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Table Of Contents
Introduction
Vitiligo represents a chronic, non-infectious dermatological condition belonging to the group of dyschromias. Clinically it manifests as sharply demarcated, porcelain-white achromic macules and patches distributed on cutaneous surfaces and mucosae. Lesions develop secondary to destruction or marked dysfunction of epidermal melanocytes—specialised neuroectodermal cells governing melanin biosynthesis and melanogenesis transfer. Although the disorder does not endanger somatic survival, it frequently provokes profound psycho-emotional distress owing to conspicuous cosmetic disfigurement.
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1. Etiology of the disease
Vitiligo represents a chronic, acquired dermatologic condition categorized within the group of dyschromias, manifesting through achromic, milky-white macules and patches distributed on cutaneous surfaces and mucosal epithelium. Such lesions develop as a consequence of selective melanocyte destruction or functional arrest, processes linked to autoimmune-mediated apoptosis of pigment-producing cells synthesizing melanin. Although the disorder is medically benign and non-contagious, the conspicuous pigmentary defect precipitates substantial psychosocial morbidity and diminished quality of life. Epidemiological surveys indicate a global prevalence ranging from 1% to 3% of the population; initial lesions typically emerge during adolescence or early adulthood, between 10 and 30 years, though onset may occur at any stage.
Although the etiopathogenesis of vitiligo has not been definitively elucidated, contemporary dermatological research characterizes the disorder as polyetiologic. Its development reflects synergistic interplay among polygenic inheritance, autoimmune dysregulation, oxidative stress, and diverse external environmental triggers.
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2. Oxidative stress in the pathogenesis of vitiligo and methods of its correction
Oxidative stress denotes a pathological condition of tissues marked by surplus oxygen-centered radicals—collectively termed reactive oxygen species (ROS) such as superoxide anion, hydrogen peroxide, hydroxyl radical, and singlet oxygen—whose extreme chemical reactivity provokes oxidation and subsequent structural modification of proteins, carbohydrates, lipids, and nucleic acids. ROS are key redox regulatory intermediates in numerous intracellular metabolic cascades. Under physiological circumstances, rates of ROS generation and detoxification remain equilibrated by antioxidant defense systems, thereby shielding cellular macromolecules from oxidative injury while permitting redox-dependent signaling. These molecules modulate cell activity via Ca2+ homeostasis, induction of protein phosphorylation, phospholipid hydrolysis, and triggering of transcription factors. They also contribute to synthesis of bioactive mediators and orchestrate innate and adaptive immune reactions. Principal sources of cellular ROS involve leakage of electrons from mitochondrial and microsomal electron-transport chains as well as altered activity of flavin- or nicotinamide-dependent dehydrogenases. Excess unpaired-electron compounds inflict extensive lesions on genomic DNA, precipitating apoptosis or necrosis. The dominant, clinically relevant manifestation of radical-induced cytotoxicity is uncontrolled lipid peroxidation.
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