Abstract

Background. Emerging evidence suggests a strong interaction between the gut, gut microbiota and liver. Derangement of gut flora, particularly small intestinal bacterial overgrowth (SIBO), occurs in a large percentage of patients with non-alcoholic fatty liver disease (NAFLD) and plays an important role in its pathogenesis. Aim. Study of the frequency of SIBO in various forms of non-alcoholic fatty liver disease, as well as the possibilities of its pathomorphosis as a result of eradication of SIBO as a result of the use of rifaximin or multicomponent probiotic. Material and methods. There were investigated 125 patients with non-alcoholic fatty liver disease (70 men, 55 women aged 18 to 65 years, mean age 37±6.7 years) developed at obesity or type 2 diabetes mellitus, including 85 patients with liver steatosis (group1) and 40 patients with non-alcoholic steatohepatitis (group 2). Patients with concomitant SIBO (70 patients) was treated with rifaximin or multicomponent probiotic. As the main endpoints of the study, the frequency of achieving eradication of SIBO was evaluated (estimated from the results of a repeated H2-lactulose hydrogen test after treatment), as well as a decrease in the severity of liver steatosis by steatometry and a decrease / normalization of transaminase levels 3 months after the start of the treatment. Secondary endpoints included the change in BMI and the HOMA-IR index 3 months after the start of the treatment. Results. SIBO in patients with non-alcoholic fatty liver disease was significantly more frequent than in control (p <0.005), and in patients with non-alcoholic steatohepatitis – significantly more often than in patients with liver steatosis (80 % vs 47.1 %, P <0.01). Eradication of SIBO after use of rifaximin was recorded in 30 of 36 patients with non-alcoholic fatty liver disease (83.3 %), including 16 of 20 patients with steatosis (80 %) and 14 of 16 (87.5 %) patients with non-alcoholic steatohepatitis. In the group of patients taking multicomponent probiotics after treatment, eradication of SIBO was noted in 12 of 36 patients (33.3 %), including 7 patients with steatosis (35 %) and 5 patients (31.3 %) with non-alcoholic steatohepatitis Conclusion. The investigation shows that the eradication of small intestinal bacterial overgrowth has the positive influence on the natural course of NAFLD and use of rifaximine should be discussed as a perspective therapeutic strategy at this pathology

Highlights

  • Non-alcoholic fatty liver disease is probably the most common chronic diffuse liver disease in the world

  • That non-alcoholic fatty liver disease develops on average in 95 % of obese patients, and non-alcoholic steatohepatitis develops in 20% of patients with steatosis [1].If the simple hepatic steatosis usually has a favorable prognosis, non-alcoholic steatohepatitis tends to progress to fibrosis, cirrhosis, hepatocellular carcinoma and liver failure that requires a liver transplantation [2]

  • The use of rifamixin accompanied by the decrease of the liver steatosis (р=0,065) and body mass index, leading to the reliable decrease of ALT level in patients with non-alcoholic steatohepatitis(р

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Summary

Introduction

Non-alcoholic fatty liver disease is probably the most common chronic diffuse liver disease in the world. Non-alcoholic fatty liver disease includes the wide spectrum of pathological changes in the liver, from the simple steatosis to steatosis with an inflammation (non-alcoholic steatohepatitis), fibrosis and cirrhosis. In 1998 a classical “double hit” hypothesis was proposed that explains the pathogenesis of non-alcoholic fatty liver disease and its progression to non-alcoholic steatohepatitis. In this model the first “hit” is represented by the deposition of fats in the liver which is promoted by insulin resistance, whereas for the second “hit” is necessary the development of an inflammatory process supported by the cytokines system with secretion of high amounts of tumor necrosis factor-alpha (TNF-α) [3]. New experimental and clinical findings made it possible to propose a model of “multiple hits” that determine the occurrence of non-alcoholic steatohepatitis which is obviously a result of the combined effect of genetic, social, behavioral factors and environmental ones [4]

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