Abstract
50 patients with chronic pancreatitis (CP) aged from 45 to 63 including 23 patients with CP and normal body index (1st group), 27 patients with CP and obesity of the 1st degree (2nd group) were examined in the research. The diagnosis of CP exacerbation was made on the basis of anamnesis, clinical and ultrasonography findings with biochemical substantiation of hyper-fermentation syndrome. The diagnosis of obesity was made on the basis of the body mass index increasing (BMI) more than 30 kg/m2. A comparative analysis of the morphological structure of the pancreatic tissue received during autopsy of patients with CP on the background of obesity and normal body mass, died due to various reasons including complications of metabolic syndrome, has been made. In obese patients pancreas morphologically characterized by replacement of the pancreas acinar epithelial by fibrous tissue and a significant increase the number of adipocytes, which is the basis of exocrine pancreatic insufficiency. Patients with chronic pancreatitis and obesity presented considerable metabolic changes of the extracellular matrix components assuming a reliable increase of the intensity of collagen synthesis, glycoproteins content, molecular hyper-production of cellular adhesion and acute phase proteins, increased catabolism of fucoglycoproteins against a reliable decrease of seromucoids and ceruloplasmin content with antioxidant properties in the blood. Increase of proteolytic blood activity and inhibition of collagenolysis processes due to the decrease of matrix metalloproteinase-1 activity, increase of inhibitory effect power of the tissue and plasma inhibitors of proteolysis and collagenolysis were found in patients with CP on the background of obesity.
Highlights
Patients with chronic pancreatitis and obesity presented considerable metabolic changes of the extracellular matrix components assuming a reliable increase of the intensity of collagen synthesis, glycoproteins content, molecular hyper-production of cellular adhesion and acute phase proteins, increased catabolism of fucoglycoproteins against a reliable decrease of seromucoids and ceruloplasmin content with antioxidant properties in the blood
Progressing of chronic pancreatitis (CP) of any etiology is based on proteinase-inhibitory imbalance followed by diffuse fibrosis of the pancreas caused by the activation of the connective tissue system due to the destruction of the acinar epithelium, polymorphocellular infiltration of the pancreatic tissue with immune-competent cells under the influence of an increasing expression and activation of cellular adhesion factors, hyperproduction of pro-inflammatory cytokines, growth factors of anabolic action, acidosis, hypoxia etc. [1, 2, 4, 5]
At the preliminary stage of our studies [6] involving a comparative analysis of the morphological structure of the pancreas obtained during autopsy of patients with chronic pancreatitis against obesity and normal body weight died due to different causes including complications of metabolic syndrome, we have proved that in patients with obesity chronic pancreatitis from morphological point of view is characterized by statistically more valuable progressing fibrous reconstruction of the organ
Summary
Patients with chronic pancreatitis and obesity presented considerable metabolic changes of the extracellular matrix components assuming a reliable increase of the intensity of collagen synthesis, glycoproteins content, molecular hyper-production of cellular adhesion and acute phase proteins, increased catabolism of fucoglycoproteins against a reliable decrease of seromucoids and ceruloplasmin content with antioxidant properties in the blood. The intensity of proteolytic processes is controlled by a number of tissue and plasma proteinase inhibitors (α2macroglobulin (α2-МG), α1-inhibitor of proteinase (α1-ІP), antithrombin III, tissue inhibitor of matrix metalloproteinase-1 (ТІМP-1) etc.) [3, 6, 8]. Imbalance of this system can result in prevailing of the processes of protein catabolism performing structural (cellular membrane components) and transport functions, which is a powerful damaging factor [8, 9]. Objective of the study: to find the availability of interrelations between the condition of functioning of the proteinase-inhibitor system and connective tissue in the mechanisms of progressing of the chronic pancreatitis in patients with obesity
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