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      Plasma diamine oxidase level predicts 6-month readmission for patients with hepatitis B virus-related decompensated cirrhosis

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          Abstract

          Background and aims

          Hepatitis B virus-related decompensated cirrhosis is difficult to cure but has a high readmission rate due to multiple complications. Our aim was to investigate the diagnostic potential value of plasma diamine oxidase (DAO) for 6-month readmission of patients with HBV-related decompensated cirrhosis.

          Methods

          A total of 135 patients with HBV-related decompensated cirrhosis were prospectively collected at the onset of discharge of hospital, and then were followed up for at least 6 months with the readmission as the primary outcome. The plasma DAO level was measured using enzyme linked immunosorbent assay. In addition, 120 age and sex matched patients with HBV-related compensated cirrhosis were included as controls.

          Results

          A total of 36 patients (36.7%) with decompensated cirrhosis admitted to hospital during the 6-month follow up. The plasma DAO level of readmission group [21.1 (14.5; 29.0) ng/ml] was significantly higher than that in the non-readmission group [12.7 (9.3; 18.0) ng/mL, P < 0.001]. Multivariate analysis showed that the plasma DAO level (HR = 1.102, P < 0.05) and hepatic encephalopathy (HE) (HR = 5.018, P < 0.05) were independent factors for 6-month readmission of decompensated cirrhosis. DAO level showed higher area under the curve of receiver operating characteristic (AUROC) than HE (0.769 vs. 0.598, P < 0.05) and Child-Pugh-Turcotte (CPT) score (0.769 vs. 0.652, P < 0.05) for predicting 6-month readmission rate, with the best cut-off value as 19.7 ng/mL. Furthermore, plasma DAO level (HR = 1.184, P < 0.05) was an independent factor and has the higher AUROC than CPT score for the onset of recurrent HE (0.905 vs. 0.738, P < 0.05) during the 6-month follow up.

          Conclusions

          Plasma DAO level > 19.7 ng/mL predicts high rate of 6-month readmission in patients with HBV-related decompensated cirrhosis.

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          Most cited references32

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          Enteric dysbiosis associated with a mouse model of alcoholic liver disease.

          The translocation of bacteria and bacterial products into the circulation contributes to alcoholic liver disease. Intestinal bacterial overgrowth is common in patients with alcoholic liver disease. The aims of our study were to investigate bacterial translocation, changes in the enteric microbiome, and its regulation by mucosal antimicrobial proteins in alcoholic liver disease. We used a mouse model of continuous intragastric feeding of alcohol or an isocaloric diet. Bacterial translocation occurred prior to changes observed in the microbiome. Quantitative changes in the intestinal microflora of these animals were assessed first using conventional culture techniques in the small and large intestine. Although we found no difference after 1 day or 1 week, intestinal bacterial overgrowth was observed in the gastrointestinal tract of mice fed alcohol for 3 weeks compared with control mice fed an isocaloric liquid diet. Because <20% of all gastrointestinal bacteria can be cultured using conventional methodologies, we performed massively parallel pyrosequencing to further assess the qualitative changes in the intestinal microbiome following alcohol exposure. Sequencing of 16S ribosomal RNA genes revealed a relative abundance of Bacteroidetes and Verrucomicrobia bacteria in mice fed alcohol compared with a relative predominance of Firmicutes bacteria in control mice. With respect to the host's transcriptome, alcohol feeding was associated with down-regulation in gene and protein expression of bactericidal c-type lectins Reg3b and Reg3g in the small intestine. Treatment with prebiotics partially restored Reg3g protein levels, reduced bacterial overgrowth, and lessened alcoholic steatohepatitis. Alcohol feeding is associated with intestinal bacterial overgrowth and enteric dysbiosis. Intestinal antimicrobial molecules are dysregulated following chronic alcohol feeding contributing to changes in the enteric microbiome and to alcoholic steatohepatitis. Copyright © 2010 American Association for the Study of Liver Diseases.
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            Role of innate immunity and the microbiota in liver fibrosis: crosstalk between the liver and gut.

            Liver fibrosis occurs as a wound-healing scar response following chronic liver inflammation including alcoholic liver disease, non-alcoholic steatohepatitis, viral hepatitis, cholestatic liver disease and autoimmune liver diseases. The liver has a unique vascular system within the gastrointestinal tract, as the majority of the liver's blood supply comes from the intestine through the portal vein. When the intestinal barrier function is disrupted, an increase in intestinal permeability leads to the translocation of intestine-derived bacterial products such as lipopolysaccharide (LPS) and unmethylated CpG containing DNA to the liver via the portal vein. These gut-derived bacterial products stimulate innate immune receptors, namely Toll-like receptors (TLRs), in the liver. TLRs are expressed on Kupffer cells, endothelial cells, dendritic cells, biliary epithelial cells, hepatic stellate cells, and hepatocytes. TLRs activate these cells to contribute to acute and chronic liver diseases. This review summarizes recent studies investigating the role of TLRs, intestinal microbiota and bacterial translocation in liver fibrosis, alcoholic liver disease and non-alcoholic steatohepatitis.
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              Gut--liver axis: the impact of gut microbiota on non alcoholic fatty liver disease.

              To examine the impact of gut microbiota on non alcoholic fatty liver disease (NAFLD) pathogenesis. Emerging evidence suggests a strong interaction between gut microbiota and liver. Receiving approximately 70% of its blood supply from the intestine, the liver represents the first line of defence against gut-derived antigens. Intestinal bacteria play a key role in the maintenance of gut-liver axis health. Disturbances in the homeostasis between bacteria- and host-derived signals at the epithelial level lead to a break in intestinal barrier function and may foster "bacterial translocation", defined as the migration of bacteria or bacterial products from the intestinal lumen to mesenteric lymph nodes or other extraintestinal organs and sites. While the full repertoire of gut-derived microbial products that reach the liver in health and disease has yet to be explored, the levels of bacterial lipopolysaccharide, a component of the outer membrane of Gram-negative bacteria, are increased in the portal and/or systemic circulation in several types of chronic liver diseases. Derangement of the gut flora, particularly small intestinal bacterial overgrowth, occurs in a large percentage (20-75%) of patients with chronic liver disease. In addition, evidence implicating the gut-liver axis in the pathogenesis of metabolic liver disorders has accumulated over the past ten years. Complex metabolic diseases are the product of multiple perturbations under the influence of triggering factors such as gut microbiota and diet, thus, modulation of the gut microbiota may represent a new way to treat or prevent NAFLD. Copyright © 2012 Elsevier B.V. All rights reserved.
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                Author and article information

                Contributors
                wangdoc876@126.com
                Journal
                Virol J
                Virol. J
                Virology Journal
                BioMed Central (London )
                1743-422X
                18 September 2019
                18 September 2019
                2019
                : 16
                : 115
                Affiliations
                [1 ]GRID grid.452402.5, Department of Hepatology, , Qilu Hospital of Shandong University, ; Wenhuaxi Road 107#, Jinan, 250012 China
                [2 ]ISNI 0000 0004 1761 1174, GRID grid.27255.37, Institute of Hepatology, , Shandong University, ; Wenhuaxi Road 107#, Jinan, 250012 China
                [3 ]GRID grid.452402.5, Department of Nuclear Medicine, , Qilu Hospital of Shandong University, ; Wenhuaxi Road 107#, Jinan, 250012 China
                Author information
                http://orcid.org/0000-0002-6297-0147
                Article
                1219
                10.1186/s12985-019-1219-4
                6751599
                31533748
                ca658e52-4f26-4083-9431-f7ec6887ee64
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 22 June 2019
                : 5 September 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100002855, Ministry of Science and Technology of the People's Republic of China;
                Award ID: 2017ZX10202202
                Award ID: 2018ZX10302206
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2019

                Microbiology & Virology
                decompensated liver cirrhosis,hepatitis b virus,intestinal microecology,diamine oxidase,readmission

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