Immunobiochemical characteristics of ulcerative skin lesions

Abstract

The article presents immuno-biochemical aspects of the pathogenesis of ulcerative skin lesions. 44 patients with UC aged 23 to 64 years were examined. All patients underwent clinical, immunological, biochemical, microbiological and statistical studies. The results of the study showed the failure of the cytokine status in the direction of hyperproduction of pro- (TNF-alpha, IL-6) and hypoproduction of antiinflammatory cytokines (IL-4, IL-10), an increase in the level of procalcitonin by 2.9 times against the background of increased contamination of opportunistic flora staphylococcus spp. in the lesions. The pathogenesis of trophic ulcers (TU), regardless of their origin, is based on similar mechanisms caused by disorders of microcirculation, cellular activity, extracellular matrix synthesis (EMS), release of growth factors and neovascularization [1,4,7-11,13]. At the same time, the leading factor in the development of ulcerative lesions is the deterioration of the microcirculatory system (MCS) caused by venous hypertension, which determines the earliest symptoms of chronic venous insufficiency (CVI), including macro and microcirculatory disorders in the venous bed, biophysical, biochemical and immunological processes, as well as impaired lymphatic drainage, affecting the course of reparative processes in the tissues of the legs. [2,3, 5]. However, the presence of immune shifts and the presence of a constant factor that causes and supports inflammation leads to the formation of a continuous cascade of perivascular cellular reactions with a pathological transformation of the substances released during this process [8,9]. In this aspect, it is important to evaluate the immunobiochemical processes in the mechanism of development of trophic ulcers.