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Summary. Aim. To evaluate the features of acute alimentary pancreatitis and the risk of complications in patients with a combination of PRSS1 and SPINKI1 gene mutations. Materials and methods. 70 patients with acute alimentary pancreatitis were examined. The mean age was 45.4±13.87 years. The study group included 48 (68.57 %) men and 22 (31.43 %) women. In 34 (48.57 %) patients there was a severe course of acute pancreatitis, in 25 (35.72 %) – moderate severity, in 11 (15.71 %) – mild. Complicated disease was diagnosed in 59 (84.29 %) patients, 11 (15.71 %) – uncomplicated. The severity of the course and the presence of complications were evaluated using the Atlanta Classification, 2012. The polymorphism of the PRSS1 and SPINKI1 genes was determined by all subjects. Statistica 13 was used for statistical analysis. Results and discussion. The combined effect of the PRSS1 and SPINKI1 gene mutation is associated with a higher risk of severe alimentary pancreatitis. The presence of a combined mutational status increases the chances of developing peritonitis, pleurisy, pancreatic accumulation, pseudocysts and pancreatogenic diabetes mellitus. In addition, these patients have proven significantly higher chances of formation of purulent peritonitis, phlegmon, suppuration of pseudocysts, development of systemic complications – systemic inflammatory response syndrome and multiple organ failure syndrome. Conclusions. The reliable connection between the presence of a combination of mutations of the studied genes and the development of severe course of acute alimentary pancreatitis and the formation of complications have been proved.

Purpose of the study. To evaluate changes of bands nuclear neutrophils level and their dynamics parameters during treatment in patients with acute alimentary pancreatitis based on repeated measurements and taking into account the severity of the course. Materials and methods. Seventy patients with acute alimentary pancreatitis were examined, who treated in Surgical Department of Vinnitsa Regional M. I. Pirogov Clinical Hospital. Average age was 45,4 ± 13,87 years. Severe pancreatitis was found in 34 (48,57%) people, in 25 (35,72%) – moderate, 11 (15,71%) persons had mild forms. The severity of the disease was assessed using the Atlanta classification (2012). To achieve aim of study the repeated measurements of the stabs neutrophils levels were performed for all patients. Statistical analysis was performed using STATISTICA 13. Results. The significant difference between the stabs neutrophils values identified in patients with acute alimentary pancreatitis was proved, taking into account the severity of the course, both during the primary measured (p = 0,04), during treatment (p = 0,004), and after its completion (p < 0,00001). The significant increase of stabs neutrophils level associated with increasing severity of acute pancreatitis, as in the primary treatment of patients (τ = 0,23, p = 0,005), with determination during treatment (τ = 0,31, p = 0,0001) and after its termination (τ = 0,49, p ≤ 0,00001) was determined. When comparing the indexes of stabs neutrophils determined by repeated measurements, a rapid and continuous decrease of their values was found, as a whole in the group – by 3,76 times, and in the groups with a mild course of the inflammatory process – 6,75 times, the average degree of severity – in 5,11 times and severe forms – 3,05 times. Conclusions. High informativeness of evaluation stabs neutrophils level and their dynamic during repeated measurements in patients with acute alimentary pancreatitis taking into account the severity of the course has been proved. Keywords: acute alimentary pancreatitis, stabs neutrophils level, inflammatory process, damage to the pancreas, acute pancreatitis of alimentary genesis.

Purpose of the study. To determine the rate of SPINK1 mutation status in patients with acute pancreatitis of alimentary genesis and to determine the prognostic value of allele status of the gene for the assessment of severity and the formation of complicated course. Materials and methods. 70 patients with acute alimentary pancreatitis underwent examination, 48 (68,57%) men and 22 (31,43%) women. Average age made 45,4 ± 13,87 years. Severe course of acute pancreatitis was diagnosed in 34 (48,57 %) persons, in 25 (35,72%) – moderate severity, in 11 (15,71%) – mild cases. Complicated clinical course of acute pancreatitis was recorded in 59 (84,29%) patients of the group, in the rest patients – 11 (15,71%) clinical course had uncomplicated nature. The severity of clinical course and structure of complications were assessed according to the classification of Atlanta (2012). In order to predict the severity of acute pancreatitis repeated measurements related to the level of band neutrophils, amylase and glucose were taken. Statistical analysis was performed by means of program STATISTICA (StatSoft Statisticа v.10). Outcomes. Mutation of SPINK1 gene was statistically found in most cases in patients with acute alimentary pancreatitis with heavy – 16 (47,06%) and moderate severity level – 8 (32,0%) (р = 0,02). The presence of SPINK1 mutation status is related to statistically higher chances of severe clinical course (OR=3,11, CI(1,08–8,92), р = 0,03). In patients with heterozygotic mutations of SPINK1 we have established statistically higher chances for the formation of pancreatic aggregation (OR = 4,5, CI (1,36–14,93), p = 0,01), pseudocysts (OR = 3,58, CI (1,01–12,74), p = 0,04) and pleural empyema (OR = 15,0, CI (1,56–143,83), p = 0,004).The carriers of homozygotic mutations of SPINK1 have higher risks for the development of peritonitis (OR = 12,89, CI (1,01–164,48), p = 0,04), pleurisy (OR = 12,89, CI (1,01–164,48),p = 0,04) and systemic complications (OR = 2,61, CI (2,14–13,14), p = 0,02). Conclusion. Consequently, we have established a high informative value of identification of SPINK1 mutation status in patients with acute pancreatitis of alimentary genesis regarding the prediction of severity level of inflammatory process and the formation of complicated clinical course. Keywords: acute alimentary pancreatitis, SPINK1 mutation status, SPINK1 polymorphism, pancreatitis, gene of pancreatictrypsin inhibitor.