الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
In vitiligo, an acquired depigmenting skin disease, melanocytes are gradually and selectively lost, resulting in the appearance of milky white macules and patches. Cosmetic and psychological distress brought on by vitiligo can lead to issues with body image, self-esteem, and sexual relationships.
It’s yet unknown what causes vitiligo specifically. The pathophysiology of vitiligo has been explained by a number of notions, including autoimmune, oxidative stress, neurological, and hereditary explanations.
Clinically speaking, there are two main types of vitiligo: SV and NSV. Additionally, there are three main subtypes of the latter: universal, acrofacial, and generalized vitiligo.
Treatment options for vitiligo can be broadly divided into two categories: medicinal and surgical. Phototherapy and systemic and topical immunosuppressants are used in medical treatment to assist in stabilizing depigmented lesions and promote repigmentation. When a patients’ condition is stable and their response to medical therapy is poor, surgery may be considered.
The preferred phototherapy for both active and/or generalized vitiligo is NB-UVB (311 nm). Owing to its excellent safety record in both pediatric and adult populations, as well as its lack of systemic adverse effects, NB-UVB phototherapy has been the first choice for patients whose vitiligo affects more than 10% of BSA.
Autophagy, which translates as ”self-eating,” is an internal catabolic process in which proteins and organelles within cells are transported to lysosomes for breakdown; the byproducts of this degradation are subsequently recycled back into the cells for utilization. One of the earliest known markers of autophagy in humans is beclin 1. Free beclin 1 is an inducer of autophagy that is commonly used as a marker to control the start of autophagy.
The purpose of this study was to examine the impact of NB-UVB phototherapy on serum beclin 1 levels in active non-segmental vitiligo patients and establish a correlation between these levels and the severity and activity of the disease.
Thirty patients with active NSV were included in this study, both before and after NB-UVB phototherapy, along with thirty healthy control participants. For six months, the patients underwent twice-weekly NB-UVB treatments, and before and following the completion of the therapy, serum beclin 1 levels were assessed using ELISA kit.
Signs of activity after therapy were significantly less than those before treatment.
Following NB-UVB phototherapy, vitiligo patients’ post-treatment VIDA values were significantly lower than their pre-treatment values (P=0.013), indicating a significant reduction in disease activity.
VASI was lower significantly following therapy than it was prior to treatment.(P <0.001).
Compared to pre-treatment readings, post-treatment VES was significantly lower. (P <0.001).
No statistically significant difference was observed in serum beclin 1 levels neither between vitiligo patients and controls nor between pre-treatment and post-treatment values.
No significant relation between pre-treatment serum level of beclin 1 and gender, vitiligo family history or pre-treatment activity signs was detected. In addition, no significant relation between post-treatment serum level of beclin 1 and post-treatment activity signs was detected.