TRPM2 Gene Polymorphism, NLRP3 Inflammasome Expression in Vitiligo Patients

NCT ID: NCT07232238

Last Updated: 2025-12-31

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

ACTIVE_NOT_RECRUITING

Total Enrollment

60 participants

Study Classification

OBSERVATIONAL

Study Start Date

2025-10-20

Study Completion Date

2027-05-01

Brief Summary

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This study investigates the relationship between Transient Receptor Potential Melastatin 2 (TRPM2) gene polymorphism and Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome expression in patients with vitiligo. Vitiligo is a common autoimmune depigmenting disorder characterized by melanocyte destruction associated with oxidative stress and immune dysregulation.

TRPM2 is a calcium-permeable cation channel activated by oxidative stress, while NLRP3 inflammasome activation promotes inflammation through interleukin-1β (IL-1β) and interleukin-18 (IL-18) release. This study aims to evaluate TRPM2 genetic variants, NLRP3 expression levels, and their possible correlation with disease severity measured using the Vitiligo Area Scoring Index (VASI).

Detailed Description

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Vitiligo is a chronic autoimmune depigmenting disorder characterized by selective loss of melanocytes. Oxidative stress plays a central role in triggering melanocyte damage. Transient Receptor Potential Melastatin 2 (TRPM2) is a calcium-permeable cation channel activated by reactive oxygen species (ROS). Activation of TRPM2 leads to increased intracellular calcium (Ca2+) influx and mitochondrial dysfunction, contributing to melanocyte apoptosis.

The Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is an intracellular multiprotein complex activated by cellular stress signals, including Ca2+ influx, ROS, and mitochondrial injury. NLRP3 activation results in caspase-1 activation and the release of pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18), which further contribute to melanocyte destruction.

Evidence suggests an interaction between TRPM2 activation and NLRP3 inflammasome signaling, particularly under oxidative stress conditions. However, this relationship has not been studied in vitiligo patients. This study investigates TRPM2 gene polymorphism, evaluates NLRP3 expression levels, and explores their association with disease presence and severity.

Conditions

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Vitiligo

Keywords

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TRPM2, NLRP3, oxidative stress, inflammasome, genetic polymorphism

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

CROSS_SECTIONAL

Study Groups

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Vitiligo Patients

Participants clinically diagnosed with vitiligo, recruited from the Dermatology Outpatient Clinic, Aswan University Hospital. Peripheral blood samples will be collected for TRPM2 gene and NLRP3 inflammasome analysis.

No interventions assigned to this group

Healthy Controls

Age- and sex-matched healthy individuals without autoimmune or inflammatory disorders, recruited as controls. Blood samples will be analyzed similarly for comparison.

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

\- Adult patients (aged 18 years and older) clinically diagnosed with vitiligo, either newly diagnosed or not on treatment for at least 3 months before the study.

Exclusion Criteria

* Any participant with associated inflammatory disease (such as infections or autoimmune disorders).
* Patients with chronic diseases including cardiac, hepatic, hematologic, or renal disorders, or malignancies.
* Patients who had recent major surgical procedures.
* Patients with segmental vitiligo.
* Vitiligo patients who have received treatment within 3 months prior to the study.
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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Aswan University

OTHER

Sponsor Role lead

Responsible Party

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Mostafa Ahmed Maher Sayed

Principal Investigator / MD Candidate

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Mostafa Ahmed Maher, M.B.B.Ch.

Role: PRINCIPAL_INVESTIGATOR

Faculty of Medicine, Aswan University

Locations

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Aswan University Hospital

Aswān, Aswan Governorate, Egypt

Site Status

Countries

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Egypt

Related Links

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https://www.aswu.edu.eg/faculty-of-medicine

Faculty of Medicine, Aswan University official website.

Other Identifiers

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897/1/24

Identifier Type: -

Identifier Source: org_study_id