The article presents a detailed literature review on the role of intestinal dysbiosis, including bacterial overgrowth syndrome, as well as increasing intestinal permeability in the pathogenesis of the main pancreatic diseases: acute and chronic pancreatitis (AP and CP), autoimmune pancreatitis, pancreatic cancer. Thus, according to the results of meta-analysis, populations of Enterobacteriaceae and Enterococcus were larger in all patients with AP as compared with healthy. There was no difference between the groups with severe and mild AP. Number of Bifidobacterium was lower in all patients with AP as compared with healthy. In severe AP, level of endotoxin and cytokines in blood was higher than in mild AP and in healthy. Participation of Helicobacter pylori in pathogenesis of autoimmune pancreatitis via molecular mimicry is assumed. In addition, Helicobacter pylori may have significance in development of pancreatic adenocarcinoma. In CP, rate of syndrome of bacterial overgrowth has been studied in numerous studies, since dysbiosis halts the effect of enzyme preparations, causes worsening of clinical manifestations. According to the results of meta-analysis, patients with CP are characterized by quantitative and qualitative changes in the composition of intestinal microbiome: decrease of Bifidobacterium and Lactobacillus, and increase of Enterobacteriaceae. The authors also preseented their own data. Recent data suggest a connection between the oral microbiota, tongue plaque and pancreatic adenocarcinoma. Pancreatic cancer is characterized by decrease of Neisseria elongate, Streptococcus mitis, and increase of Porphyromonas gingivalis and Granulicatella adiacens. Recent reports have found that oral microbiota may be important in increasing the risk of pancreatic cancer. The conclusion is drawn on the prospects of studying the intestinal microbiota in pancreatic diseases and the need for its participation in the pathogenesis of this disease.
The article presents data on classification, pathogenesis, clinical picture, diagnosis and differentiated treatment tactics, as well as practical algorithm for recognizing and preventing the development of drug-induced liver injury. Pathogenesis of drug-induced liver injury is analyzed, mechanisms of drug metabolism are explained, metabolism phases are described. Four main mechanisms of the pathological effect of drugs on the liver are identified: direct toxic effect on hepatocytes; toxic effect of drug metabolites; immunoallergic liver injury; idiosyncrasy. Peculiar attention is paid to the pathogenesis of drug-induced cholestasis. Direct hepatotoxic reactions develop according to the cytolytic (hepatocellular, parenchymal), cholestatic or mixed option. The most commonly diagnosed clinical variant of drug-induced liver injury is drug-induced hepatitis. Five forms of hepatitis induced by the use of pharmacological agents are distinguished: drug-induced hepatitis with an isolated increase in transaminases (anti-TB drugs, methyldopa, amiodarone, statins); acute hepatitis with jaundice; pseudo-surgical form of acute hepatitis: abdominal pain, fever, jaundice, enlarged gall bladder (cytostatics, antidepressants, antiarrhythmic drugs); severe forms of acute hepatitis with liver failure; chronic drug hepatitis. International diagnostic criteria, basic data on morphological liver changes are presented. Action of ursodeoxycholic acid is explained. It has a litholytic, anticholestatic, cytoprotective, immunomodulating, anti-inflammatory, antitoxic, hypocholesterolemic effect, modulates apoptosis, has a differentiated effect on the regeneration of hepatocytes.
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