Background Non-alcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome. Within the spectrum of NAFLD, non-alcoholic steatohepatitis (NASH) in combination with hepatic inflammation and fibrosis can lead to liver cirrhosis and hepatocellular carcinoma. Dysbiosis was reported to contribute to NASH pathogenesis. This study aimed to determine the effects of fructo-oligosaccharides (FOS) on steatohepatitis and visceral adiposity in an obese mouse model of NASH. Methods Twelve newborn C57BL/6 J male mice were subcutaneously injected with monosodium glutamate (MSG) to induce obesity on a conventional diet. Six mice were also administered 5% FOS via drinking water from 10 weeks of age. At 18 weeks, histological characteristics of the liver and epididymal fat were compared between the groups. Hepatic mRNA expression of lipid metabolism enzymes and SCFA in feces and sera were measured. Results Hepatic steatosis, inflammatory cell infiltration, and hepatocyte ballooning in the liver and increased hepatic mRNA expression of fatty acid synthase and glycerol-3-phosphate acyltransferase were observed in the MSG-treated mice. FOS treatment improved the liver pathology and blunted the increases in the mRNA expression levels of lipid metabolism enzymes. In addition, FOS inhibited adipocyte enlargement and formation of crown-like structures and reduced the M1 macrophage frequency in the epididymal fat of the MSG mice (39.4% ± 3.0% vs. 22.8% ± 0.7%; P = 0.001). FOS increased not only the fecal concentrations of n-butyric acid (0.04 ± 0.01 vs. 0.38 ± 0.14 mg/g, P = 0.02), propionic acid (0.09 ± 0.03 vs. 0.42 ± 0.16 mg/g, P = 0.02), and acetic acid (0.65 ± 0.16 vs. 1.48 ± 0.29 mg/g, P = 0.03) but also the serum concentration of propionic acid (3.9 ± 0.5 vs. 8.2 ± 0.5 μmol/L, P = 0.001). Conclusions FOS ameliorates steatohepatitis, visceral adiposity, and chronic inflammation by increasing SCFA production.

A 44-year-old Japanese woman was admitted to our hospital with fatigue and an altered liver function. She had been receiving atorvastatin treatment for 10 months. Although no jaundice was seen, the patient's serum alkaline phosphatase and γ-glutamyl transpeptidase levels were markedly elevated. Based on the results of a drug-induced lymphocyte-stimulation test, her liver disease was diagnosed as atorvastatin-induced hepatic injury. Subsequently, anti-mitochondrial antibodies (AMAs) were detected in her serum; however, a liver biopsy specimen did not show the characteristic features of primary biliary cholangitis. We herein report the detection of AMAs accompanied by drug-induced hepatic injury caused by atorvastatin.

Background: The recent improvement of peroral cholangioscopy (POCS) maneuverability has enabled the precise, targeted biopsy of bile duct lesions under direct cholangioscopic vision. However, as only small-cup biopsy forceps can pass through the scope channel, the resulting small sample size may limit the pathological diagnosis of biopsy specimens. This study compared the diagnostic abilities of POCS-guided biopsy and conventional fluoroscopy-guided biopsy for bile duct cancer. Method: This multicenter, retrospective cohort study included patients exhibiting bile duct stricture with suspected cholangiocarcinoma in whom POCS-guided and fluoroscopy-guided biopsies were performed in the same session. The primary endpoint was the diagnostic sensitivity for malignancy. The size and quality of the biopsy specimens were also compared. Result: A total of 59 patients were enrolled. The sensitivity of POCS-guided biopsy was similar to that of fluoroscopy-guided biopsy (54.0% and 64.0%, respectively). However, when the modalities were combined, the sensitivity increased to 80.0%. The mean specimen size from POCS-guided biopsy was significantly smaller than that from fluoroscopy-guided biopsy. The specimen quality using fluoroscopy-guided biopsy was also better than that using POCS-guided biopsy. Conclusions: The diagnostic sensitivity of POCS-guided biopsy is still insufficient, mainly because of the limited specimen quantity and quality. Therefore, conventional fluoroscopy-guided biopsy would be helpful to improve diagnostic sensitivity.

An 86-year-old woman from Japan was admitted to our hospital with jaundice. Endoscopic ultrasonography (EUS) revealed a highechoic wall thickening and mass lesion with an irregular or papillary surface in the gallbladder. Moreover, mobile hyperechoic lesions were observed in the gallbladder and common bile duct. Contrast-enhanced EUS showed inhomogeneous hyperenhancement patterns within the gallbladder wall thickening and mass lesion without any invasion out of the gallbladder wall (Figure 1). The opening of the papilla of Vater and outflow of mucus from the papilla were endoscopically confirmed. Endoscopic retrograde cholangiography showed filling defects within the dilated common bile duct, with slight movement and changes in shape. Peroral cholangioscopy (POCS) showed the mucinous material continued to flow out of the cystic duct and no obvious tumor in cystic and common bile duct (Figure 2). Based on these findings, intracholecystic papillary neoplasm (ICPN) localized in the gallbladder and jaundice due to mucinous production was diagnosed, and laparoscopic cholecystectomy was performed without extended surgical resection.