Gastroenterology and Hepatology From Bed to Bench Journal
Volume:8 Issue: 2, Spring 2015

Gastric cancer is the third most common cause of cancer-related death in the world. It is now wellestablished that Helicobacter pylori infection predispose individuals toward gastric adenocarcinoma later in life. It has since been classified as a class I carcinogen by the World Health Organization. Research suggests that the oncogenic effects of Helicobacter pylori can occur through a variety of mechanisms, including the indirect inflammatory effects of Helicobacter pylori on the gastric mucosa and the direct epigenetic effects of Helicobacter pylori on individual cells. Whilst infected with Helicobacter pylori, a combination of environmental and host-dependent factors determines the likelihood of developing gastric cancer. Controversy remains regarding the effects of eradication of Helicobacter pylori on the prevention of further progression of gastric lesions and the possibility for regression of atrophic gastritis. The aim of this review is to synthesis different elements that contribute to the step-wise progression of normal gastric mucosa to gastric adenocarcinoma. This review helps clinicians to better identify those infected individuals who are at high risk of developing gastric cancer and implement the necessary investigations and treatment.

Gastric adenocarcinoma is one of the most common malignancies worldwide. Many ethological causes have been introduced among which helicobacter pylori, as a gram-negative bacterium has been considered as an important pathological facilitating factor. This agent is also associated with different digestive diseases, such as gastritis, peptic ulcer, and mucosa-associated lymphoid tissue lymphoma. Recently, scientists have been described some molecular aspects that show the role of some apoptotic genes and proteins; for example: P53, Bcl, C-Myc and Rb-suppressor systems in the H. pylori pathogenesis. Also the relationship between nitric oxide (NOSi genotype) with H. pylori infection has been shown. The aim of this mini-review is to explain better these genetically aspects of H.pylori pathogenesis.

The objective of this study was to evaluate the time trend of Helicobacter pylori (H. pylori) prevalence and presence of intestinal Metaplasia over the period of seven years among gastritis Iranian patients. H. pylori is the major causal factor in chronic gastritis. Its acquisition leads to a chronic, usually lifelong, inflammation of the gastric mucosa, which may gradually progress to atrophy with intestinal metaplasia in a significant proportion of infected individuals. Patients and H. pylori and intestinal Metaplasia data among 14,860 consecutive gastritis patients, who referred to the gastrointestinal department of Tehran’s Taleghani Hospital in Iran from 2008 to 2014, was examined by sex and age group. The patients were divided into six age groups (16-30, 30-40, 40-50, 50-60 and >70). The chi-square test was used to compare the qualitative variables. The overall prevalence rate among patient with H. pylori infection was 83.5% 12406/14860) and 11,394 (84.1%) of them were related to the gastritis. The prevalence rate of H. pylori among patient with severe gastritis was significantly higher (P<0.05) compared to mild and moderate gastritis. In addition, the prevalence of H. pylori decreased with age and has been declined in recent years. The presence of intestinal metaplasia increased with age (P<0.05). The results of this study showed that the prevalence of H. pylori infection in Iranian population has been declined in recent years; nevertheless it seems to be highly prevalent in Iran. We also find a significant positive relationship between H. pylori infection and gastritis. There is no association between sex and infection, however in contrast with the most studies its prevalence decreased with age.

The current investigation aimed to evaluate ruminant raw milk as a reservoir source of Helicobacter pylori and analyze the diversity of cagA and vacA genotypes as H. pylori virulence factors to find any relationship between these genotypes in human and animal H. pylori strains. The way of transmission of Helicobacter pylori as one of the most controversial bacteria in the world, which colonizes the human gastric tissue and is responsible for several gastric diseases is still unknown. The possibility of zoonotic transmission of H. pylori is feasible, but is not proven in ruminant reservoirs. Overall 210 cows, sheep, goats, camels and buffalos’ raw milk samples and 100 human gastric biopsies were collected in this survey. We applied PCR assays to identify H. pylori, vacA and cagA genes. Statistical tests were applied for data analysis. Totally 12(16%) cow, 8(13.79%) sheep, 2 (4.76%) goat, 2(13.33%), buffalo 4 20%) and 82 (82%) of human specimens were confirmed to be H. pylori positive. Among which s1a/m2 genotype was more frequent in isolated H. pylori strains and statistically significant between strains. Based on statistical analyses the 1b allele of sheep had a significant association with human strains. The current survey was prompted by our previous report. According to both results we can conclude that sheep may act as a reservoir for H. pylori and transmit this bacterium to human via its milk. Extended assessments in other geographical regions and other animals are recommended.

Our aim was to determine the EPIYA-cagA Phosphorylation sites and dupA gene in H. pylori isolates among patients with upper gastrointestinal diseases. Pathogenicity of the cagA-positive Helicobacter pylori is associated with EPIYA motifs and higher number of EPIYA-C segments is a risk factor of gastric cancer, while duodenal ulcer promoting gene (dupA) is determined as a protective factor against gastric cancer. Patients and A total of 280 non-repeated gastric biopsies obtained from patients undergoing endoscopy from January 2013 till July 2013. Samples were cultured on selective horse blood agar and incubated in microaerophilic atmosphere. The isolated organisms were identified as H. pylori by Gram staining and positive oxidase, catalase, and urease tests. Various motif types of cagA and the prevalence of dupA were determined by PCR method. Out of 280 specimens, 128 (54.7%) isolated organisms were identified as H. pylori. Of 120 H. pylori isolates, 35.9% were dupA positive and 56.26% were cagA positive, while cagA with ABC and ABCC motifs were 55.5% and 44.5%, respectively. Fifty six percent of the isolates with the ABCC motif have had dupA genes. We also found a significant association between strains with genotypes of dupA-ABC and duodenal ulcer disease (p = 0.007). The results of this study showed that the prevalence of cagA-positive H. pylori in Shiraz was as high as in western countries and higher numbers of EPIYA-C segments were seen in gastric cancer patients. We may also use dupA as a prognostic and pathogenic marker for duodenal ulcer disease and cagA with the segment C for gastric cancer and gastric ulcer disease in this region.

The purpose of this investigation was to determine the oipA and dupA genes of Helicobacter pylori isolates from west of Iran; Chaharmahalo Bakhtiyari region and find their relationship with the severity of the gastroduodenal diseases. Helicobacter pylori is an organism responsible for many gastroduodenal diseases. Many studies suggest that genetic diversity in H. pylori virulence factors such as oipA and dupA genes is high among isolates of different geographic regions and may cause more severe diseases. Patients and In this cross-sectional study, gastric biopsy specimens were taken from 150 patients suffering from gastroduodenal diseases. The presence of ureC, dupA and oipA genes was tested by polymerase chain reaction (PCR). Overall, 123 (82%) H. pylori strains were isolated from 150 specimens. dupA gene was detected in 41 (33.33%) H.pylori-positive specimens. There was a reverse correlation between this gene and gastric cancer. The oipA gene was found in 88 (71.54%) samples and statistically there was no association between this gene and gastric disorders. As statistical analyses revealed, the presence of the dupA was more common in isolates with the oipA negative. Based on our findings, the presence of dupA gene can be considered as a marker for the onset of severe diseases. However, the oipA gene cannot be regarded for prediction of gastroenterology diseases. Meanwhile, extended molecular epidemiology researches in other populations are recommended.

The aim of this study was to evaluate the Helicobacter pylori eradication in the group receiving standard -dose twice a day for two weeks and continue taking amoxicillin for 4 weeks. Helicobacter pylori is the major etiological cause of chronic gastritis, gastric and duodenal ulcers, gastric cancer and lymphoma. Therefore, patients should be treated after diagnosis of H. pylori infection. Patients and A total of 66 consecutive patients with rapid urease test during endoscopy or biopsy positive for H. pylori were enrolled in this clinical trial study during 2013-2014. Patients were divided randomly into two groups. Group A (standard dose) received omeprazole (20 mg), amoxicillin (1 g), and clarithromycin (500 mg), all two times a day for two weeks. Group B received standard dose like group A and in patients with H.pylori infection amoxicillin were continued for 4 weeks. After completion of treatment, patients did not receive any treatment for a month and then stool antigen was performed to evaluate the H.pylori. The rate of successful HP eradication was significantly higher in group A (90.9% V.s 63.6%; p=0.017). Inflation and bitter mouth were found in 8 and 13 patients in group A and 7 and 9 patients in group B, respectively. The incidence of adverse effects was the same (p=0.437). Increased duration of antibiotic therapy to four weeks significantly raises the rate of successful HP eradication with standard triple therapy without significant increase in adverse effects.