Síndrome de supercrescimento bacteriano do intestino delgado associada à síndrome metabólica e à doença hepática gordurosa não alcoólica

Abstract

Non-alcoholic fatty liver disease (NAFLD) has multifactorial etiopathogenesis, and in most cases is associated with metabolic syndrome (MS). The intestinal microbiota has potential involvement in both metabolic disorders and NAFLD. The aim of this study was to evaluate the intestinal microbiota in NAFLD patients with different metabolic profiles. Thirty-six patients with biopsy-proven nonalcoholic steatohepatitis (NASH) were evaluated. Subjects were divided into two groups according to their metabolic profile. We selected 16 patients with MS, 13 female, with mean age of 49.5 years. In the group without MS, there were 20 patients, 15 male, with mean age of 47.5 years. Their characteristics in relation to liver disease and intestinal microbiota were analyzed. The groups were similar in the laboratory and histological evaluation of liver disease. For microbiota evaluation, a breathing test for small intestinal bacterial overgrowth (SIBO) and in situ fluorescence hybridization (FISH) fecal microbiota analysis were performed. Breathing test was positive in 43.8% of patients with MS and 50% of those without MS. There was a high frequency of SIBO in both groups, with no significant difference between them. The fecal microbiota analysis showed significant difference in order Verrucomicrobiales. Its average concentration was 0.84 x 108 cells g-1 in the group without MS and 1.44 x 108 cells g-1 in those with MS (p 0.01). Verrucomicrobiales quantification also inversely correlated with serum ferritin and hepatocyte ballooning, markers of inflammation associated with NASH. This order of bacteria, through its representative in the human microbiota, Akkermansia muciniphila, is associated with intestinal mucosa protection and better metabolic profile. Given these findings, it is suggested that the lower concentration of Verrucomicrobiales is associated with higher inflammatory activity in patients with NAFLD without MS, in which the etiopathogenesis of the disease does not have its classic metabolic substrate.