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العنوان
Hepatitis C virus infection could be a risk factor for adult-onset vitiligo in Egyptian patients :
المؤلف
Dawood, Eman Mohamed Abdel-khalik .
هيئة الاعداد
باحث / ايمان محمد عبدالخالق داوود
مشرف / محمد عبد الواحد جابر
مشرف / راندا محمد صديق
الموضوع
Vitiligo. Pigmentation disorders. Skin Diseases Egypt.
تاريخ النشر
2024.
عدد الصفحات
80 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الأمراض الجلدية
الناشر
تاريخ الإجازة
10/7/2024
مكان الإجازة
جامعة المنوفية - كلية الطب - الجلدية والأمراض النتاسلية
الفهرس
Only 14 pages are availabe for public view

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from 107

Abstract

Vitiligo is an acquired depigmenting skin disorder, resulting from melanocyte destruction and characterized by patches of the skin losing their pigment. The patches of skin affected become white and usually have sharp margins. Moreover, the hair from the skin may also become white, and the inside of the mouth and nose may also be involved.
Typically, both sides of the body are affected. Often the patches begin on areas of skin that are exposed to the sun, thus it is more noticeable in people with dark skin. The exact etiology of vitiligo is still unknown, and several factors may contribute to its pathogenesis. It is believed to be due to genetic susceptibility that is triggered by an environmental factor such that an autoimmune disease occurs which results in the destruction of skin pigment cells.
Risk factors include a family history of the condition or other autoimmune diseases, such as hyperthyroidism, alopecia areata, and pernicious anemia. Hepatitis C Virus (HCV) is a hepatotropic and lymphotropic virus that is prevalent in Egypt. chronic HCV infection is frequently asymptomatic and only discovered when extra-hepatic manifestations (EHMs) develop. About 74% of patients with chronic HCV infection develop at least one EHM during their lifetime.
About 17% of them had at least one dermatological manifestation. The most common dermatological manifestations of HCV are lichen planus (LP), mixed cryoglobulinemia (MC) and porphyria cutanea tarda. The relationship between chronic HCV infection and vitiligo has not been established yet. A high prevalence of vitiligo among HCV reactive patients has been reported in some studies.
Summary 
61
The aim of this study was to measure the prevalence of HCV sero- reactivity among vitiligo patients and if HCV may be a triggering factor for adult-onset vitiligo, particularly in regions with a high prevalence of HCV.
This was a cross-sectional descriptive study that carried out on 100 patients confirmed with vitiligo admitted to Dermatology Department at Menoufia University and El-Bagour General Hospital
Summary of results of present study:
In the present study, The mean age of patients with vitiligo (30.32 ± 4.75) range(22 – 42),while the mean duration of these patient at vitiligo onset was 27.2 ± 4.47 years with a disease duration of 3.3 ± 1.21 and mean of vitiligo extension was(17.18 ± 3.42) measured by BSA involvement. About 16% of patients with vitiligo reported past family infection with vitiligo and only 11% of patients had a positive consanguinity status.
Regarding vitiligo subtype among patients, the most common finding was generalized type with 84%, followed by Acrofacial 12%, and universal 4%. The zero VIDA score was the most reported score among patients with vitiligo with 54%. HCV-reactivity was reported in 21% of the studied patients.
There was no observed significance between HCV-reactive and non-reactive regarding vitiligo subtype, VIDA score, features of activity, VISA score, or extent of BSA.
The prevalence of HCV-seroreactivity was 21% among patients with a vitiligo. All of them had adult-onset vitiligo, with a prevalence of HCV-seroreactivity of 34.6% among patients with adult-onset vitiligo.
Summary 
62
There was a significant association between HCV- seroreactivity and adult onset vetiligo (p< 0.01). Moreover Age and age of vetiligo onset were much higher in HCV-reactive patients compared to non-reactive patients (p<0.01 for all).
There was no significant difference between the two studied groups regarding gender, consanguinity, family history, or duration of disease.