Ignite Creation Date:
2025-12-24 @ 12:22 PM
Ignite Modification Date:
2026-01-20 @ 6:31 AM
Study NCT ID:
NCT04803461
Status:
UNKNOWN
Last Update Posted:
2021-03-17
First Post:
2021-03-13
Is Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Catecholamines Level in Vitiligo Patients Before and After Excimer Light
Sponsor:
Assiut University
Organization:
Study Overview
Official Title:
Catecholamines Level in Urine and Serum in Stable Non-segmental Vitiligo Patients Before and After Excimer Light
Status:
UNKNOWN
Status Verified Date:
2021-03
Last Known Status:
NOT_YET_RECRUITING
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 an acquired cutaneous disorder of pigmentation, with a 1-2% incidence worldwide, without predilection for sex or race. People affected by vitiligo have a vast reduction of quality of life, caused by the color contrast between healthy pigmented skin and the depigmented vitiligo patches due to death of melanocytes, which may cause psychological problems to the patient.
Detailed Description:
Despite much research, the etiology of vitiligo and the causes of melanocyte death are not clear. Conventionally, there have been three hypotheses to explain the pathogenesis of vitiligo: neural, immune and self-destructive, but none can completely explain the disease and are probably interrelated.
From therapeutic and prognostic viewpoint, vitiligo is broadly classified in two major subtypes, segmental vitiligo (SV) including focal lesions confined to a segment of the body that does not progress towards generalized disease; and non-segmental vitiligo (NSV) which comprises all generalized usually symmetrical forms, including acrofacial vitiligo.
The increased release of catecholamines (CA) from the autonomic nerve endings in the micro-environment of melanocytes in the affected skin areas might be involved in the aetiopathogenesis of vitiligo through two main mechanisms: a direct cytotoxic action of CA and/or their o-diphenol catabolites and an indirect action, skin and mucosa arterioles possess receptors, activation of which by CA discharge may cause a severe vasoconstriction, leading to epidermal and dermal hypoxia with excessive production of toxic oxyradicals generated by different pathways.In both cases, a genetic predisposition due to insufficient radical scavengers in the affected areas should be taken into account.
First line of non-surgical therapy includes topical corticosteroid therapy and phototherapy (solar exposition, Psoralen + UVA (PUVA), narrowband UVB (NB-UVB). (8-10). The NB-UVB is now considered as the best treatment for extensive vitiligo vulgaris due to its relatively good efficacy and excellent tolerance .
Contrary to the majority of laser devices, the 308-nm excimer laser is not a ''destructive'' form of therapy but induces photobiological effects similar to selective UVB phototherapy (311-312 nm).As for UVB phototherapy, it could be judged that the efficiency of the 308-nm excimer laser in treating vitiligo depends on immunomodulatory effects (induction of the secretion of cytokines, T-lymphocytes apoptosis) and stimulation of melanocyte migration and proliferation from the niche located in hair follicles. The 308-nm excimer laser allows a selective treatment of the lesions. This device has already shown interesting results in post-resurfacing leukoderma.
From therapeutic and prognostic viewpoint, vitiligo is broadly classified in two major subtypes, segmental vitiligo (SV) including focal lesions confined to a segment of the body that does not progress towards generalized disease; and non-segmental vitiligo (NSV) which comprises all generalized usually symmetrical forms, including acrofacial vitiligo.
The increased release of catecholamines (CA) from the autonomic nerve endings in the micro-environment of melanocytes in the affected skin areas might be involved in the aetiopathogenesis of vitiligo through two main mechanisms: a direct cytotoxic action of CA and/or their o-diphenol catabolites and an indirect action, skin and mucosa arterioles possess receptors, activation of which by CA discharge may cause a severe vasoconstriction, leading to epidermal and dermal hypoxia with excessive production of toxic oxyradicals generated by different pathways.In both cases, a genetic predisposition due to insufficient radical scavengers in the affected areas should be taken into account.
First line of non-surgical therapy includes topical corticosteroid therapy and phototherapy (solar exposition, Psoralen + UVA (PUVA), narrowband UVB (NB-UVB). (8-10). The NB-UVB is now considered as the best treatment for extensive vitiligo vulgaris due to its relatively good efficacy and excellent tolerance .
Contrary to the majority of laser devices, the 308-nm excimer laser is not a ''destructive'' form of therapy but induces photobiological effects similar to selective UVB phototherapy (311-312 nm).As for UVB phototherapy, it could be judged that the efficiency of the 308-nm excimer laser in treating vitiligo depends on immunomodulatory effects (induction of the secretion of cytokines, T-lymphocytes apoptosis) and stimulation of melanocyte migration and proliferation from the niche located in hair follicles. The 308-nm excimer laser allows a selective treatment of the lesions. This device has already shown interesting results in post-resurfacing leukoderma.
Study Oversight
Has Oversight DMC:
False
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?: