Viewing Study NCT05869942



Ignite Creation Date: 2024-05-06 @ 7:01 PM
Last Modification Date: 2024-10-26 @ 2:59 PM
Study NCT ID: NCT05869942
Status: NOT_YET_RECRUITING
Last Update Posted: 2023-05-22
First Post: 2023-05-10

Brief Title: Histochemical Study of Vitiligo in Sohag University Hospital Patients
Sponsor: Sohag University
Organization: Sohag University

Study Overview

Official Title: Histological and Histochemical Study of Vitiligo Pathogenesis in Sohag University Hospital Patients
Status: NOT_YET_RECRUITING
Status Verified Date: 2023-05
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief Summary: Vitiligo is a common acquired idiopathic disorder characterized by depigmentation of the skin hair and mucous membranes in the form of macules and patches due to selective melanocyte destruction Incidence of Vitiligo is about 05 to 2 of the worlds population and its incidence continues to increase Vitiligo can appear at any age group especially in the second and third decades of life About one-third of vitiligo patients are children under ten years old Vitiligo can be classified into non-segmental segmental mixed and unclassifiableundetermined types Vitiligo has a negative impact on patients quality of life by decreasing their self-confidence and causing significant psychological distress
Detailed Description: The pathogenesis of vitiligo is still unclear but some theories can explain it such as oxidative stress autoimmunity autocytotoxicity genetic factors neural and melanocytorrhagy Loss of pigment which occur in vitiligo may be due to two main causes absence of melanocytes andor the inability of melanocytes to produce and store melanin in melanosomes in the process of melanogenesis

High mobility group box protein B1 HMGB1 normally presents in the nucleus to maintain genomic stabilization and regulate gene transcription but HMGB1 can be released outside the cell due to exposure to stressful factors such as oxidative stress and function as a damage-associated molecular pattern DAMP protein leading to strong proinflammatory effects Recent data showed that HMGB1 is overexpressed in both blood and lesional specimens from vitiligo patients Moreover oxidative stress triggers the release of HMGB1 from keratinocytes and melanocytes indicating that HMGB1 may participate and play a crucial role in the pathological process of vitiligo

HMGB1 Directly induces Melanocyte apoptosis through stimulation with reactive oxidative stress ROS or ultraviolet B UVB in vitro which significantly increases the release of HMGB1 from keratinocytes which inhibits the expression of melanogenesis-related molecules such as microphthalmia- associated transcription factor MITF tyrosinase-related proteins and the gp100 protein in a paracrine manner and finally activate caspase-3 to trigger melanocyte apoptosis

Study Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: False
Is a FDA Regulated Device?: False
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: None