[The prevalence of autoimmune endocrine diseases in vitiligo patients].

Vitiligo is a common polygenic autoimmune disease in which the foci of depigmentation are formed on the skin and/or mucous membranes as a result of the death of melanocytes. There are several hypotheses for the pathogenesis of the disease, the leading role among them is played the autoimmune hypothesis. This review summarizes the available literature data on the prevalence and structure of comorbid endocrine autoimmune pathology in vitiligo patients. In most studies conducted in Europe, America and Asia the prevalence of autoimmune thyroid diseases (including autoimmune thyroiditis and Graves disease), diabetes mellitus and autoimmune adrenal insufficiency was higher in vitiligo patients than in the general population. The results of some studies indicate a frequent association of vitiligo with autoimmune polyglandular syndromes. In the structure of comorbid pathology the highest prevalence was in autoimmune thyroid diseases. A number of studies have established a higher prevalence of autoimmune endocrine diseases in women, as well as in nonsegmental vitiligo patients and in cases of family history of vitiligo and/or other autoimmune diseases. In addition, it was shown that the prevalence of endocrine diseases increases with increasing area of depigmentation. The data obtained justify the advisability of conducting a timely examination of vitiligo patients with the aim of early detection of comorbid diseases and the appointment of appropriate treatment. Further studies are needed to investigate the effect of the identified associations on the course of vitiligo and comorbid endocrinopathies, as well as the effectiveness of therapy and the quality of life of patients.

[The intensification of lipid peroxidation in the skin for the suppression of experimental dermatitis]. / Usilenie perekisnogo okisleniia lipidov v kozhe dlia podavleniia éksperimental'nogo dermatita.

Guinea pig experiments making use of spectrofluorometry have revealed reduced level of Schiff's bases in skin biopsy specimens obtained from foci of allergic contact dermatitis induced by 2,4-dinitrochlorobenzene (DNCB). Iron sulfate electrophoresis resulted in a decrease of the sensitization and of the allergic contact dermatitis intensity, as well as in enhancement of lipid peroxidation in the skin. These data permit a supposition that reduction of lipid peroxidation is one of the pathogenetic mechanisms of delayed type hypersensitivity, and that lipid peroxidation enhancement in the skin by iron sulfate electrophoresis is one of the possible mechanisms of suppressing allergic contact dermatitis.