The Role of Identification of Spink1 Gene Mutation Status in Patients With Acute Pancreatitis of Alimentary Genesis for the Predicting the Severity of Clinical Course and Formation of Complications

Abstract

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.