BORTO is a safe and effective treatment for gastric varices.

The endoscopic finding of YWN could be observed at any site of the gastric mucosa in H. pylori-associated gastritis, and represented histological lymphoid follicles.

Although PCR-based in situ hybridization (PCR-ISH) can be used to determine the distribution and localization of pathogens in tissues, this approach is hampered by its low specificity. Therefore, we used a highly specific and sensitive PCR-ISH method to reveal the lobular distribution and intracellular localization of hepatitis B virus (HBV) and HCV in chronic liver disease and to clarify the state of persistent HBV and HCV infection in the liver. HBV genomic DNA was detected in almost all hepatocytes, whereas HBV RNA or protein was differentially distributed only in a subset of the HBV DNA-positive region. Further, HCV genomic RNA was detected in almost all hepatocytes and was localized to the cytoplasm. HCV RNA was also detected in the epithelium of the large bile duct but not in endothelial cells, portal tracts, or sinusoidal lymphocytes. In patients with HBV and HCV coinfection, HCV RNA was localized to the noncancerous tissue, whereas HBV DNA was found only in the cancerous tissue. Using this novel PCR-ISH method, we could visualize the staining pattern of HBV and HCV in liver sections, and we obtained results consistent with those of real-time detection (RTD)-PCR analysis. In conclusion, almost all hepatocytes are infected with HBV or HCV in chronic liver disease; this finding implies that the viruses spreads throughout the liver in the chronic stage.Hepatitis B virus (HBV) and hepatitis C virus (HCV) are the primary causative agents of chronic liver disease (2, 9, 17). HBV infection remains a global health problem; it is estimated that 350 million individuals are persistently infected with the virus and that approximately 15% to 25% of these individuals will die due to the sequelae of the infection (23, 29). Further, more than 170 million people are infected with HCV worldwide (21). HCV has a single-stranded RNA genome (8, 19), does not have canonical oncogenes, and can easily establish chronic infection without integration into the host genome (3,20), resulting in hepatic steatosis and hepatocellular carcinoma (HCC) (28). The viruses share a similar route of transmission, such as via the transfusion of infected blood or body fluids or use of contaminated needles.Several studies have shown that 10% to 35% of the individuals infected with HBV also have HCV infection, although the prevalence varies depending on the population studied (4, 32, 34). The relationship between coinfection and acceleration of malignant transformation remains unclear, but HBV and HCV coinfection seems to alter the natural history of both HBVrelated and HCV-related liver disease (2, 12). HCV has been shown to inhibit HBV gene expression (7, 15). The high prevalence of occult HBV infection may indicate that HCV also inhibits HBV replication (34). Most epidemiological studies of HBV have been performed by using diagnostic serological assays (16). We recently used a novel, highly sensitive diagnostic PCR method to demonstrate that the HBV genome is detectable in the sera of a substantial proportion of patients with chronic HCV infectio...

Background:We evaluated the endoscopic microvascular architecture of the gastric mucosa in portal hypertension patients using the prototype of narrow band imaging (NBI). Material and Methods: The study included 103 Helicobacter pylori-negative patients with chronic liver disease (22 without portal hypertension (group 1), 81 with portal hypertension (group 2)). Results: (i) Abnormality of collecting venules, reddening mucosa, red spots, a mosaic-like pattern, and gastric antral vascular ectasia (GAVE) were observed on the gastric mucosa, and an obscure change in collecting venules (73% vs 14%; P < 0.001), reddening mucosa (49% vs 5%; P < 0.001), red spots (36% vs 5%; P < 0.01) and a mosaic-like pattern (40% vs 5%; P < 0.01) were more frequently observed in group 2 than in group 1. (ii) On magnifying endoscopy with NBI, the mucosa with an obscure change in collecting venules was demonstrated as dilation of the capillaries surrounding the gastric pits in various degrees, and reddening mucosa was observed as extended and swollen gastric pits and various degrees of dilated and convoluted capillaries surrounding the gastric pits. Red spots were demonstrated as extended and swollen gastric pits, dilated and convoluted capillaries surrounding the gastric pits, and intramucosal hemorrhage around these capillaries. GAVE was recognized as partial and marked dilatation of the capillaries surrounding the gastric pits. Conclusion: Abnormality of collecting venules, swelling of gastric pits, dilatation of capillaries surrounding the gastric pits, intramucosal hemorrhage around capillaries, and partial and marked dilatation of the capillaries were observed on the gastric mucosa in portal hypertension patients.