The priority areas of current research in pancreatology are to study the mechanisms of functioning loss of pancreatic tissue and its replacement by connective tissue. In damage of acinar pancreatic cells defined role belongs to the complex process of cell-cell interactions that are activated under the influence of immune and non-immune factors. So, in the development of fibrous changes of pancreas at chronic pancreatitis as a consequence of dynamic actions as cytokines, chemokines, growth factors and other factors are there damages of balance between processes of synthesis and degradation of cellular proteins extra matrix of accumulation and degradation. It was studied of TGF-β1, IL-6, IL-10, IL-18, IL-8 in patients with complicated pancreatic pseudocyst. TGF-β1 was significantly increased in all groups of patients with pseudocyst in average by 584,4%, 476,5% and 363,5% compared with the control group (р0,05). The level of IL-18 was higher in the first group of patients on the average of 86% in the second group it was to 24,1% and in the third one it was 27,2% compared to control (р0,05). A similar trend is noted also for IL-6 and IL-8 against the backdrop of increase of IL-10, respectively on the average of 30,2 times (I type pancreatic pseudocyst), 30,9 times (II type of pancreatic pseudocyst) and 23,6 times while type III pseudocyst contained (р0,05). The possible increase in the level of IL-10 is a compensatory attempt to reduce sick body produce inflammatory cytokines, which continues lasting. However, levels of inflammatory cytokines in patients with the third type of pseudocyst (21,5%) were lower than in patients with the first type of pancreatic pseudocyst to 27,1% than in patients with the second type of pancreatic pseudocyst. Correlation analysis showed that among patients and state levels of TGF-1, IL-6, 8, 10 and 18 in serum there were positive connections, and for all levels of performance Spearman correlation coefficient there were respectively 0,69; 0,68; 0,57; 0,73 and 0,82 (р <0,001). Performance analysis of the ratio of IL-18 / IL-10 (control was 81,3, and the first type of pseudocysts was 5,0, the second type of pancreatic pseudocysts was 3,26; the third type of pancreatic pseudocysts contained 4,4) revealed its significant reduction (in an average of 93,8%, 96% and 94,6%, p<0,05) in all patients, despite the fact that the average level of proinflammatory cytokines they had a much higher performance appropriate control group. The data indicate a leading role of TGF-β1 in the development of intra- and perіlobulаris fibrosis regardless of the trigger mechanism of pancreatitis and its complications. It was established that the determination of circulating TGF-β1 may reflect different stages of the course and severity of pancreatitis complications that develop in different terms from the moment the disease. IL-10, a powerful TGF-β1, controls the regeneration phase, reduces fibrosis and atrophy and IL-18 stimulates apoptosis. Thus, our findings support the hypothesis that activation of proinflammatory cytokine IL-18 and anti-inflammatory cytokine IL-10 can form a link between the risk factors for complications in patients with different types of pancreatic pseudocyst.
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