Total of metaplastic cases), characterized by structures similar to the pyloric glands in the lamina propria. Intestinal type, which characterized by the presence of goblet cells and enterocitlike cells, was detected in only 16 (4 cases) of all the metaplastic patients. No difference was found in the distribution of the two metaplastic types between the two groups (p = 0.602). Regarding iNOS and ROS expression, the immunoreactive scores were both significantly higher in H. pylori-positive gallbladder mucosa compared to H. pylori-negative mucosa (p = 0.012 and 0.000, respectively) (Figure 6 and 7). However, in our study, there were only 3 of the NT 157 manufacturer slides showed positive H. Licochalcone A site pylori staining and enhanced iNOS or ROS expressions occurring simultaneously in the same area.DiscussionThe presence of H.pylori in gallbladder mucosa was first confirmed by Kawaguchi et al in 1996. [18] However, although H.pylori has been found 3.5 16574785 times more frequently in presence of chronic cholecystitis, whether this agent contributes in the pathogenesis of this biliary disease is still poorly understood. [19] Firstly, it is difficult to verify the potential entry routes of H.pylori to the gallbladder including either ascending duodenum infection or the portal system circulation pathway. [20,21] Secondly, since successful demonstration of H.pylori in gallbladder was mostly based on the indirect detection methods such as PCR for H.pylorispecific components rather than direct bacterial culture, some investigators believe that H.pylori is only a “stagger” but not an “invader” in biliary system. [22,23]. 1315463 Consistent with one previous report from Turkey [24] in our study, H.pylori was isolated in 20.55 (67/259) of the patients using culture, staining of gallbladder mucosa and PCR for specific 16s rRNA gene. Among the above three techniques, nest PCR still showed the highest sensitivity. We found that H.pylori in the stomach was strongly associated with the infection of this bacterium in gallbladder mucosa. Our data also showed a significant correlation between chronic cholecystitis and a few H.pylori-related diseases such as chronic gastritis, gastric ulcer and duodenal ulcer. Considering that H. pylori-16s rRNA in gallbladder and gastric-duodenal mucosa from the same individual patient had completely identical sequences, we hypothesize that H.pylori in the gastrointestinal system might be a potential candidate for increasing the risk of chronic inflammation of the gallbladder. H. pylori might reach the biliary system via sphincter of Oddi by the reflux mechanism. Bacteria colonized in the stomach and small intestine in patients with sphincterotomy and biliary enteric anastomoses, recurrent cholangitis and sphincter of Oddidysfunction might be the cause of secondary gallstones and cholecystitis. [25,26]. The presenting study revealed that H.pylori-infected gallbladder mucosa has a significantly higher prevalence of adenomyomatosis (GAM) than non-infected mucosa (52.24 versus 35.52 , p = 0.012). GAM is a benign, degenerative condition characterized by proliferation of the mucosal epithelium and hypertrophy of the muscularis mucosae accompanying with grossly formed mucosal invagination and intramural Rokitansky-Aschoff sinuses. [27] GAM can be diagnosed preoperatively through ultrasound, CT scan or MRI. [28,29] Incidence rate of GAM is reported to be 25.8 ?2 in chronic cholecystitis patients based on the cholecystectomy specimens. [30,31] Some investigators strongl.Total of metaplastic cases), characterized by structures similar to the pyloric glands in the lamina propria. Intestinal type, which characterized by the presence of goblet cells and enterocitlike cells, was detected in only 16 (4 cases) of all the metaplastic patients. No difference was found in the distribution of the two metaplastic types between the two groups (p = 0.602). Regarding iNOS and ROS expression, the immunoreactive scores were both significantly higher in H. pylori-positive gallbladder mucosa compared to H. pylori-negative mucosa (p = 0.012 and 0.000, respectively) (Figure 6 and 7). However, in our study, there were only 3 of the slides showed positive H. pylori staining and enhanced iNOS or ROS expressions occurring simultaneously in the same area.DiscussionThe presence of H.pylori in gallbladder mucosa was first confirmed by Kawaguchi et al in 1996. [18] However, although H.pylori has been found 3.5 16574785 times more frequently in presence of chronic cholecystitis, whether this agent contributes in the pathogenesis of this biliary disease is still poorly understood. [19] Firstly, it is difficult to verify the potential entry routes of H.pylori to the gallbladder including either ascending duodenum infection or the portal system circulation pathway. [20,21] Secondly, since successful demonstration of H.pylori in gallbladder was mostly based on the indirect detection methods such as PCR for H.pylorispecific components rather than direct bacterial culture, some investigators believe that H.pylori is only a “stagger” but not an “invader” in biliary system. [22,23]. 1315463 Consistent with one previous report from Turkey [24] in our study, H.pylori was isolated in 20.55 (67/259) of the patients using culture, staining of gallbladder mucosa and PCR for specific 16s rRNA gene. Among the above three techniques, nest PCR still showed the highest sensitivity. We found that H.pylori in the stomach was strongly associated with the infection of this bacterium in gallbladder mucosa. Our data also showed a significant correlation between chronic cholecystitis and a few H.pylori-related diseases such as chronic gastritis, gastric ulcer and duodenal ulcer. Considering that H. pylori-16s rRNA in gallbladder and gastric-duodenal mucosa from the same individual patient had completely identical sequences, we hypothesize that H.pylori in the gastrointestinal system might be a potential candidate for increasing the risk of chronic inflammation of the gallbladder. H. pylori might reach the biliary system via sphincter of Oddi by the reflux mechanism. Bacteria colonized in the stomach and small intestine in patients with sphincterotomy and biliary enteric anastomoses, recurrent cholangitis and sphincter of Oddidysfunction might be the cause of secondary gallstones and cholecystitis. [25,26]. The presenting study revealed that H.pylori-infected gallbladder mucosa has a significantly higher prevalence of adenomyomatosis (GAM) than non-infected mucosa (52.24 versus 35.52 , p = 0.012). GAM is a benign, degenerative condition characterized by proliferation of the mucosal epithelium and hypertrophy of the muscularis mucosae accompanying with grossly formed mucosal invagination and intramural Rokitansky-Aschoff sinuses. [27] GAM can be diagnosed preoperatively through ultrasound, CT scan or MRI. [28,29] Incidence rate of GAM is reported to be 25.8 ?2 in chronic cholecystitis patients based on the cholecystectomy specimens. [30,31] Some investigators strongl.
