Aim: to review the common risk factors and links in the pathogenesis of functional gastrointestinal disorders (FGID) to optimize therapy of patients with a combination of multiple FGID.Key points. FGID occurs in more than 40 % of people globally, mainly affecting the working-age population in young and middle-aged subjects. At the same time, more than 30 % of patients have a combination of 2 or more functional gastrointestinal (GI) disorders i.e. overlap syndrome. Common links in the pathogenesis of FGID include disorders of gut-brain interaction, visceral hypersensitivity, changes in intestinal microbiota, overproduction of proinflammatory cytokines, impaired epithelial permeability and motor activity of the gastrointestinal tract. The combination of FGID in various gastrointestinal segments is associated with more pronounced clinical symptoms (mutual burden syndrome). Common risk factors and pathogenetic links of the functional disorders enables reducing the number of prescribed medications when several FGIDs overlap in one patient, which also increases adherence to therapy. Treatment of FGID includes adjustment of risk factors and drug therapy. As a pathogenetically justified pharmacotherapy of overlap syndrome, Kolofort, highly diluted antibodies to TNF-α, histamine and brain-specific protein S-100, is of interest.Conclusion. Kolofort has demonstrated high efficacy and safety including among patients with overlap FGID enabling to consider it as the treatment of choice in these patients.

Cholesterol pseudopolyps are the most common variant of gallbladder polyps (GP). Their development is pathogenetically connected with the components of metabolic syndrome, especially with dislipoproteinemia and nonalcoholic fatty liver disease (NAFLD). Lipid metabolism disorder in the form of increased levels of total cholesterol, low-density lipoproteins (LDL), decreased high-density lipoproteins (HDL), as well as steatosis and liver inflammation lead to disorders of enterohepatic circulation (EHC) of bile acids, changes in rheological properties of bile, which, eventually, can lead to uptake of excess bile cholesterol by epithelium of GP in form of micelles. Infiltration of microvilli with bile micelles causes activation of tissue macrophages and triggers subclinical microinflammation of GB wall. When neighboring microvilli, crowded with foamy cells, merge, cholesterol pseudopolyp is formed, which represents a focal form of GB cholesterosis. The main drug that influences the recovery of EHC and physicochemical properties of bile is ursodeoxycholic acid (UDCA). There is also evidence that UDCA can improve parameters of lipid metabolism, liver enzymes, reduce the severity of hepatic steatosis. The use of UDCA in patients with polyposis form of GB cholesterosis has demonstrated positive results against cholesterol polyps. Glycyrrhizic acid (GA), which has anti-inflammatory, antioxidant, antifibrotic, and other beneficial properties, can improve the effectiveness of therapy for GB polyps by acting on the subclinical microinflammation component of the GB wall. In a prospective observational study, the use of fixed combination of UDCA with GA in patients with cholesterol polyps of GB and NAFLD for 3 months resulted in reduction of polyp number and size in more than 50% of patients, which was accompanied by significant improvement of lipid spectrum and liver enzymes parameters. Further studies of UDCA+GA combination in the combination of these pathologies are required.