الفهرس 
VitiligoOnly 14 pages are availabe for public view
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Abstract
Vitiligo is an acquired depigmenting cutaneous disorder characterized by the loss of melanocytes from the epidermis. It affects approximately 0.5% of the population worldwide. The characteristic lesion is a totally amelanotic, non scaly, chalky-white macule with distinct margins. The mechanism by which melanocytes are lost is not fully understood. There are three major hypotheses for the pathogenesis of vitiligo. The first and most acceptable hypothesis considers vitiligo as an autoimmune disease. The second is the neural hypothesis which suggests that accumulation of a neurochemical substance decreases melanin production. Finally, the biochemical hypothesis implies auto-destruction of melanocytes as a result of cytotoxic by-products of melanin synthesis
Vitamin B12 is a water-soluble vitamin that is naturally present in some in foods and available as a dietary supplement and a prescription medication. Because vitamin B12 contains the mineral cobalt, compounds with vitamin B12 activity are collectively called “cobalamins”. Methylcobalamin and 5-deoxyadenosylcobalamin are the metabolically active forms of vitamin B12. Vitamin B12 is required for the development, myelination, and function of the central nervous system; healthy red blood cell formation; and DNA synthesis.
Vitamin B12 status is typically assessed by measurements of serum or plasma vitamin B12 levels. The cutoff between normal vitamin B12 levels and deficiency varies by method and laboratory, but most laboratories define subnormal serum or plasma values as those lower than 200 or 250 pg/mL.
Causes of vitamin B12 deficiency include difficulty absorbing vitamin B12 from food, lack of intrinsic factor (e.g., because of pernicious anemia), surgery in the gastrointestinal tract, prolonged use of certain medications (e.g., metformin or proton pump inhibitor), and dietary deficiency.
Cutaneous manifestations associated with vitamin B12 deficiency are skin hyperpigmentation, vitiligo, angular stomatitis, and hair changes. It is believed that patients with vitiligo are more likely to have pernicious anemia and vitamin B12 deficiency. Vitamin B12 are major determinants of homocysteine (Hcy) levels, and a nutritional deficiency in it cause hyperhomocysteinemia. Hcy also leads to inhibition of tyrosinase enzyme by binding with copper at its active site, resulting in reversible hypopigmentation.
This study included 40 patients with vitiligo and 40 age and sex matched healthy controls. The serum vitamin B12 was measured in cases and controls with ELISA and it was correlated to disease activity, severity and disease duration.
We found that serum level of vit B12 was decreased in cases in comparison to control, and there is inverse relation between vitamin B12 deficiency, VASI score, VIDA score and disease duration.
So, this study confirms that vitamin B 12 is a very efficient and simple biomarker for vitiligo cases. We recommended the estimation of serum vitamin B12 among the work up of vitiligo patients and we think that supplements might be of great value for vitiligo patients.