A New Biomarker in Patients with Vitiligo: A Case-Control Study

The word vitiligo is possibly derived from “Vitellius” meaning white leather patches. [1] This disease is acquired lack of pigmentation following the absence of epidermal melanocytes [1]. The destruction of melanocytes is the result of depigmented macules clinically seen in this disease. Although its cause is unknown, several theories have been presented such as autoimmunity, autocytotoxicity, oxidative stress and neurohormonal complications [2-4], the most common of which is autoimmunity with a genetic background [3]. Vitiligo often begins in childhood or young adulthood [2]. Almost half of the affected individual sure initially afflicted before the age of 20 and its prevalence decreases with age. Its global prevalence has been estimated to be 1-2% [2,4]. It equally affects men and women and there is no association between skin type and vitiligo [3]. Vitiligo presents in the form of hypo pigmented macules or white patches with varying degrees of depigmentation. Vililigo is classified based on the extent of involvement and the distribution of depigmentation [2]. The most common manifestation of vitiligo is the generalized type in the form of bilateral symmetrical depigmentations on the face, neck, extensor surfaces or bony surfaces on the hands, feet, wrists, axilla and mucosal surfaces [1,3]. The acrofacial type occurs on the fingers and periorificial areas with circular patterns. The focal type presents as focal depigmented macules without any dermatological pattern. The segmental types has asymmetrical dermatological pattern accompanied by autoimmune diseases. In the universal type, hypopigmentation is seen in all body surfaces [2,4]. In most patients, the depigmentation begins in areas exposed to sunlight [2]. Volume 3 Issue 6 2016