. 2004. “Parametric Modeling of Narrowband UV‐B Phototherapy for Vitiligo Using a Novel Quantitative Tool: The Vitiligo Area Scoring Index.” Archives of Dermatology 140, no. 6: 677–683. [DOI] [PubMed] [Google Scholar]
  15. Hu, Z. , and Wang T.. 2023. “Beyond Skin White Spots: Vitiligo and Associated Comorbidities.” Frontiers in Medicine 10: 1072837. [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. Katz, E. L. , and Harris J. E.. 2021. “Translational Research in Vitiligo.” Frontiers in Immunology 12: 624517. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. King, B. , Ohyama M., Kwon O., et al. 2022. “Two Phase 3 Trials of Baricitinib for Alopecia Areata.” New England Journal of Medicine 386, no. 18: 1687–1699. [DOI] [PubMed] [Google Scholar]
  18. McKesey, J. , and Pandya A. G.. 2019. “A Pilot Study of 2% Tofacitinib Cream With Narrowband Ultraviolet B for the Treatment of Facial Vitiligo.” Journal of the American Academy of Dermatology 81, no. 2: 646–648. [DOI] [PubMed] [Google Scholar]
  19. Mohammad, T. F. , Al‐Jamal M., Hamzavi I. H., et al. 2017. “The Vitiligo Working Group Recommendations for Narrowband Ultraviolet B Light Phototherapy Treatment of Vitiligo.” Journal of the American Academy of Dermatology 76, no. 5: 879–888. [DOI] [PubMed] [Google Scholar]
  20. Mumford, B. P. , Gibson A., and Chong A. H.. 2020. “Repigmentation of Vitiligo With Oral Baricitinib.” Australasian Journal of Dermatology 61, no. 4: 374–376. [DOI] [PubMed] [Google Scholar]
  21. Narayan, V. S. , Uitentuis S. E., Bekkenk M. W., and Wolkerstorfer A.. 2021. “What is Successful Repigmentation in Vitiligo From the Point of View of Patients?” British Journal of Dermatology 184, no. 1: 165–166. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Nicolaidou, E. , Antoniou C., Stratigos A. J., Stefanaki C., and Katsambas A. D.. 2007. “Efficacy, Predictors of Response, and Long‐Term Follow‐Up in Patients With Vitiligo Treated With Narrowband UVB Phototherapy.” Journal of the American Academy of Dermatology 56, no. 2: 274–278. [DOI] [PubMed] [Google Scholar]
  23. Njoo, M. D. , Das P. K., Bos J. D., and Westerhof W.. 1999. “Association of the Köbner Phenomenon With Disease Activity and Therapeutic Responsiveness in Vitiligo Vulgaris.” Archives of Dermatology 135, no. 4: 407–413. [DOI] [PubMed] [Google Scholar]
  24. Rosmarin, D. , Pandya A. G., Lebwohl M., et al. 2020. “Ruxolitinib Cream for Treatment of Vitiligo: A Randomised, Controlled, Phase 2 Trial.” Lancet 396, no. 10244: 110–120. [DOI] [PubMed] [Google Scholar]
  25. Rosmarin, D. , Passeron T., Pandya A. G., et al. 2022. “Two Phase 3, Randomized, Controlled Trials of Ruxolitinib Cream for Vitiligo.” New England Journal of Medicine 387, no. 16: 1445–1455. [DOI] [PubMed] [Google Scholar]
  26. Rothstein, B. , Joshipura D., Saraiya A., et al. 2017. “Treatment of Vitiligo With the Topical Janus Kinase Inhibitor Ruxolitinib.” Journal of the American Academy of Dermatology 76, no. 6: 1054–1060.e1. [DOI] [PubMed] [Google Scholar]
  27. Song, H. , Hu Z., Zhang S., Yang L., Liu Y., and Wang T.. 2022. “Effectiveness and Safety of Tofacitinib Combined With Narrowband Ultraviolet B Phototherapy for Patients With Refractory Vitiligo in Real‐World Clinical Practice.” Dermatologic Therapy 35, no. 11: e15821. [DOI] [PubMed] [Google Scholar]
  28. Su, X. , Luo R., Ruan S., et al. 2023. “Efficacy and Tolerability of Oral Upadacitinib Monotherapy in Patients With Recalcitrant Vitiligo.” Journal of the American Academy of Dermatology 89, no. 6: 1257–1259. [DOI] [PubMed] [Google Scholar]
  29. Taylor, P. C. , Weinblatt M. E., Burmester G. R., et al. 2019. “Cardiovascular Safety During Treatment With Baricitinib in Rheumatoid Arthritis.” Arthritis & Rhematology 71, no. 7: 1042–1055. [DOI] [PMC free article] [PubMed] [Google Scholar]
  30. van Geel, N. , Grine L., De Wispelaere P., Mertens D., Prinsen C. A. C., and Speeckaert R.. 2019. “Clinical Visible Signs of Disease Activity in Vitiligo: A Systematic Review and Meta‐Analysis.” Journal of the European Academy of Dermatology and Venereology 33, no. 9: 1667–1675. [DOI] [PubMed] [Google Scholar]
  31. van Geel, N. , Lommerts J., Bekkenk M., et al. 2016. “Development and Validation of the Vitiligo Extent Score (VES): An International Collaborative Initiative.” Journal of Investigative Dermatology 136, no. 5: 978–984. [DOI] [PubMed] [Google Scholar]
  32. Xu, Z. , Xuan Y., Li Y., et al. 2024. “A Prospective Observational Study of Oral Abrocitinib and Narrow‐Band Ultraviolet‐B in Refractory Progressive Vitiligo.” Journal of the American Academy of Dermatology 91, no. 3: 590–592. [DOI] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Figure S1‐S4

PCMR-38-0-s001.docx (3.6MB, docx)

Data Availability Statement

The data underlying this article cannot be shared publicly due to the privacy of individuals that participated in the study. The data will be shared on reasonable request to the corresponding author.

Articles from Pigment Cell & Melanoma Research are provided here courtesy of Wiley

RESOURCES