Cover Page

Cite item


Aim: to examine the role of immune, biochemical and hormonal factors in the regulation of melanogenesis in patients with chromatopathy. Patients and methods: we observed 226 patients with various forms dyschromia skin. Age of the patients was in the range of 16 to 55 years. The frequency of females (n =157) prevailed over the male sex (n =69) 2,3 times. The disease duration ranged from 3 weeks to 12 years. For the study of melanogenesis in vitiligo, nevi and melasma were studied parameters of the immune, endocrine and lipid peroxidation — antioxidant system. Results: melanocytes are responsible for the change in concentration a- chromatophorotropic hormone and adrenocorticotropic hormone (ACTH) decrease or increase melanogenesis. Activation process is also associated with UFOs. Comparison of the level of system components lipid peroxidation (LPO) – antioxidant system (AOS) suppressor (CD8 +) lymphocyte activity vitiligo patients showed that the most pronounced suppressive effect was observed in patients with high levels of lipid peroxidation. At the same time, patients with hyperpigmentation found a significant negative relationship with СD4+. It should be noted a negative relationship CD16+-lymphocytes with indicators pituitary- adrenal axis in patients Dyschromias (r = -0,318 vitiligo, r = -0,512, r = -0,4578 — in nevi and melasma, respectively). Conclusions: the results showed that vitiliginozny process, especially actively expressed, proceeds with the intensification of lipid peroxidation processes, changes in the state of AOS and immunity. With the increased level of hyperpigmentation CD95+-cells led to a weakening of apoptosis and cause increase in the number of melanocytes. When there is insufficient apoptosis hyperpigmentation, hypopigmentation and when — excessive apoptosis. To find mechanisms regulating skin pigmentation necessary to determine a-chromatophorotropic hormone, adrenocorticotropic hormone and neutral endopeptidase.

About the authors

R. G. Ismaylov

Azerbaijan Medical University, Baku
Urban Skin Venereal Dispensary, Baku, Republic of Azerbaijan

Author for correspondence.

кандидат медицинских наук, главный врач Городского кожного венерологического диспансера г. Баку Минздрава Азербайджанской Республики
Адрес: AZE-1005, Баку, ул. Толстого, д. 135, тел.: (99412) 594-35-34



  1. Кошевенко Ю.Н. Витилиго. Клиника, этиология, патогенез, лечение, реабилитация, профилактика. М.: Медицина. 2002. 644 c.
  2. Барабой В.А. Структура, биосинтез меланоцитов, их биологическая роль, перспективы применения. Усп. совр. биол. 2000; 117: 86–92.
  3. Mishima Y. New era of cell re-discovery led to the control of melanogenesis/melanoma: A scientific journey into terra incognita. Pigment Cell Res. 2001; 14: 47–70.
  4. Prota G. Melanins, melanogenesis and melanocytes: looking at their functional significance from the chemist’s viewpoint. Pigment Cell Res. 2000; 13: 283–293.
  5. Клиническая дерматовенерология. Т. II. Под ред. Ю.К. Скрипкина, Ю.С. Бутова. М.: ГЭОТАР-Медиа. 2009. 928 с.
  6. Kovacs S.O. Vitiligo. J. Am. Acad. Dermatol. 1998; 38 (5): 647–668.
  7. Moretti S., Spallanzani A., Amato L., Hautmann G., Gallerani I., Fabbri P. Vitiligo and epidermal microenvironment: possible involvement of keratinocyte-derived cytokines. Arch. Dermatol. 2002; 138 (2): 273–274.
  8. Rimoldi D., Muehlethaler K., Salvi S., Valmori D., Romero P., Cerottini J.C., Levy F. Subcellular localization of the melanoma-associated protein Melan-AMART1 influences the processing of its HLA-A2-restricted epitope. J. Biol. Chem. 2001; 276 (46): 43189–43196.
  9. Gleason B.C., Nascimento A.F. HMB-45 and Melan-A are useful in the differential diagnosis between granular cell tumor and malignant melanoma. Am. J. Dermatopathol. 2007; 29 (1): 22–27.
  10. Westerhof W., d’Iscia M. Vitiligo puzzle: the pieces fall in place. Pigment. Cell. Res. 2007; 20 (5): 345–359.
  11. Dell Anna M.L., Picardo M. A review and a new hypothesis for non-immunological pathogenetic mechanisms in vitiligo. Pigment. Cell. Res. 2006; 19: 406–411.
  12. Gopal K.V., Rama Rao G.R., Kumar Y.H. Vitiligo: a part of a systemic autoimmune process. Indian J. Dermatol. Venerol. Leprol. 2007; 73: 162–165.
  13. Le Poole I.C., Luiten R.M. Autoimmune etiology of generalized vitiligo. Curr. Dir. Autoimmune. 2008; 10: 227–243.
  14. Rashtak S., Pittelkow M.R. Skin involvement in systemic autoimmune diseases. Curr. Dir. Autoimmun. 2008; 10 (3): 44–58.
  15. Скрипкин Ю.К., Лезвинская Е.М. Кожа — орган иммунной системы. Вестн. дерматол. и венерол. 1989; 10: 14–18.
  16. Mari B., Checler F., Ponziio G., Peyron J.F., Manie S., Farahifar D., Rossi B., Auberger P. Jurkat T cells express a functional neutral endopeptidase activity (CALLA) involved in T cell activation. EMBO J. 1992; 11 (11): 3875–3885.
  17. Гланц С. Медико-биологическая статистика. Пер. с англ. Под ред. Н.Е. Бузикашвили, Д.В. Самойлова. М.: Практика. 1999. 200 с.
  18. Ветров Я.Я., Иванова Л.В., Крейле И.Э. Цитокины. Гематология и трансфузиология. 2000; 4: 46–49.

Copyright (c) 2015 "Paediatrician" Publishers LLC

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies