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Related to vitiligo: Ceroid


condition that causes irregular patches of skin to lose pigment and turn white. The exact cause is unknown, but it occurs when the immune system attacks and destroys melanocytes, the cells that make pigment; the skin does not become raised or painful. Commonly affected areas are the face, elbows and knees, hands and feet, and genitals. Vitiligo can appear at any age and may worsen over time; it is more noticeable in individuals with darker skin. Treatments include ultraviolet light therapy, topical corticosteroid or immunosuppressive creams or gels, skin grafts from normally pigmented areas, opaque foundation makeup and skin dyes to camouflage the affected area, and the depigmenting of the remaining normal skin in extensive cases. Although affected areas sunburn easily and may be associated with certain skin cancers, research has found that a common gene mutation may increase both the chance of vitiligo and lower the risk of melanoma, the most serious form of skin cancer.



a pigmentation disorder manifested by the disappearance of normal pigment from patches of skin. The cause is unknown. It usually starts in youth (more often in females) with the appearance of white spots of different sizes and shapes on unchanged skin. The spots gradually enlarge and coalesce, forming extensive milky-white patches. The hairs on the affected areas turn gray. Foci of vitiligo may occur anywhere on the skin. The affected individuals experience no internal sensations. Treatment consists in using drugs that increase the sensitivity of skin to ultraviolet rays and then exposing the skin to these rays.


A skin disease characterized by an acquired ochromia in areas of various sizes and shapes.
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Investigation on the integrity of phase II detoxification pathway in the epidermis of vitiligo patients showed that the transcript levels of Nrf2 as well as the downstream detoxification genes NQO-1, GCLC, and GCLM are upregulated in the lesional epidermis compared with the matched nonlesional skin [42].
In summary, imbalance between oxidative and antioxidative processes and excess reactive oxygen species in the active vitiligo skin are thought to be pathogenic events in vitiligo.
Our study aimed to investigate the presence of dry eye in vitiligo patients with objective
While type 3 groups comprises with autoimmune thyroid disease, myasthenia gravis, thymoma, Sjogren's syndrome, pernicious anemia, idiopathic thrombocytopenic purpura (ITP), Addison's disease, diabetes, vitiligo, autoimmune hemolytic anemia, systemic lupus erythematosus (SLE) and dermatitis herpetiformis.
A genetic component to vitiligo has long been suspected, due to the fact that incidence is higher among family members of affected individuals than in the general population.
Koga classified vitiligo into two clinical types: vitiligo non segmentalis (type A) and vitiligo segmentalis (type B).
VanStockum continues to write books, articles, and frequently speaks at vitiligo conferences.
Enrichment in pathway showed that differentially expressed proteins for both the vitiligo stages were involved in complement cascade, clotting cascade, sequestering of ions, and reverse cholesterol transport.
The study included 11 patients with vitiligo affecting at least 1% of body surface area.
There are a few pathogenic theories on vitiligo, all of them drawing on genetic factors and several changes in the immune activity:
To analyse patient compliance to narrow band ultraviolet B (NBUVB) phototherapy in patients of vitiligo, and to evaluate factors affecting the compliance.