The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with Barrett's esophagus in Japan

OBJECTIVES: The acidity of the refluxate into the esophagus is a key factor for the pathogenesis of gastroesophageal reflux disease. Helicobacter pylori (H. pylori) infection can influence gastric acid secretion. We have reported that H. pylori infection prevents reflux esophagitis by decreasing gastric acid secretion in Japanese patients, but the role of this organism in Barrett's esophagus is unclear. The aim of this study was to investigate the prevalence of H. pylori infection and gastric acid secretion in Japanese patients with reflux esophagitis with or without Barrett's esophagus. METHODS: We enrolled 112 reflux esophagitis patients who were examined for the status of H. pylori and acid secretion in this study. They were divided into three groups, according to the presence or absence of Barrett's esophagus as follows: reflux esophagitis group without Barrett's esophagus (reflux esophagitis alone) (80 patients); short-segment Barrett's esophagus group (16 patients); and long-segment Barrett's esophagus group (LSBE) (16 patients). Age- and sex-matched control subjects were also assigned to the 80 patients with reflux esophagitis alone. The prevalence of H. pylori infection was determined by histology, rapid urease tests, and serum IgG antibodies. Gastric acid secretion was evaluated by the endoscopic gastrin test (EGT). RESULTS: The overall prevalence of H. pylori infection in the reflux esophagitis patient group (24.1%) was significantly lower than the control group (71.2%) (odds ratio 0.13, 95% confidence interval 0.07-0.24; p < 0.0001). The prevalence of H. pylori infection in the patients with Barrett's esophagus tended to be lower than that in the patients with reflux esophagitis alone (reflux esophagitis alone; 30.0%, SSBE; 18.7%, LSBE; 0%), especially in the patients with LSBE compared with the reflux esophagitis alone group (p < 0.01). The EGT value of the respective reflux esophagitis patient group was significantly higher than the control group. The EGT value in the patients with Barrett's esophagus tended to be higher than that in the patients with reflux esophagitis alone, but the difference was not statistically significant. When examined in H. pylori-negative subjects, no difference was found in the EGT value between the control subjects and the patients with reflux esophagitis alone, but it was significantly higher in patients with Barrett's esophagus than the control subjects (p < 0.05). On the other hand, when examined in the H. pylori-positive subjects, the EGT value was significantly higher in the patients with reflux esophagitis alone than in the control subjects (p < 0.01). CONCLUSIONS: H. pylori infection may play a protective role in the development of Barrett's esophagus, especially in the development of LSBE in Japan. Gastric acid hypersecretion may be concerned with the development of Barrett's esophagus in addition to the absence of H. pylori infection.     

Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett's esophagus, Barrett's dysplasia, and Barrett's adenocarcinoma

OBJECTIVE: This study was undertaken to prospectively determine the prevalence of gastric H. pylori infection in Barrett's esophagus and Barrett's complicated by dysplasia or adenocarcinoma. METHODS: The prevalence of H. pylori was determined in Barrett's esophagus patients compared to a control population of patients with gastroesophageal reflux disease (GERD) only. All patients had a minimum of 10 gastric surveillance biopsies obtained. H. pylori colonization was determined upon the basis of hematoxylin and eosin and use of a modified Giemsa and or Steiner's silver stain of all gastric biopsy specimens. RESULTS: Two hundred and eighty-nine Barrett's patients and 217 GERD control patients were included in the study. H. pylori was found in 95/289 (32.9%) of the Barrett's patients, compared with 96/217 (44.2%) of the GERD controls (NS). Forty-seven of the Barrett's patients had low-grade dysplasia/indefinite dysplasia, 14 high-grade dysplasia, and 20 Barrett's adenocarcinoma. When Barrett's was subgrouped according to absence of dysplasia, and presence of low-grade dysplasia, high-grade dysplasia, or adenocarcinoma, H. pylori prevalence was found to be significantly less for patients with Barrett's high-grade dysplasia (14.3%) and adenocarcinoma (15.0%) versus patients with GERD alone (44.2%), Barrett's alone (35.1%), or Barrett's with low-grade dysplasia (36.2%) (p = 0.016). This difference could not be explained by differences between Barrett's esophagus patients infected with H. pylori and those who were not with respect to gender, smoking history, alcohol consumption, use of proton pump inhibitor, or length of Barrett's mucosa. CONCLUSIONS: Barrett's high-grade dysplasia and adenocarcinoma are significantly more prevalent in patients who are not infected with H. pylori. H. pylori appears to have a protective effect against the development of Barrett's adenocarcinoma.     

Relationship of gastric Helicobacter pyloriinfection to Barrett＇s esophagus and gastro-esophageal reflux disease in Chinese

AIM:To evaluate the relationship of Helicobacter pylori infection to reflux esophagitis (RE), Barrett‘s esophagus (BE)and gastric intestinal metaplasia (IM).METHODS:RE,BE and gastric IM were determined by upper endoscopy. Patients were divided into 2 groups; those with squamocolumnar junction (SCJ) beyond gastroesophageal junction (GEJ)≥3cm (group A), and those with SCJ beyond GE.1 &lt;3cm (group B). Biopsy specimens were obtainedend escopically from just below the SCJ, gastric antrum along the greater and lesser curvature. Pathological changes and Hpylorr infection were determined by HE staining, Alcian blue staining and Giemsa staining.RESULTS:The prevalence of Hpyloriinfection was 46.93%.There was no difference in the prevalence between males and females.The prevalence of Hpyloriinfection decreased stepwise significantly from RE grade I to Ⅲ.There was no difference in the prevalence between the two groups, and between long-segment and short-segment BE. In distal stomach, prevalence of Hpyloriinfection was significantly higher in patients with IM than those without IM.CONCLUSION: There is a protective role of Hpyloriinfectuion to GERD. There may be no relationship between Hpylori infection of stomach and BE. Hpyloriinfection is associated with the development of IN in the distal stomach.     

CagA-positive strains of Helicobacter pylori may protect against Barrett's esophagus

OBJECTIVE: Helicobacter pylori (H. pylori) colonization is associated with chronic gastritis, peptic ulcer disease, and adenocarcinoma of the distal stomach. However, the role of H. pylori strain variation in complicated gastroesophageal reflux disease, especially Barrett's esophagus, is unknown. Therefore, the aim of this study was to evaluate the prevalence of colonization by cagA+ and cagA- H. pylori strains in the spectrum of gastroesophageal reflux disease, including Barrett's esophagus. METHODS: A total of 251 patients undergoing endoscopy were categorized into four groups: controls, patients with gastroesophageal reflux disease alone, and patients with short- and long-segment Barrett's esophagus. All patients underwent upper endoscopies with biopsies and serum collections. H. pylori and degree of mucosal inflammation in gastric biopsies were assessed and serological assessment made for H. pylori and cagA status. RESULTS: The overall prevalence of H. pylori colonization in the study population was 35% (95% confidence interval = 29.5-41.4%) which did not differ significantly among the groups. However, colonization by cagA+ H. pylori strains was significantly more prevalent among controls (11/25; 44%) and patients with gastroesophageal reflux disease (13/36; 36%) than in patients with short-segment (2/10; 20%) or long-segment Barrett's esophagus (0/18; 0%). Patients with Barrett's esophagus were less likely to be colonized by cagA+ H. pylori strains than reflux patients without Barrett's esophagus (odds ratio = 0.27, 95% confidence interval = 0.11-0.67, p = 0.004). CONCLUSIONS: Colonization by cagA+ H. pylori strains may be protective against the formation of short- and long-segment Barrett's esophagus and its malignant complications.     

Role of gastritis pattern on Helicobacter pylori eradication

Helicobacter pylori eradication rate following standard triple therapy is decreasing. Identification of predictive factors of therapy success would be useful for H. pylori management in clinical practice. This study aimed to evaluate the role of different gastritis patterns on the efficacy of the currently suggested 14-day triple therapy regimen. One-hundred and seventeen, consecutive, non-ulcer dyspeptic patients, with H. pylori infection diagnosed at endoscopy, were enrolled. All patients received a 14-day, triple therapy with lansoprazole 30?mg, clarithromycin 500?mg and amoxicillin 1?g, all given twice daily. Bacterial eradication was assessed with ¹³C-urea breath test 4?C6?weeks after completion of therapy. H. pylori infection was cured in 70.1% at ITT analysis and 83.7% at PP analysis. The eradication rate tended to be lower in patients with corpus-predominant gastritis as compared to those with antral-predominant gastritis at both ITT (66.1 vs 74.5%) and PP (80.4 vs 87.2%) analyses. The multivariate analysis failed to identify factors associated with therapy success. However, 14-day triple therapy does not achieve acceptable H. pylori cure rate in Italy, and should be not recommended in clinical practice.     

Treatment of Helicobacter pylori infection in atrophic gastritis

Helicobacter pylori(Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis(AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows:(1) Cure of infection, resolution of inflammation and normalization of gastric functions;(2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and(3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric p H, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroupof patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG.     

CagA-positive Helicobacter pylori infection is not associated with decreased risk of Barrett's esophagus in a population with high H. pylori infection rate

Background & aim  

The role that H. pylori infection plays in the development of and Barrett's esophagus (BE) is uncertain. We tested the hypothesis that infection with cagA+ Helicobacter pylori strains protects against the development of BE.     

HTLV-I infection and the low prevalence of Helicobacter pylori infection in Japan

HTLV-I retrovirus infection and Helicobacter pylori infection are common in Japan; however a report in this issue shows a significantly low prevalence of H. pylori in patients infected with HTLV-I. The reasons for this may be due to differences in genetic susceptibility of the infections, the gastric milieu in HTLV-I being unable to support H. pylori, or because antimicrobial therapy in HTLV-I infection has eradicated H. pylori in this susceptible population. Similarities between HIV-1, another retroviral infection, and the prevalence of H. pylori are noted.     

Lymphocytic gastritis and Helicobacter pylori infection in gastric lymphoma.

Lymphocytic gastritis and primary gastric lymphoma are rare conditions with unknown aetiology. It has recently been suggested that Helicobacter pylori has a role in the pathogenesis of both of them. The occurrence of lymphocytic gastritis and H pylori was studied in a series of patients with primary gastric lymphoma. The cases of primary gastric lymphomas (n = 35) diagnosed in years 1970-1993 were identified. The specimens of 22 cases contained gastric mucosa sufficiently so that the number of intra-epithelial lymphocytes, severity of gastritis, and occurrence of H pylori could be studied. Lymphocytic gastritis was detected in seven of 22 patients (32%), and in most cases both in antral and body mucosa. Atrophy of the body glands was significantly more severe in lymphocytic gastritis patients. H pylori was detected in 13 of all 22 patients (59%); two of seven lymphocytic gastritis patients (29%), and 11 of 15 (73%) of patients without lymphocytic gastritis were H pylori positive. Patients with gastric lymphoma have significantly increased prevalence of lymphocytic gastritis. Rarity of H pylori in these patients might be connected with atrophic changes in body mucosa. Further studies are needed to show the significance of lymphocytic gastritis as a precursor of gastric lymphoma.     

Barrett's oesophagus and Helicobacter pylori

Abstract In order to demonstrate the presence of Helicobacter pylori in the metaplastic epithelium of Barrett's oesophagus and to evaluate its possible association with this entity, we examined 29 cases of Barrett's oesophagus where concomitant antral biopsies were also available. These cases were compared with an equal number of age and sex matched controls of uncomplicated reflux oesophagitis. H. pylori was present in 11 of 29 cases of Barrett's oesophagus (38%). No increase in the frequency of H. pylori antral gastritis was found in patients of Barrett's oesophagus compared to the control group of uncomplicated reflux oesophagitis. The positivity of Barrett's oesophagus for H. pylori correlated with the presence of H. pylori antral gastritis ( P < 0.05), although in two cases of H. pylori -positive Barrett's oesophagus antral biopsies were negative for H. pylori. No difference was found in the severity of inflammatory and dysplastic changes of H. pylori- positive and H. pylori -negative Barrett's oesophagus. Presence of H. pylori does not seem to alter the natural history of Barrett's oesophagus.     

Kawamura分类法在评价幽门螺杆菌感染和胃炎中的价值

目的 探讨Kawamura分类法在诊断幽门螺杆菌(H.pylori)感染和评价胃黏膜炎症及萎缩程度中的价值。方法 在放大内镜下观察71例H.pylori感染患者的胃体上段大弯侧和小弯侧胃黏膜的腺管开口(COs)。根据腺管开口特点分为“白边黑点(white-edged dark spot)”型、“白色(white)”型、“纯白色(dense white pit，DWP)”型，分别取病理活检。对患者行H.pylori根除治疗，6个月后对根除成功的65例患者复查胃镜，比较根除治疗前后3种分型的分布及不同分型胃黏膜炎症活动度和萎缩程度的差异。结果 H.pylori根除后3种分型的分布与根除前比较差异有统计学意义(P<0.001)。根除治疗前以“white”型为主，根除治疗后以“white-edged dark spot”型为主。“white-edged dark spot”型、“white”型、“DWP”型胃黏膜的炎症程度依次升高，每两组间炎症活动度分布比较差异均有统计学意义(P<0.001)。不同Kawamura分型胃黏膜萎缩程度分布比较差异无统计学意义(P>0.05)。结论 Kawamura分类法有助于评价H.pylori感染及胃黏膜炎症活动度，但在评价胃黏膜萎缩程度方面无显著优势。     

慢性胃炎结节状改变与幽门螺杆菌感染的关系研究

目的　探讨慢性胃炎结节状改变与幽门螺杆菌 (Hp)感染的关系。方法　对 2 0 0 1～2 0 0 2年中胃镜检查发现的慢性胃炎结节状改变患者进行Hp检测 ,对Hp阳性患者 ,进行Hp根除治疗 ,随访 6个月 ,观察其胃镜下的改变。结果　 4 939例胃镜检查患者中共发现 1 3例慢性胃炎结节状改变 ,占检查总人数的 0 2 6 %。平均年龄 2 9岁 ,均为女性患者。主要症状均为上腹部疼痛。所有患者均有Hp感染。Hp根除成功后 ,症状和胃镜下结节状表现消失 ,病理证实胃黏膜下淋巴滤泡也随之消失。结论　慢性胃炎结节状改变可作为Hp阳性胃炎的内镜下的表现之一。     

Barrett's esophagus is characterized by the absence of Helicobacter pylori infection and high levels of serum pepsinogen I concentration in Japan

Background and Aim:  It has been reported that patients with Barrett's esophagus (BE) may have gastric acid hypersecretion. Serological markers such as serum pepsinogen or gastrin have been used to estimate the gastric secretory function. The aim of this study was to compare the serum pepsinogen and gastrin concentrations in view of Helicobacter pylori infection status between BE patients and the controls.
Methods:  Thirty-six patients with long-segment BE were enrolled in this study. Three age- and sex-matched controls were assigned to each patient. Serum pepsinogen and gastrin concentrations were measured by radioimmunoassay and H. pylori infection was determined by histology and serum IgG antibodies.
Results:  Helicobacter pylori infection was present in 4 of 36 patients (11%) with BE and in 80 of 108 controls (74%), being less prevalent in BE patients than in the controls ( P  < 0.0001). When examined in the H. pylori -negative subjects, both the serum pepsinogen I and pepsinogen II concentrations in BE patients were significantly higher than those in the controls (mean pepsinogen I:BE 51.0 ± 14.0 ng/mL vs control 38.9 ± 13.5 ng/mL, P  = 0.0012; mean pepsinogen II:BE 10.8 ± 4.0 ng/mL vs control 7.9 ± 2.0 ng/mL, P  = 0.0097). There was no significant difference in the serum gastrin levels between BE patients and the controls irrespective of the H. pylori infection status.
Conclusions:  Most of the Japanese BE patients are characterized by the absence of H. pylori infection and high levels of serum pepsinogen. Determination of the serum pepsinogen level in combination with the H. pylori infection status could be a useful serological marker for BE screening.     

Chronic gastritis and Helicobacter pylori

Helicobacter pylori is the major cause of chronic gastritis. The predominant anatomic distribution of the gastritis is antral in the majority of individuals. In a small minority, the corpus is predominantly involved. The former pattern is associated with duodenal ulceration in some patients, but the majority of those infected never develop either symptoms or disease. The latter form is associated with the development of gastric ulcer and carcinoma and may be protective against the development of Barrett's esophagus. It is the physiological changes associated with the histological changes and the, as yet poorly, defined host response, which are of paramount importance in determining the evolution of a disease or whether the infected individual remains asymptomatic and disease free. This article addresses the various relationships between H. pylori infection, histology, gastric physiology, and disease.     

Trend toward a reduced prevalence of Helicobacter pylori infection, chronic gastritis, and gastric cancer in Japan

It is speculated that declines in H. pylori infection and gastritis over the past few decades may lead to a decline in gastric cancer in Japan, supplemented by excellent procedures for the early detection of gastric cancer. Because H. pylori infection rarely is acquired in adult life, once it is eradicated, reinfection would not be expected in adult patients. It seems likely that adequate treatment of H. pylori infection would provide long-term protection against gastric cancer.