Measurement Serum Levels of Vitamin B12 in vitiligo Patients
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Keywords
Melanin, Autoimmune diseases, Vitamin B12
Abstract
Vitiligo is a skin disease caused by a disorder in the work of the immune system that attacks melanocytes causing "to kill them and the loss of melanin pigment in the skin, several theories have been proposed to understand the causes of the occurrence of the disease, including the theory of autoimmune diseases, oxidative stress, neurological and genetic factors, including those related to exposure to some chemicals and the appearance of the disease may be associated with a decrease or increase in some vitamins, including vitamin B12, the aim of this research was to learn more about this vitamin because of its important effects on the system Blood and nervous system and its complex relationship to the skin and its association with the onset of the disease by measurement level's of concentration of vitamin B12 .
Methods: The current study included 120 participants as the control group (who appeared to be in good health) and 100 participants with vitiligo. These samples were obtained between 1 October to 15 December 2022, from the Dermatological Consultation Unit of the Imam Sadiq Teaching Hospital in the Babylon Governorate. ELISA test kits were used to measure the amount of vitamin B12 concentration in the serum of all patients and the control group.
Results: Serum for vitamins B12 levels significant decrease at the probability level (P≤0.05) of patient's with vitiligo, while evaluating the same-criteria rates for the control group.
Conclusions: In the current study, it was revealed Patients with vitiligo reported reduced serum for vitamins D levels compared to control group had.
References
2. Dell'Anna, M. L. Et al. Membrane lipid alterations as a possible basis for melanocyte degeneration in vitiligo. J. Invest. Dermatol. 5, 1226–1233 (2007).
3. Jimbow, K., Chen, H., Park, J. S. & Thomas, P. D. Increased sensitivity of melanocytes to oxidative stress and abnormal expression of tyrosinase-related protein in vitiligo. Br. J. Dermatol. 1, 55–65 (2001).
4. Boissy, R. E. & Manga, P. On the etiology of contact/occupational vitiligo. Pigment Cell Res. 3, 208–214 (2004).
5. Hasse, S., Gibbons, N. C., Rokos, H., Marles, L. K. & Schallreuter, K. U. Perturbed 6-tetrahydrobiopterin recycling via decreased dihydropteridine reductase in vitiligo: more evidence for H2O2 stress. J. Invest. Dermatol. 2, 307–313 (2004).
6. Schallreuter, K. U., Elwary, S. M., Gibbons, N. C., Rokos, H. & Wood, J. M. Activation/deactivation of acetylcholinesterase by H2O2: more evidence for oxidative stress in vitiligo. Biochem. Biophys. Res. Commun. 2, 502–508 (2004).
7. Dell'Anna, M. L. Et al. Membrane lipid defects are responsible for the generation of reactive oxygen species in peripheral blood mononuclear cells from vitiligo patients. J. Cell. Physiol. 1, 187–193 (2010).
8. Le Poole, I. C., van den Wijngaard, R. M., Westerhof, W. & Das, P. K. Tenascin is overexpressed in vitiligo lesional skin and inhibits melanocyte adhesion. Br. J. Dermatol. 2, 171–178 (1997).
9. Gauthier, Y., Cario-Andrè, M., Lepreux, S., Pain, C. & Taieb, A. Melanocyte detachment after skin friction in non lesional skin of patients with generalized vitiligo. Br. J. Dermatol. 148, 95–101 (2003).
10. Rokos, H., Beazley, W. D. & Schallreuter, K. U. Oxidative stress in vitiligo: photo-oxidation of pterins produces H(2)O(2) and pterin-6-carboxylic acid. Biochem. Biophys. Res. Commun. 4, 805–811 (2002).
11. Moore, J., Wood, J. M. & Schallreuter, K. U. Evidence for specific complex formation between alpha-melanocyte stimulating hormone and 6(R)-L-erythro-5,6,7,8-tetrahydrobiopterin using near infrared Fourier transform Raman spectroscopy. Biochemistry 46, 15317–15324 (1999).
12. Schallreuter, K. U. Et al. Epidermal H(2)O(2) accumulation alters tetrahydrobiopterin (6BH4) recycling in vitiligo: identification of a general mechanism in regulation of all 6BH4-dependent processes? J. Invest. Dermatol. 1, 167–174 (2001).
13. Bellei, B. Et al. Vitiligo: a possible model of degenerative diseases. Plos ONE 3, e59782 (2013).
14. Salem, M. M. A. E. L. Et al. Enhanced DNA binding capacity on up-regulated epidermal wild-type p53 in vitiligo by H2O2-mediated oxidation: a possible repair mechanism for DNA damage. FASEB J. 23, 3790–3807 (2009).
15. Xavier, J. M., Morgado, A. L., Solá, S. & Rodrigues, C. M. Mitochondrial translocation of p53 modulates neuronal fate by preventing differentiation-induced mitochondrial stress. Antioxid. Redox Signal. 21, 1009–1024 (2014).
16. Paradisi, A. Et al. Markedly reduced incidence of melanoma and nonmelanoma skin cancer in anonconcurrent cohort of 10,040 patients with vitiligo. J. Am. Acad. Dermatol. 71, 1110–1116 (2014).
17. Teulings, H. E. Et al. Decreased risk of melanoma and nonmelanoma skin cancer in patients with vitiligo: a survey among 1307 patients and their partners. Br. J. Dermatol. 168, 162–171 (2013).
18. Dell'Anna, M. L. Et al. Alterations of mitochondria in peripheral blood mononuclear cells of vitiligo patients. Pigment Cell Res. 16, 553–559 (2003).
19. Dell'Anna, M. L. Et al. Mitochondrial impairment in peripheral blood mononuclear cells during the active phase of vitiligo. J. Invest. Dermatol. 117, 908–913 (2001).
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