Helicobacter pylori infection among offspring of patients with stomach cancer

BACKGROUND & AIMS: A positive family history is associated with an increased risk of stomach cancer. We compared the prevalence of Helicobacter pylori infection, a known risk factor for stomach cancer, between subjects with and without parental history of stomach cancer to evaluate a potential role of H. pylori infection in familial aggregation of stomach cancer. METHODS: A total of 1351 men and women aged 30-74 years who participated in the German Health and Nutrition Survey conducted in the western part of Germany in 1987-1988 were included in the study. Detailed information on sociodemographic factors, nutritional factors, and parental history of cancer was obtained by standardized interviews. Serum samples were analyzed for immunoglobulin G antibodies against H. pylori by enzyme-linked immunosorbent assay. RESULTS: The prevalence of H. pylori infection was much higher (69%) among subjects with a parental history of stomach cancer than among other subjects (44%). This association persisted after control for potential confounders by multiple logistic regression (adjusted odds ratio, 2.7; 95% confidence interval, 1.3-5.9), and was particularly strong among subjects below age 55 (adjusted odds ratio, 5.1; 95% confidence interval, 1.6-16.1). CONCLUSIONS: These results suggest that familial aggregation of stomach cancer may be explained at least partly by familial clustering of H. pylori infection.     

Helicobacter pylori of remnant stomach and optimal dose of amoxicillin for eradicating Helicobacter pylori

BACKGROUND/AIMS: The optimal dose of antibiotics for Helicobacter pylori eradication is not known. The aim of this study was to evaluate optimal dose of antibiotics (amoxicillin) for eradication of H. pylori in the remnant stomach. METHODOLOGY: Biopsy specimens were obtained from 77 patients who underwent gastrectomy for gastric cancer. H. pylori was subsequently diagnosed by rapid urease test and culture. Gastritis was assessed by scoring. Patients with positive H. pylori were eligible for the eradication study. Amoxicillin 750 mg per day for 2 weeks and omeprazole 20 mg per day for 8 weeks were administered to them. Endoscopic reexamination and 13C-urea breath test were performed 12 weeks after the initiation of treatment. RESULTS: The positive rate of H. pylori was 38.9% in the remnant stomach. Eradication rate was 50.0%. Mean dose of amoxicillin in effective cases was 14.1 +/- 1.5 mg/kg/day. This was significantly higher than that in non-effective cases (12.5 +/- 1.5 mg/kg/day). Remnant gastritis was significantly improved after complete eradication. CONCLUSIONS: H. pylori was present in 38.9% of patients who underwent gastrectomy for gastric cancer. The optimal dose of amoxicillin was 15.6 mg/kg/day for 14 days with omeprazole-amoxicillin therapy.     

幽门螺杆菌与胃癌关系的研究现状

幽门螺杆菌与胃癌关系的研究现状郭飞胡伏莲贾博琦幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ，Ｈｐ）自分离出来迄今已有十几年的历史，大量的研究证明Ｈｐ是引起人类慢性胃炎的主要因素，且其与消化性溃疡密切相关，感染Ｈｐ的人群中，以消化性溃疡病的检出率最...     

Helicobacter pylori and gastric cancer

Infection with Helicobacter pylori is now recognized as the primary cause of peptic ulcers and their recurrence. Compelling evidence has also been found linking H. pylori infection to gastric cancer, the second most common cancer in the world. Given the high rate of patient morbidity and mortality associated with gastric cancer, any method by which one can reduce the occurrence of the disease or increase its early detection is desirable. The strong correlation with H. pylori infection and the current availability of easily administered tests for the detection of the pathogen argue for screening at least those individuals with a family history of gastric cancer or other risk factors. This article reviews the association between H. pylori and gastric cancer and the pathologic changes that the infection produces in the gastric mucosa, as well as the cost-effectiveness of universal testing and eradication of the infection in H. pylori-positive individuals to reduce gastric cancer.     

Helicobacter pylori and gastric cancer

Gastric cancer despite a declining incidence remains a significant cause of morbidity and mortality world wide. There is strong epidemiological and histological evidence to associate Helicobacter pylori infection with the subsequent development of gastric cancer. The exact pathophysiological mechanisms involved remain to be elucidated. There is evidence to relate Helicobacter pylori infection and subsequent inflammation with an increase in gastric epithelial cell proliferation and with the induction of apoptosis. Such alterations in cellular dynamics may promote the development of mitogenic cell lines by inducing DNA damage. Studies have shown that following successful treatment, proliferation rates return to normal. At what histological stage, eradication is of benefit is less clear. It is likely that following the development of atrophy or intestinal metaplasia eradication will only slow progression. It would, therefore, seem logical, that to establish any benefit for a population, treatment should be employed at an earlier stage. As yet, an at risk group has not been identified, and as such population screening cannot be advised, mainly as a result of financial implications and the risk of promoting the development of resistant strains. Recent studies have explored the rules of bacterial factors, CagA and VacA status, host factors, HLA type, and environmental factors as determinants of outcome. Results have been variable. The establishment of an at risk group would enable selective screening and treatment, and thus prevent the development of gastric carcinoma as a result of Helicobacter pylori infection in the long-term.     

Helicobacter pylori and gastric cancer

Abstract This review focuses on the similarities between the epidemiology of gastric cancer and the epidemiology of Helicobacter pylori. Their demographic patterns and the results of studies regarding familial and environmental risk factors are described. The association of gastric cancer and H. pylori infection with both gastric ulcer and chronic atrophic gastritis is also characterized and the possibility that a H. pylori infection could lead to gastric cancer is discussed.     

Helicobacter pylori infection and precancerous lesions of the stomach

H. pylori infection is associated with a slightly increased risk of gastric cancer. However, the risk is much higher in the subgroup of infected patients who have atrophic gastritis and extensive intestinal metaplasia. In those subjects, H. pylori acts as a trigger of the sequence which begins as atrophic gastritis with intestinal metaplasia and evolves towards immature forms of intestinal metaplasia and dysplasia. It seems that factors different from H. pylori (diet, genetical background, etc.) might have an influence on how often gastric precancerous lesions appear in H. pylori-infected subjects. Effective prevention of gastric carcinoma would require identification of the patients at risk in an early step of the process. Preventive measures would include H. pylori eradication and changes in the diet (i.e., increase of vitamin C and carotenoid intake). Preliminary data suggest that H. pylori eradication cannot revert intestinal metaplasia. However, it is possible that eradication of the bacteria would prevent progression towards immature forms of intestinal metaplasia and dysplasia.     

Helicobacter pylori related and non-related lesions in the stomach

Gastric lesions may arise in gastric mucosa of patients with gastritis or gastropathies due to different etiopathogenic factors. As most lesions of the stomach result from a chronic infection of gastric mucosa with Helicobacter pylori (H. pylori), a possible classification of gastric lesions based on etiology may distinguish H. pylori-related lesions from those arising in a gastric mucosa not colonized from the bacterium. The repertoire of lesions one may find in the stomach is limited and different pathologies may present with a similar macroscopic aspect. Clinically relevant lesions of the stomach that are or are not associated with H. pylori infection include gastric ulcer, gastric atrophy, gastric neoplasia, and metastasis from other cancers. The detection or exclusion of an H. pylori infection in patients with gastric lesions has important consequences for the clinical management. In the present review we focus on H. pylori-related and non-related peptic lesions in the stomach.     

Prevalence of Helicobacter pylori in the residual stomach after gastrectomy for gastric cancer

BACKGROUND/AIMS: In recent years, the role of Helicobacter pylori in gastritis of the residual stomach has attracted much attention. We investigated the prevalence of Helicobacter pylori in the residual stomach after distal gastrectomy for gastric cancer, as well as the correlations between Helicobacter pylori positivity and clinical characteristics or the severity of gastritis in the residual stomach. METHODOLOGY: The subjects were 66 patients with gastric cancer who underwent distal gastrectomy with Billroth I reconstruction at our department. Helicobacter pylori was detected by the 13C-urea breath test, and patients were considered to be Helicobacter pylori-positive if the delta 13C value was > 2.5@1000. RESULTS: The overall Helicobacter pylori positivity rate of the gastrectomy patients was a high 80.3%, with the rate being especially high in patients under 60 years of age and in those tested less than 5 years after surgery. There was a close relationship between Helicobacter pylori positivity and the severity of gastritis. CONCLUSIONS: Helicobacter pylori infection appears to cause the development of gastritis. Helicobacter pylori eradication needs to be taken into consideration in the management of Helicobacter pylori-positive patients after gastrectomy.     

Gastric cancer prevention and Helicobacter pylori

Journal of Gastroenterology -