Journal Digest: January 28, 2026

Case Reports in Dermatological Medicine | Drug-Induced Phototoxicity in Vitiligo: The Role of Hydrochlorothiazide in Photosensitivity Dermatitis

This case study highlights drug-induced phototoxic dermatitis in a patient with vitiligo, emphasizing the role of hydrochlorothiazide (HCTZ) as a trigger in UV-vulnerable skin. A 54-year-old man with generalized vitiligo developed pruritic erythematous papules confined to sun-exposed depigmented areas of the hands and face. The eruption was initially mistaken for a fungal infection and did not respond to antifungals, but a review of medications identified olmesartan–HCTZ as a likely culprit. Thiazide diuretics can absorb UV radiation and generate reactive oxygen species, causing direct cellular injury in phototoxic reactions. In vitiligo, the absence of melanin removes a key photoprotective and antioxidant defense, allowing deeper UV penetration and amplifying oxidative damage and inflammation. The clinical pattern and timing favored a phototoxic rather than photoallergic mechanism. Management included discontinuation of HCTZ and strict photoprotection.¹

Health Science Reports | Evaluation of Oxidative Stress in Red Blood Cells From Vitiligo Patients and Its Correlation With Disease Severity and Activity: A Cohort Case-Control Study

A case–control study investigated systemic oxidative stress in vitiligo by assessing red blood cell (RBC) antioxidant enzymes and plasma lipid peroxidation markers, and correlating findings with disease severity and activity. Thirty patients with vitiligo were compared with 30 age- and sex-matched healthy controls. Spectrophotometric analysis showed significantly higher RBC superoxide dismutase (SOD) activity and plasma malondialdehyde (MDA) levels in patients, alongside significantly reduced catalase and glucose-6-phosphate dehydrogenase (G6PD) activities (p < 0.05 for all). Oxidative stress markers correlated with clinical parameters: SOD and MDA levels positively correlated with Vitiligo Extent Score (VES) and were highest in universal vitiligo, while catalase and G6PD showed negative correlations with disease extent. Patients with active disease (higher VIDA scores) demonstrated greater oxidative imbalance, with elevated SOD and MDA and lower catalase and G6PD levels²

Clinical, Cosmetic and Investigational Dermatology | Integrative Multi-Omics and Experimental Analyses Identify TAPBP as a Key Mediator Linking Genetic Susceptibility to Melanocyte Dysfunction in Vitiligo

This integrative multi-omics study explored how genetic risk translates into melanocyte vulnerability in vitiligo, identifying TAPBP (tapasin) as a key mediator. Researchers combined GWAS data from FinnGen (n = 466,064), blood eQTL data (n = 31,684), and single-cell RNA sequencing of lesional skin. Cross-omic analyses highlighted TAPBP as genetically associated with vitiligo susceptibility and significantly upregulated in lesional melanocytes, with enrichment of antigen processing and MHC class I presentation pathways. Transcription factor analysis identified STAT2, a type I interferon pathway effector, as a likely upstream regulator, linking interferon signaling to altered antigen presentation. Functional validation in human melanocytes showed that TAPBP overexpression increased HLA class I expression, suppressed proliferation, and induced apoptosis. These findings suggest that a STAT2–TAPBP axis enhances melanocyte immunogenicity, promoting CD8⁺ T-cell recognition and cytotoxicity.³

Journal of the European Academy of Dermatology and Venereology | Efficacy of Ritlecitinib for Vitiligo Treatment Stratified by Baseline Demographic and Clinical Characteristics: Post Hoc Analysis of a Phase 2b Study

A post hoc analysis of a phase 2b trial (NCT03715829) evaluated whether baseline demographic and clinical factors influenced response to ritlecitinib in active non-segmental vitiligo. Patients received ritlecitinib 50 mg once daily, with or without a loading dose, during a 24-week dose-ranging period and a 24-week extension. Efficacy was measured by achievement of ≥75% improvement in Facial Vitiligo Area Scoring Index (F-VASI75). Among 184 patients in the dose-ranging period and 90 in the extension, overall response rates increased from 8.7% at week 24 to 26.7% at week 48, indicating greater repigmentation with longer treatment. Clinically meaningful responses were observed across all analyzed subgroups, including age, sex, Fitzpatrick skin type, disease duration, prior treatment, and facial involvement. Numerical differences seen at week 24—such as higher responses in males, darker skin types, treatment-naïve patients, and those without leukotrichia—generally diminished by week 48. Only small, nonsignificant trends remained for lower BMI, absence of leukotrichia, and fewer comorbidities.⁴

Japanese Journal of Dermatology | Elevated Risk of Herpes Zoster in Vitiligo Patients: A Nationwide Population-Based Cohort Study of Taiwan

This nationwide, population-based cohort study from Taiwan assessed whether vitiligo is independently associated with herpes zoster (HZ) risk. Using the Longitudinal Health Insurance Database (2010–2022), investigators identified patients with vitiligo and matched them 1:4 with non-vitiligo controls via propensity scores for age, sex, index date, and comorbidities, yielding 79,910 individuals. HZ incidence was significantly higher in the vitiligo group than controls (7.78% vs 2.72%, p < 0.001). After adjustment, vitiligo remained an independent risk factor for HZ (aaHR 1.532). Risk increased with age and was greater in women. Subgroup analyses showed the highest susceptibility among vitiligo patients receiving systemic therapies, particularly cyclosporine (aHR 1.891), methotrexate (aHR 1.981), and systemic corticosteroids (aHR 1.474). Dermatologists should consider this baseline vulnerability when prescribing systemic agents and discuss preventive strategies, including zoster vaccination, especially for older and female patients.⁵

References

1. Parga AD, Dubin C, Rudikoff D. Drug-Induced Phototoxicity in Vitiligo: The Role of Hydrochlorothiazide in Photosensitivity Dermatitis. Case Rep Dermatol Med. 2025;2025:4302190. Published 2025 Dec 26. doi:10.1155/crdm/4302190

2. Saleh YSN, Mohammed GF, Anani M, Bandy A, Bahaj SS, Marie RE. Evaluation of Oxidative Stress in Red Blood Cells From Vitiligo Patients and Its Correlation With Disease Severity and Activity: A Cohort Case-Control Study. Health Sci Rep. 2026;9(1):e71699. Published 2026 Jan 7. doi:10.1002/hsr2.71699

3. Shi J, Guo M, Fu L, He J, Hu Y. (2026). Integrative Multi-Omics and Experimental Analyses Identify TAPBP as a Key Mediator Linking Genetic Susceptibility to Melanocyte Dysfunction in Vitiligo. Clinical, Cosmetic and Investigational Dermatology, 19, 1–10. https://doi.org/10.2147/CCID.S577486

4. Pandya AG, Hamzavi I, Ghosh P, Ezzedine K, Harris JE, Adiri R, Chen S, Peeva E, Yamaguchi Y. (2026), Efficacy of Ritlecitinib for Vitiligo Treatment Stratified by Baseline Demographic and Clinical Characteristics: Post Hoc Analysis of a Phase 2b Study. JEADV Clinical Practice. https://doi.org/10.1002/jvc2.70193

5. Lin BS, Chung CH, Weng TH, et al. Elevated Risk of Herpes Zoster in Vitiligo Patients: A Nationwide Population-Based Cohort Study of Taiwan. J Dermatol. Published online January 9, 2026. doi:10.1111/1346-8138.70140