Amaç: Kronik hepatit B virus infeksiyonu morbidite ve mortalitenin önemli bir nedenidir. Tenofovir disoproksil fumarat ve entekavir, hepatit B virus infeksiyonu tedavisinde ruhsatl› ilaçlard›r. Biz, kronik hepatit B nin tenofovir ve entekavir ile

The severity of Helicobacter pylori-related diseases varies greatly among infected individuals and seems to be influenced by both host and bacterial factors. Infection with a cytotoxin-associated gene pathogenicity island (Cag PAI)-positive H. Pylori strain causes a higher grade of gastric mucosal inflammation than an infection caused by a negative strain. Furthermore, such an infection is associated with severe atrophic gastritis and gastric adenocarcinoma. NOD1 protein is a cytosolic pattern recognition receptor that responds to peptidoglycan delivered by H. Pylori cag pathogenicity island. The aim of this study is to investigate whether the presence of the NOD1 G796A polymorphism has any influence on the clinical outcomes of Cag PAI-positive H. Pylori. Both Helicobacter pylori and CagA-positive 150 patients were considered eligible for the study. In this selected group, NOD1 G796A was detected by using polymerase chain reaction/restriction fragment length polymorphism. Activity and severity of gastritis, atrophy, intestinal metaplasia and Helicobacter pylori density were assessed in body and antral biopsies. Also post-therapy controls for predicting Helicobacter pylori persistence were done. The correlations of these parameters were determined by SPSS 15 packet program for statistical analysis. Of the 150 CagA-positive patients, 57 had (38%) heterozygote (GA), and 29 had (19.3%) homozygote (AA) mutant variants of NOD1. The other 64 patients had (42.7%) wild-type DNA(GG). NOD1 796A allele carriers had higher risk for antral atrophy (OR = 13.35, 95% CI = 5.12-34.82) and antral intestinal metaplasia (OR = 2.71, 95% CI = 1.26-5.80). Carriage of the single nucleotide polymorphism of NOD1 G796A proved to be a significant risk factor for the Helicobacter pylori therapy failure (OR = 4.62, 95% CI = 1.67-12.79). Our results suggest that carriage of the NOD1 G796A mutation increases the susceptibility of gastric epithelial cells for intestinal metaplasia and atrophy when infected by CagA-positive Helicobacter pylori strains. Additionally, it increases the ratio of eradication failure.

Ulcerative colitis (UC) pathogenesis includes the altered gut microbiota, environmental factors, and human immune and genetic predisposition. Recently, its association with reduced bifidobacteria quantity in the microbiota is reported. Xyloglucan, a plant-based prebiotic oligosaccharide, causes increase in bifidobacteria quantity. In this article, we share the results of our UC cases treated by intracolonic single-dose administration of Bifidobacterium animalis subsp. lactis and xyloglucan combination. Intracolonic single-dose administration of 200 billion colony-forming units (CFUs) of B. animalis subsp. lactis and 4 g of xyloglucan combination was administrated to 10 severe UC patients, who were either unresponsive or had inadequate response to treatment. All patients continued treatment after the procedure. Treatment responses were evaluated by colonoscopic, laboratory, and clinical examination after 6 weeks. Intracolonic single-dose administration of B. animalis subsp. lactis and xyloglucan was found effective in the mucosal healing and resolution of colonic symptoms in UC patients. Intracolonic administration of B. animalis subsp. lactis and xyloglucan in UC is a new single-strain and strain-specific prebiotic combination method. It is easy to apply and has no observable side effect. Its effectiveness on mucosal healing could be attributed to the enhancement of non-stimulatory status and biodiversity in colonic mucosa. Nonetheless, it is still necessary to develop diagnostic strategies to determine the patients to whom this method would be the most applicable.

In patients with recurrent duodenal ulcers and/or apical stricture with accompanying CBD dilatation, extrahepatic cholestasis and cholangitis, EOCBD into the duodenal bulb should be considered.