title: [Regulation of melanogenesis in the dyschromia of skin].
abstract: OBJECTIVE
  To examine the role of immune, biochemical and hormonal factors in the regulation of melanogenesis in patients with chromatopathy.
  
  
  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 CD4+. 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.
authors: R G
authors: RG
authors: Ismaĭlov
mesh_terms: D000293:Adolescent; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000975:Antioxidants / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007378:Interleukins / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D008544:Melanocytes / Q000502:physiology*; D008875:Middle Aged; D009506:Nevus / Q000378:metabolism; D010859:Pigmentation Disorders / Q000378:metabolism* / Q000473:pathology*; D012878:Skin Neoplasms / Q000378:metabolism; D014820:Vitiligo / Q000378:metabolism / Q000473:pathology; D055815:Young Adult; D019014:fas Receptor / Q000378:metabolism
chemical_list: D000975:Antioxidants; C491901:FAS protein, human; D007378:Interleukins; D019014:fas Receptor; D000324:Adrenocorticotropic Hormone