الفهرس 
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Abstract
Summary
Vitiligo is an acquired, non-contagious disease characterized by progressive patchy, multifocal depigmentation of skin, with or without depigmentation of overlying hair, and mucous membranes results from loss of melanocytes from the involved areas. Although non-contagious, the phenotype of this disorder has high impact on the psychological behavior of the affected individuals than their physical ability more often leads to social isolation.
Vitiligo is a multifactorial disorder, related to both genetic and non-genetic factors. It is generally agreed that there is an absence of functional melanocytes in vitiligo skin due to their destruction. Several hypotheses have been proposed to explain the pathophysiology of melanocytes destruction including autoimmune, genetic, self-destruction, oxidative stress and neural theories.
The metabolic syndrome (MetS) is a major and escalating public-health and clinical challenge worldwide in the wake of urbanization, surplus energy intake, increasing obesity, and sedentary life habits.
Autoimmunity and oxidative stress in patients with vitiligo can trigger certain systemic manifestations due to inflammatory and immunological pathogeneses, as well as skin involvement. It is believed that an oxidative imbalance is responsible for the development of both MetS and vitiligo. Melanin in the adipose tissue has anti-inflammatory and antioxidant effects.
A decreased number of melanocytes as well as decreased melanogenesis in the adipose tissue might reduce the anti-inflammatory effects of the melanocytes, and cause an increased production of the free oxygen radicals in vitiligo, which is responsible for MetS. In addition, other mechanisms may contribute to the development of MetS in patients with vitiligo, such as insulin resistance, lipid profile disturbances and other metabolic disorders, due to the increased inflammatory cytokines and autoimmune reactions of the melanocytes. An increased level of homocysteine, which is a tyrosinase inhibitor, may also be a contributing factor to the development of MetS in vitiligo patients. These very complicated mechanisms involving many systems may have affected the results of this study, since every system associated with MetS affected by vitiligo may not be affected at the same time. Each system might be affected differently over time.
The aim of this study was to investigate the association between metabolic syndrome and vitiligo pathogenesis and to assess its clinical significance among patients, but there was no relation between them according to the results of the study. Furthermore, the relationship between metabolic syndrome and vitiligo was not correlated. The present study included 50 patients suffering from vitiligo (group A). In addition, 30 apparently healthy individuals of matched age and sex as a control group (group B). Blood samples were taken from all participants for evaluation of blood glucose levels both fasting and two hours post prandial, serum triglycerides (TGs), serum total cholesterol (TC), high density lipoprotein cholesterol (HDL-c), serum low density lipoprotein cholesterol (LDL-c). All patients were subjected to full clinical examination and full history taking
In addition, the results proved that there was no significant statistical difference between patients and control as regard age, blood pressure, waist circumference, post-prandial blood sugar and fasting blood sugar, HDL and LDL, TG., T. Cholesterol. (p-value > 0.05).
Finally, there was no significant statistical difference between patients and control as regard metabolic syndrome. (p-value > 0.05)
In conclusion, there was no relation between mets and vitiligo according to the results of the study.