NCT06768840

Vitiligo, New Treatment and Serum s100B

Serum s100B in Generalized Vitiligo and Its Relation to Oral Baricitinib, Narrow Band Ultraviolet (B) Therapy

• Status: Recruiting
• Phase: Phase 2 / Phase 3
• Study type: Interventional
• Enrollment: 50 (estimated)
• Sponsor: South Valley University · Academic / Other
• Sex: All
• Age: 10 Years – 75 Years
• Healthy volunteers: Accepted

Summary

vitiligo is an autoimmune depigmenting skin disorder characterized by milky white macules or patches, with 2% worldwide prevalence. Vitiligo has unexpected course that significantly influences on patient's quality of life and self-esteem. Multiple medications have been introduced for vitiligo treatment, in this study we work on one of systemic JAK inhibitors

Detailed description

Vitiligo, an autoimmune depigmenting disorder has a worldwide prevalence of 0.5%-2.0%. distinguished by distinct, varying-shaped depigmented macules and patches. Vitiligo is thought to be a benign condition that mostly affects appearance, although it usually has a significant negative influence on patients' quality of life and self-esteem. It may also put them at higher risk of developing skin cancer and sunburn. 85%-90% of cases are generalized vitiligo, also known as non-segmental vitiligo (NSV), which is characterized by a symmetric body distribution. A number of factors contribute to the multifactorial pathophysiology of vitiligo, including metabolic disorders, oxidative stress, hereditary vulnerability, and autoimmune response. Of these, cell-mediated immunity plays a major role in melanocytes destruction .The interferon-gamma (IFN-γ), C-X-C motif chemokine ligands (CXCL9/10), and C-X-C motif chemokine receptor (CXCR3) signaling axis (IFN-γ-CXCL9/10-CXCR3 or ICC axis) has been identified as a critical mediator for the recruitment of autoimmune CXCR3+ CD8+ T cells. High amounts of INF-γ and tumor necrosis factor alpha (TNF-α) are produced by these cells, which encourage melanocytes (MC) detachment and apoptosis. MCs detachment is prevented by inhibiting IFN-γ signaling pathway, which is regulated by Janus kinase-signal transducer and activator of transcription (JAK-STAT). Treatment goals for vitiligo include arresting, re-pigmentation of existing lesions, and maintenance of re-pigmentation. Only generic immunosuppressants, including oral and topical corticosteroids, calcineurin inhibitors, phototherapy, and surgical procedures, are available as the current traditional therapeutics for vitiligo. One of the primary lines of treatment for generalized vitiligo is narrowband ultraviolet B (NB-UVB) phototherapy, which is always enhanced by combining it with other therapies. JAK inhibitors target the JAK/STAT signaling pathway and are now approved to treat many immune diseases. It was reported that individuals with vitiligo treated with JAK inhibitors had higher rates of re-pigmentation especially when combined with ultraviolet or sun exposure. Given IFN-γ signaling is specially mediated by JAK1 and JAK 2. Baricitinib is a small molecule, which mainly targets the JAK1 and JAK2 subtypes, is already used in dermatology to treat inflammatory dermatoses that are caused by JAK/STAT signaling. The cytosolic calcium-binding S100 protein family has a variety of intracellular and extracellular activities. A damage-associated molecular pattern protein called S100B has been suggested as a gauge of melanocyte cytotoxicity.

Conditions

• Vitiligo, Generalized

Interventions

Type	Name	Description
DRUG	Baricitinib	oral baricitinib 4mg for adults and 2mg for children 10-16 years for group A
DRUG	oral mini pulse	pulse dose of oral dexamethasone 2.5mg for adults for two consecutive days per week and half the dose for children
RADIATION	Narrow Band UVB Treatment	narrowband ultraviolet rays B phototherapy two sessions per week

Timeline

• Start date: 2024-10-02
• Primary completion: 2025-08-01
• Completion: 2025-10-01
• First posted: 2025-01-10
• Last updated: 2025-01-10

Locations

1 site across 1 country: Egypt