Aim: to present a rare clinical case of multiple post-traumatic intra-abdominal splenosis in combination with type 2 macroamylasemia, chronic pancreatitis in a 27-year-old woman, clinically manifested like a palpable mass in the right iliac region.Main results. In the first part of the article, a detailed analysis of the medical history is given, the results of archival imaging studies and the data of laboratory and instrumental examination at the time of treatment are presented. The literature review presents modern definitions of splenosis, as well as brief information about the anatomy and physiology of the spleen.Conclusion. The diagnostic process requires a detailed analysis of the history of the disease, the performance of laboratory studies in combination with modern imaging studies, as well as a thorough study of the literature data.

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic fatty pancreatic disease (NAFPD) develop against the background of metabolic syndrome, systemic insulin resistance, oxidative stress, changes in lipid and carbohydrate metabolism. There are a number of similarities between NAFLD and NAFPD: the natural course of diseases proceeds from steatosis through inflammation to fibrosis and cancer, one of the etiopathogenetic factors is the disbalance of bile acids synthesis and low expression of farnesoid receptor X (FXR). One of the possible methods of treatment NAFLD and NAFPD is a correction of the biosynthesis of bile acids and increase FXR expression with FXR agonists. Ursodeoxycholic acid (UDCA) is a selective FXR agonist. It has a multipled spectrum of actions: anticholestatic, anti-apoptic, antioxidant, cytoprotective, antifibrotic, hypocholesterolemic, immunomodulatory, hepatoprotective. The ability of UDCA correct lipid and carbohydrate metabolism in combination with anti-inflammatory and antiapoptic effects may be of great importance for the treatment of NAFLD and NAFPD. The article reviews the results of clinical and experimental studies describing the efficacy of UDCA in NAFLD and some pancreatic diseases. It has been suggested that the therapy of UDCA can reduce the severity of NAFLD and NAFPDand improve the functional activity of hepatocytes and β cells. The need for randomized clinical trials was emphasized in order to make an informed decision on the expediency of including UDCA in the treatment of NAFLD and NAFPD.

Physiological features of amylase synthesis and excretion are considered in the article, presence of other sources of amylase synthesis different from pancreas and salivary glands is emphasized. Definitions of hyperenzymemia and macroamylasemia (MAE) are given. MAE is a state characterized by presence of circulating complexes of normal serum amylase with protein or carbohydrates in blood. There are 3 types of MAE: first — classical (constant hyperamylasemia, decreased amylase level in urine, high blood concentration of macroamylase complexes); second — hyperamylasemia with slightly decreased amylase activity in urine, macroamylase/normal amylase ratio is less than in the first type; third — normal blood and urine amylase activity, low macroamylase/normal amylase ratio. Pathogenesis is explained by connection of blood amylase and acute phase protein in different inflammatory, infectious diseases, malabsorption. MAE clinical manifestations could be absent, sometimes abdominal pain is possible. Hyperamylasemia and reduced urine amylase activity are typical. MAE diagnostics means determination of macroamylase complexes in blood (chromatography, calculation of the clearance ratio of amylase and creatinine). The article presents clinical cases describing extra-pancreatic MAE in women with malignant ovarian lesions. The question of expediency of thorough diagnostic examination in asymptomatic MAE is raised, which may turn out to be a symptom of cancer. The lack of specific treatment for MAE is emphasized.

After the discovery of the method of ursodeoxycholic acid’s (UDCA) synthesis and the publication of evidence confirming its ability to reduce the lithogenic properties of bile, active clinical use of UDCA began in the world. This drug, which has pleiotropic effect (choleretic, cytoprotective, immunomodulatory, antiapoptic, litholytic, hypocholesterolemic), has proven its effectiveness in the treatment various diseases: primary biliary cholangitis, intrahepatic cholestasis of pregnancy, gallstone disease. Being a tertiary bile acid, UDCA stimulates bile acid synthesis by reducing the circulating fibroblast growth factor 19 and inhibiting the activation of the farnesoid X-receptor (FXR), which leads to the induction of cholesterol-7α-hydroxylase, a key enzyme in the synthesis of bile acid de novo, mediating the conversion of cholesterol into bile acids. Changes in the formation of bile acids and cholesterol while taking UDCA intake is accompanied by activation of the main enzyme of cholesterol synthesis - 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR). Under the influence of UDCA the activity of stearoyl-Coa desaturase (SCD) in visceral white adipose tissue increases. According to studies conducted in 2019, UDCA improves lipid metabolism by regulating the activity of the ACT/mTOR signaling pathway, reduces the synthesis of cholesterol, decreases the fractional synthesis rate of cholesterol and the fractional synthesis rate of triglycerides. It has been proved that UDCA is accompanied by a decrease in the level of total cholesterol and low density lipoprotein cholesterol.

After the discovery of the method of synthesis of ursodeoxycholic acid (UDCA) and the publication of evidence confirming its ability to reduce the lithogenic properties of bile, active clinical use of UDCA began around the world. This drug, in addition to the proven choleretic, cytoprotective, litholytic, anti-apoptotic effects, has a signaling activity that allows UDCA to influence metabolic syndrome components such as hyperglycemia, hypercholesterolemia. Under the influence of UDCA, FXR is activated in the liver, which leads to an increase in the activity of glycogen synthase and decrease in the level of glycaemia. Another mechanism by which UDCA affects glycaemia is mediated by the activation of the TGR5 membrane receptor under the influence of this bile acid, as well as the release of insulin from pancreatic β-cells and decrease in postprandial glycaemia. When taking UDCA, the concentration of glycosylated hemoglobin, insulin in the blood plasma decreases the effects of insulin resistance decrease. UDCA has a beneficial effect on the vascular wall, reducing the severity of atherosclerotic lesions and normalizing the average thickness of the intima-media complex. UDCA improves lipid metabolism by regulating the activity of the AKT/ mTOR-signaling pathway, reduces the synthesis of cholesterol, and decreases the fractional rate of cholesterol synthesis and the fractional rate of triglyceride synthesis. It is proved that UDCA administration is accompanied by a drop in the level of total cholesterol and cholesterol of low-density lipoproteins. Normalization of the metabolism of glucose, triglycerides, cholesterol and the insulin-signaling pathway under the influence of bile acids is the basis for the use of UDCA for the correction of metabolic syndrome, as well as its hepatological manifestations - NAFLD.