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Intrahepatic cholangiocarcinoma (ICC), a type of bile duct cancer, has a high mortality rate. Gut microbiota, bile acid metabolism, and cytokines have not been characterized in patients with ICC, and better noninvasive diagnostic approaches for ICC are essential to be established. Accordingly, in this study, we aimed to improve our understanding of changes in gut microbiota, bile acid metabolism, and cytokines in patients with ICC. We found that the α- and β-diversities of ICC were highest and that the abundances of four genera (Lactobacillus, Actinomyces, Peptostreptococcaceae, and Alloscardovia) were increased in patients with ICC compared with those in patients with hepatocellular carcinoma or liver cirrhosis and in normal individuals. The glycoursodeoxycholic acid and tauroursodeoxycholic acid (TUDCA) plasma-stool ratios (PSRs) were obviously increased in patients with ICC. Furthermore, the genera Lactobacillus and Alloscardovia positively correlated with TUDCA-PSR were combined to discriminate ICC from the other three diseases. Vascular invasion (VI) frequently led to a poor prognosis in patients with ICC. Compared with patients with ICC without VI, patients with VI had a greater abundance of the family Ruminococcaceae, increased levels of plasma interleukin (IL)-4 and six conjugated bile acids, and decreased levels of plasma IL-6 and chenodeoxycholic acid. A positive correlation between plasma taurocholic acid and IL-4 was observed in patients with ICC. Plasma TUDCA was negatively correlated with the abundance of the genus Pseudoramibacter and the survival time of patients with ICC, but had no effect on tumor size, as determined in two murine tumor models.
In this study, we identified new biomarkers, including gut microbiota, bile acids, and inflammatory cytokines, for diagnosis of ICC and prediction of VI in patients with ICC. This article is protected by copyright. All rights reserved.
This article was published in the following journal.
Name: Hepatology (Baltimore, Md.)
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A malignant tumor arising from the intrahepatic bile duct epithelium. It is composed of ducts lined by cuboidal or columnar cells that do not contain bile, with abundant stroma. (From Holland et al., Cancer Medicine, 3d ed, p1455; Stedman, 25th ed)
Impairment of bile flow due to injury to the HEPATOCYTES; BILE CANALICULI; or the intrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC).
FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cirrhosis involves the destruction of small intra-hepatic bile ducts and bile secretion. Secondary biliary cirrhosis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.
An ATP-binding cassette, sub-family B protein (P-glycoproteins) that functions in the ATP-dependent secretion of BILE SALTS into the BILE CANALICULI of HEPATOCYTES. Mutations in the ABCB11 gene are associated with progressive familial intrahepatic cholestasis 2 (see CHOLESTASIS, INTRAHEPATIC).
A benign tumor of the intrahepatic bile ducts.
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