Isolated granulomatous gastritis successfully treated by <Emphasis Type="Italic">Helicobacter pylori</Emphasis> eradication: a possible association between granulomatous gastritis and <Emphasis Type="Italic">Helicobacter pylori</Emphasis>

We report two cases of granulomatous gastritis that resolved completely with Helicobacter pylori eradication. Two Japanese women, one 61 years old and one 58 years old, presented to our hospital with epigastralgia. Endoscopy revealed multiple shallow ulcerative lesions in the gastric corpus of both patients. Biopsy specimens demonstrated acute and chronic inflammation with multiple small, noncaseating granulomas at the level of the foveolar isthmi—the junction between the pits and the glands. Both specimens were positive for Helicobacter pylori. No other causes of organic granulomatous disease could be found. Both patients were diagnosed as having isolated granulomatous gastritis and were given triple therapy for Helicobacter pylori eradication, with their fully informed consent. The granulomatous gastritis resolved after successful Helicobacter pylori eradication therapy. This report describes a possible association between isolated granulomatous gastritis and Helicobacter pylori infection. To our knowledge, this is the first report describing isolated granulomatous gastritis successfully treated by triple therapy (Helicobacter pylori eradication therapy). Received: November 12, 2001 / Accepted: March 8, 2002 Acknowledgments. We wish to thank Dr. Syoichi Fujika, Dr. Yasuhiko Kitadai, Dr. Toru Hiyama, Dr. Toshiyuki Fukuhara, Dr. Masaru Nakamura, Dr. Chiyuki Watanabe, Dr. Hiroyasu Yamada, and Dr. Masaru Imagawa for their advice and support. Reprint requests to: M. Yoshihara     

Screening of atrophic gastritis and gastric cancer by serum pepsinogen, gastrin-17 and Helicobacter pylori immunoglobulin G antibodies

OBJECTIVE: Currently the screening and diagnosis of gastric cancer and atrophic gastritis are mainly made by endoscopy and biopsy. The aim of this study was to evaluate the use of serum tests: serum pepsinogen I (PGI pepsinogen I/II ratio (PGR), gastrin‐17 (G‐17) and H. pylori‐immunoglobulin G (IgG) antibodies to screen atrophic gastritis and gastric cancer. METHODS: A total of 458 patients were recruited, and each underwent endoscopy with biopsies before the serum tests were performed. These patients were divided into five groups based on the endoscopic and histological findings: 92 patients in the atrophic gastritis group, 58 in the gastric ulcer group, 90 in the duodenal ulcer group, 141 in the gastric cancer group (40 early gastric cancer and 101 advanced gastric cancer) and 77 (including mild non‐atrophic gastritis) served as a control group. Serum samples for PGI and II, G‐17, and H. pylori‐IgG antibodies estimation were analyzed by ELISA. RESULTS: PGI and PGR values decreased significantly both in atrophic gastritis and gastric cancer groups (P < 0.01). For the best discrimination of atrophic gastritis, the cut‐off values of PGI and PGR were 82.3 µg/L and 6.05, respectively. The PGI, PGR and G‐17 values were related significantly with the grades and/or sites of atrophic gastritis (P < 0.01). Patients with atrophic corpus gastritis had low PGI and PGR values and high G‐17 level, and patients with atrophic antral gastritis had low G‐17 level. G‐17 increased significantly in the gastric cancer group (P < 0.01). PGI and PGR values were significantly lower in patients with advanced gastric cancer than in patients with early gastric cancer, while there was no difference in G‐17 level between them. The positivity rate of H. pylori‐IgG antibodies was 54.55% in the control group. The PGI level was higher in H. pylori positive patients than in H. pylori negative ones (P < 0.001), while there was no difference in G‐17 level between them. The positivity rates of H. pylori‐IgG antibodies were over 85% in all other four groups. CONCLUSIONS: Low serum PGI, PGR and G‐17 values are biomarkers of atrophic antral gastritis. Atrophic corpus gastritis can be screened by lower serum PGI, PGR and high G‐17 values. [Correction added after online publication on 2 February 2007: the preceding sentence has replaced one that read ‘Atrophic be screened by serum PGI and PGR values’]. Gastric cancer can be screened on the basis of increased serum G‐17 and remarkedly low serum PGI and PGR values. The H. pylori infection is related to the change of PG level.     

Low presence of <Emphasis Type="Italic">p53</Emphasis> abnormalities in <Emphasis Type="Italic">H. pylori</Emphasis>-infected gastric mucosa and in gastric adenocarcinoma

Background: Alterations of the p53 gene and/or its abnormal protein accumulation have been observed in gastric cancer and preneoplastic lesions. Our aim was to assess possible associations between different H. pylori strains and p53 abnormalities in patients with dyspepsia and with gastric cancer. Methods: Seventy-five dyspeptic patients and 40 patients with gastric adenocarcinoma entered the study. H. pylori status was determined by the rapid urease test, histology, and polymerase chain reaction (PCR) analysis. Overexpression of the p53 protein was evaluated by immunohistochemistry. Detection of p53 mutations was done by direct DNA sequencing. Results: Fifty-four of the 75 (72.0%) dyspeptic patients and 27 of the 40 (67.5%) gastric cancer patients showed H. pylori infection. Cytotoxin-associated gene (cagA)-positive strains were found in 31 of the 54 (58%) dyspeptic patients and in 25 of the 27 (92.6%) neoplastic patients. As regards vacA, s2 strains showed the highest prevalence among dyspeptic patients (24 of 54 patients; 44.4%), whereas s1 strains were more expressed among cancer patients (23 of 27; 85.2%). Among the dyspeptic patients, 1 patient with duodenal ulcer showed p53 overexpression. Three mutations were identified by DNA sequencing: one in a patient with normal endoscopic findings and two in patients suffering from gastritis. Among the neoplastic patients, 16 subjects (40%) showed p53 overexpression (9 had diffuse-type and 7 intestinal-type cancer). Four mutations (10%) occurred in patients with intestinal-type gastric cancer. No association between p53 abnormalities (overexpression/mutation) and H. pylori infection was found in either group of patients. Conclusions: These results lead us to hypothesize that H. pylori infection does not affect the p53 pattern in gastric mucosa. Moreover, mutations of the p53 gene do not seem to be a predominant event in gastric carcinogenesis, at least in our populations. Received: December 14, 2001 / Accepted: May 17, 2002 RID="*" ID="*"  These authors contributed equally to the work RID="*" ID="*"  These authors contributed equally to the work Acknowledgments. The authors would like to thank Mrs B. D'Attoma and Mrs P. Fiorente for their valuable technical assistance, and Mrs M.V.C. Pragnell, B.A., for her help in revising the English. Reprint requests to: A. Di Leo     

<Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection and Idiopathic Thrombocytopenic Purpura

A treatment strategy for idiopathic thrombocytopenic purpura (ITP) is considered with the aim of cure or management of the bleeding tendency. In 1998, Gasbarrini et al reported a high prevalence of Helicobacter pylori infection in patients with ITP and showed that platelet recovery occurred after eradication therapy in most cases. Since then, many studies were performed to evaluate eradication therapy. This article discusses the incidence of H pylori infection in ITP, characteristic clinical features in H pylori-positive ITP, the effectiveness of eradication on platelet count increase, and the mechanisms of development of ITP by H pylori infection. Overall, there was a positive association between H pylori infection and ITP, and eradication of bacterium was accompanied by a significant increase in platelet counts in more than 50% of H pylori-positive ITP cases. These findings suggest that H pylori infection is involved in the mechanisms of thrombocytopenia in most cases of ITP in middle-aged and older patients. This approach could be beneficial to some ITP patients, but there were some uncertainties raised. To confirm the effectiveness of eradication therapy in H pylori-positive ITP, prospective studies conducted in several countries with a new treatment protocol are required, with a large number of ITP cases and longer follow-up.     

Correlation between serum pepsinogen levels and gastric mucosal histological findings before and after Helicobacter pylori eradication therapy

Background: Helicobacter pylori causes chronic gastritis and is also associated with many other gastrointestinal diseases. The incidence of gastric cancer is thought to vary according to the degree and topography of chronic gastritis. Histological findings of specimens obtained at endoscopy are therefore important. In the present study, we investigated the correlation between these histological findings and serum pepsinogen (PG) levels. Methods: Helicobacter pylori eradication therapy was conducted in 100 H. pylori‐positive patients. Endoscopies were performed prior to, and 2 months after, eradication therapy; gastric mucosal biopsies were taken from the antrum and corpus. Helicobacter pylori infection was diagnosed using the rapid urease test, culture and histology. Using the Updated Sydney System, histological findings of inflammation, activity, atrophy and intestinal metaplasia were each graded. Blood was taken on the same two occasions for determination of serum levels of PG I and II. Results: Levels of PG I were highest in association with antrum‐predominant gastritis (APG), followed in order by pangastritis (PAN) and corpus‐predominant gastritis (CPG), with a significant difference between APG and CPG. No correlations were seen between PG II levels and gastritis topography. Examination of the relationship between PG levels and histological findings revealed significant correlations between PG I levels after eradication atrophy and intestinal metaplasia in the gastric corpus. No significant correlations were seen between PG II levels and before or after eradication histological findings. Conclusion: Our results indicate that serum PG levels may be a useful indicator of before‐eradication gastritis topography and after‐eradication gastric atrophy in the gastric corpus.     

The prevalence of <Emphasis Type="Italic">Helicobacter pylori</Emphasis> in Japanese children with gastritis or peptic ulcer disease

Background Although Helicobacter pylori infection is typically acquired in childhood, the role of H. pylori infection in gastroduodenal diseases in childhood remains to be defined. The purpose of this study was to evaluate the prevalence of H. pylori infection in children with gastritis, duodenal ulcer, and gastric ulcer.Methods This was a retrospective analysis of 283 Japanese children (mean age, 11.5 years) with non-nodular gastritis (n = 73), nodular gastritis (n = 67), duodenal ulcer (n = 100), and gastric ulcer (n = 43). H. pylori status was based on biopsy tests. Clinical symptoms at the time of endoscopy were analyzed with regard to a possible association with the infection.Results The prevalence of H. pylori in non-nodular gastritis, nodular gastritis, duodenal ulcer, and gastric ulcer was 28.8%, 98.5%, 83.0%, and 44.2%, respectively. H. pylori was significantly linked to duodenal ulcer and gastric ulcers in the age group of 10–16 years, but not in the age group of 9 years and under. In children with H. pylori infection, nodular gastritis was observed in 26.3% of gastric ulcer patients and in 74.7% of duodenal ulcer patients (P < 0.001). H. pylori infection was significantly associated with the prevalence of anemia (P < 0.05).Conclusions H. pylori is the most important causal factor for the development of duodenal ulcer in childhood. While H. pylori infection appears to be a risk factor in gastric ulcer, other causes are responsible for most cases. Nodular gastritis is the most common type of H. pylori gastritis in childhood. Chronic infection with H. pylori is associated with anemia.     

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.     

Molecular Analysis of B-Cell Clonality in <Emphasis Type="Italic">Helicobacter Pylori</Emphasis> Gastritis

The aim of our study was to identify PCR-detectable clonal B-cell population in Helicobacter pylori gastritis and assess their relation to the Wotherspoon-Isaacson (W-I) grade for gastric lymphoid infiltrates. Amplified DNA was obtained from thirty four H. pylori positive gastritis dyspeptic patients and thirty four H. pylori negative matched controls. Clonal bands were observed in 6 (2/17 W-I Grade 1, 2/13 W-I Grade 2, and 2/4 W-I Grade 3 lesions) and polyclonal smears in 24 cases (15 W-I Grade 1, 7 W-I Grade 2, and 2 W-I Grade 3). Four additional W-I Grade 2 samples with clonal bands were associated with background polyclonal smear and were not reproducible. Clonal bands were not recorded in controls. B-cell clonality was not related to W-I grades. We conclude that certain H. pylori positive gastritis patients show PCR-detectable monoclonality, which is independent of the W-I grade of gastritis and cannot be taken as evidence of an existing neoplastic lesion.     

Nodular Gastritis: An Endoscopic Indicator of <Emphasis Type="Italic">Helicobacter Pylori</Emphasis> Infection

We prospectively assessed the relationship between nodular gastritis and Helicobacter pylori infection. Of 1409 adults who underwent endoscopy for persistent dyspepsia between June 2004 and August 2005, 41 (2.9%) patients were diagnosed with nodular gastritis (11 [27%] men and 30 [73%] women). The mean age was 45.9 years. A control group of 65 patients without nodular gastritis was also evaluated. The prevalence of H. pylori infection was higher in patients with nodular gastritis than in controls (38/41 [93%] vs. 33/65 [51%]). Of 21 patients treated to eradicate H. pylori, the nodular gastritis pattern resolved or improved in 16 patients on subsequent endoscopy. This study suggests that a nodular pattern of the gastric mucosa on endocscopy is a good indicator for H. pylori infection in adults, with the high positive predictive value of 92.7%.     

Association of <Emphasis Type="Italic">Lewis</Emphasis> and <Emphasis Type="Italic">Secretor</Emphasis> gene polymorphisms and <Emphasis Type="Italic">Helicobacter pylori</Emphasis> seropositivity among Japanese-Brazilians

Background Secretor (Se) and Lewis (Le) genes are involved in the synthesis of Lewis b (Le^b) and type I antigens throughout the body, especially in the epithelial cells of gastric mucosa. Helicobacter pylori can attach to the gastric epithelial cells with the blood group antigen-binding adhesin, which binds to Le^b or H type I carbohydrate structures. In a previous study, a marked association between H. pylori seropositivity and polymorphism of the Se and Le genes was observed among Japanese outpatients of a gastroenterology clinic. The present work aims to investigate the associations between Se and Le gene polymorphisms and H. pylori infection among Japanese-Brazilians.Methods The subjects consisted of 942 healthy volunteer Japanese-Brazilians, who were tested for the presence of anti-H. pylori IgG antibodies and genotyped for Se and Le polymorphisms.Results The sex-age-adjusted odds ratios (aORs) for H. pylori seropositivity were 0.99 for the Sese genotype relative to the SeSe genotype (95% confidence interval [CI], 0.73–1.33), and 1.03 for sese relative to SeSe (95% CI, 0.71–1.48). On the other hand, the aOR for the subjects with the le allele (Lele or lele) relative to the LeLe genotype was 1.48 (95% CI, 1.07–1.79). When the Se and Le genotypes were analyzed in combination according to risk group, no statistically significant association was observed.Conclusions These results are inconsistent with previous work and may have been modulated by an external factor or some other unidentified factor. Japanese-Brazilians are genotypically the same as Japanese, but their lifestyle is adapted to that of Brazil. Further investigations are necessary to clarify this influence on susceptibility to H. pylori infection.     

Serum pepsinogen II levels are doubled with Helicobacter pylori infection in an asymptomatic population of 40,383 Chinese subjects

Pepsinogen (PG) I and II are crucial in the gastric digestive processes. This study is to examine the relationship of serum PGI, PGII, and PGI/PGII ratio with Helicobacter pylori (Hp) infection, age, sex, and body mass index (BMI) in subjects in Beijing, China.A total of 40,383 asymptomatic subjects, who underwent medical examination in Beijing Rehabilitation Hospital, were included in this study. Serum PG levels were measured using chemoluminescence techniques. The age, sex, and BMI data were collected, and Hp infection was identified with ¹³C-urea breath test. Statistical analysis was conducted with Python, Pandas and Seaborn software.Asymptomatic subjects with Hp infection (Hp+) had a significantly higher level of PGI in the serum (111 ng/mL [median]) than those without Hp infection (Hp−) (94 ng/mL, P < .001). The asymptomatic Hp+ subjects had 2-fold higher PGII levels (7.2 ng/mL) than Hp− subjects (3.2 ng/mL, P < .001). These changes produced significantly lower PGI/II ratio in Hp+ patients than in Hp− subjects (16:30, P < .001). The serum PGI and PGII levels were higher in males than in females (PGI: 104 ng/mL vs 95 ng/mL, PGII: 4.3 ng/mL vs 3.7 ng/mL, both P < .001), PGI/II ratio of males is at 95% of that in females (P < .001). PGI and PGII levels gradually increased in older people (P < .001), whereas the PGI/II ratio decreased significantly with age (P < .001). The levels of the two serum PGs were decreased and the ratio increased when BMI were higher than 28 kg/cm² (P < .05).The levels of serum PGI, especial PGII, were increased by Hp infection, and also influenced by age, sex, and BMI. Therefore, these influencing factors should be considered during clinical practice.     

Racial differences in Helicobacter pylori, serum pepsinogen and gastric cancer incidence in an urban Asian population

BACKGROUND: In Singapore, the highest incidence of gastric cancer occurs in the Chinese (C), with lower rates among Malay (M) and Indian (I) subjects. The purpose of the present paper was to examine whether racial differences in the prevalence of Helicobacter pylori and serum pepsinogen (PG) could account for this difference. METHODS: A randomized community health survey involving 7000 asymptomatic healthy individuals was conducted. Among the Chinese, Malay and Indian respondents, subjects were matched for age, gender and race and a total of 595 sera were obtained. The H. pylori seropositivity and serum PG levels were determined by ELISA. The dependency of the cumulative gastric incidence rate on H. pylori seroprevalence was evaluated by linear regression. The racial difference in the seroprevalence of H. pylori and low serum PG was determined. RESULTS: The H. pylori seroprevalence was similar between Chinese and Indian subjects, but significantly lower among Malay subjects (C, 46.3%; M, 27.9%; I, 48.1%). The gastric cancer incidence rates correlated with H. pylori seropositivity for the Chinese and Malay subjects, but not for the Indian subjects. The prevalence of low PG was highest in Indian subjects (PG I low: C, 2.1%; M, 5.4%; I, 14.2%; P < 0.0001; PG I:II ratio low: C, 5.3%; M, 5.9%; I, 12.6%; P = 0.012), even when adjusted for gender and the presence of H. pylori. CONCLUSIONS: The difference in gastric cancer incidence correlated with H. pylori seroprevalence for Chinese and Malay subjects. The lower incidence of gastric cancer among Indian subjects cannot be explained by differences in H. pylori or serum PG. Other modifying factors such as host and environmental factors may be important.     

胆汁反流性胃炎患者幽门螺杆菌感染及其胃粘膜病理学表现研究*

目的 探讨胆汁反流性胃炎（BRG）患者幽门螺杆菌（Hp）感染及其胃粘膜病理学变化。方法 我院诊治的BRG患者618例和无胆汁反流的慢性浅表性胃炎（CSG）患者1486例,采用¹⁴C-尿素呼气试验、血清抗-Hp抗体检测和对组织切片行硼酸亚甲蓝染色三种方法对受试者进行Hp感染诊断,常规行胃镜检查,参照新悉尼系统标准,将组织学上胃黏膜慢性炎性反应、炎性反应活动性、萎缩和肠上皮化生的严重程度分为无、轻、中和重4个等级。结果 BRG患者Hp感染率为32.7%（202/618）,而CSG组患者为40.6%（603/1486）,两组间无显著性差异（P>0.05）;在202例Hp阳性的BRG患者中,胃粘膜轻、中、重度炎症反应发生率分别为10.9%、61.4%和27.7%,显著重于416例Hp阴性患者的40.4%、51.7%和7.9%（P<0.05）,胃粘膜淋巴滤泡形成、肠化生和活动性炎症发生率分别为15.4%、5.4%和16.8%,也显著重于Hp阴性患者的2.7%、10.8%和0.7%（P<0.05）;603例Hp阳性的CSG患者胃粘膜轻、中、重度炎症反应发生率分别为29.2%、59.4%和11.5%,与883例Hp阴性患者的34.1%、54.0%和11.9%比,无显著性差异（P>0.05）,胃粘膜淋巴滤泡形成、肠化生和活动性炎症发生率分别为10.4%、1.8%和8.5%,与Hp阴性患者的7.8%、1.0%和5.0%比,也无显著性差异（P>0.05）;观察胃粘膜病理学轻度、中度和重度炎症情况发现,117例内镜下胃粘膜III级BRG患者炎症程度显著重于200例I级或301例II级患者（P<0.05）。结论 BRG患者无论是胃镜下表现还是胃粘膜组织病理学变化都存在明显的病变,胆汁反流和Hp感染是引起胃粘膜炎症反应的重要因素。     

<Emphasis Type="Italic">Helicobacter pylori</Emphasis>: present status and future prospects in Japan

The discovery of Helicobacter pylori has already changed the natural history of peptic ulcer disease, with most patients being cured at their first presentation. Similarly, the incidence of gastric cancer and other diseases related to H. pylori are likely to be greatly reduced in the near future. Isolation of the spiral intragastric bacterium H. pylori totally reversed the false dogma that the stomach was sterile, and it taught us that chronic infectious disease can still exist in modern society. Helicobacter pylori's unique location, persistence, and evasion of the immune system offer important insights into the pathophysiology of the gut. Also, the fact that it was overlooked for so long encourages us to think “outside the box” when investigating other diseases with obscure etiologies. We should consider such provocative scientific ideas as bridges to the future disease control.     

<Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection and hiatal hernia do not affect acid reflux and esophageal motility in patients with gastro-esophageal reflux

Background. The association of H. pylori and hiatal hernia in patients with gastroesophageal reflux disease, in terms of acidity and esophageal motility, is not well defined. The purpose of this work was to assess whether, in patients with gastroesophageal reflux, the presence of H. pylori and hiatal hernia affects the severity of esophagitis. Methods. Reflux symptoms, endoscopy, H. pylori, esophageal manometry, and 24-h pH monitoring were evaluated in 37 patients with esophageal reflux and 14 healthy volunteers. Results. A total of 75.6% of patients with esophageal reflux was positive for H. pylori; 81% had hiatal hernia, and only 43.2% showed an acid score by 24-h pHmetry. Esophageal reflux patients with H. pylori, hiatal hernia, and an acid score demonstrated higher acid parameters compared with those in healthy volunteers. Patients with an acid score who were negative for H. pylori tended toward more acid reflux events than patients with an acid score who were positive for H. pylori, a difference that did not reach significance. The same situation existed with patients with an acid score and hiatal hernia who were negative for H. pylori, but the tendency did not achieve significance. Independent analysis of patients with Savary-Miller stage II and III esophagitis showed results that were not different from the combined analysis of stage II and III patients. Amplitude and contraction-duration parameters of the esophageal wave, and the number of high-pressure and prolonged contractions were not different among the reflux groups. Wave amplitude in the lower third of the esophagus was significantly lower in esophagitis stage III patients with hiatal hernia and in esophagitis stage II and III patients, combined, with H. pylori, compared with findings in the healthy volunteers. Conclusions. These results suggest that H. pylori and hiatal hernia in patients with esophageal reflux do not constitute risk factors that affect the severity of esophagitis. Received: April 12, 2001 / Accepted: September 14, 2001     

Helicobacter pylori eradication improves gastric histology and decreases serum gastrin, pepsinogen I and pepsinogen II levels in patients with duodenal ulcer

Background and Aim: The aim of this study was to assess the gastric histopathology and serum gastrin‐17 and pepsinogens profiles in patients with duodenal ulcer before and after Helicobacter pylori eradication in a population with a very high prevalence of H. pylori. At the same time we assessed the role of H. pylori density on these variables. Methods: Eighty Caucasian patients with H. pylori–associated duodenal ulcer before treatment and 1 year after randomized eradication were studied. Among patients with unsuccessful eradication two groups were distinguished according to the data obtained after treatment: the group with negative rapid urease test and decreased bacterial density according to morphological score (partial elimination group); the group with positive rapid urease test and high bacterial density (failed eradication group). Results: One year after successful eradication, serum levels of gastrin‐17, pepsinogen I and pepsinogen II decreased. Similar changes of serum pepsinogen I and pepsinogen II levels were observed in patients with partial elimination of H. pylori infection. In the group with successful eradication, inflammation, activity, atrophy and number of lymphoid follicles in the antral mucosa fell. In the group with partial elimination, antral mucosa activity and H. pylori score reduced. Other morphological changes were statistically non‐significant. Conclusion: Patients with duodenal ulcer after successful eradication have improvement of morphological and functional characteristics of gastric mucosa.     

Effect of Helicobacter pylori infection on cyclooxygenase‐2 expression in gastric antral mucosa

OBJECTIVE: Helicobacter pylori infection is a major etiological cause of chronic gastritis. Inducible cyclooxygenase (COX‐2) is an important regulator of mucosal inflammation. Recent studies indicate that expression of COX‐2 may contribute to gastro­intestinal carcinogenesis. The aim of this study was to investigate the effects of H. pylori infection and eradication therapy on COX‐2 expression in gastric antral mucosa. METHODS: Antral biopsies were taken from 46 H. pylori‐infected patients, who also had chronic gastritis, both before and after anti‐H. pylori treatment. The COX‐2 protein was stained by using immunohistochemical methods and COX‐2 expression was quantified as the percentage of epithelial cells expressing COX‐2. Gastritis and H. pylori infection status were graded according to the Sydney system. RESULTS: Cyclooxygenase‐2 expression was detected in the cytoplasm of gastric antral epithelial cells both before and after the eradication of H. pylori. Cyclooxygenase‐2 expression in mucosa with H. pylori infection was compared with the corresponding mucosa after successful H. pylori eradication (20.1 ± 13.1%vs 13.8 ± 5.9%; P < 0.05). At the same time, COX‐2 expression in H. pylori‐infected mucosa was com­pared with the normal controls (18.0 ± 14.1%vs 12.3 ± 4.6%, P < 0.05). Expression of COX‐2 was correlated with the degree of chronic inflammation (r= 0.78, P < 0.05). CONCLUSIONS: Our results showed that H. pylori infection leads to gastric mucosal overexpression of COX‐2 protein, suggesting that the enzyme is involved in H. pylori‐related gastric pathology in humans.     

Helicobacter pylori infection and gastric function in patients with fundic atrophic gastritis

In the present study we evaluated the relation among histology, H. pylori, IgG to H. pylori, gastric emptying, and acid secretion in 43 patients with fundic atrophic gastritis. On the basis of gastric acid secretion, patients were divided into three subgroups: patients with preserved acid secretion (Group 1), patients with hypochlorhydria (Group 2), and patients with achlorhydria (Group 3). Fundic glandular atrophy was more severe in hypoachlorhydric patients than in those with preserved acid secretion (P < 0.05 vs Group 2, P < 0.005 vs Group 3). H. pylori colonization was found in 94% of patients in Group 1, in 61% of patients in Group 2, and in only 8% of patients in Group 3 (P < 0.001 vs Group 1, P < 0.05 vs Group 2). Conversely, serological positivity to H. pylori was high in all three subgroups of patients (100% in Group 1, 77% in Group 2, 92% in Group 3). Gastric emptying was delayed in atrophic patients, particularly in those with hypoachlorhydria. Our data suggest that fundic atrophic gastritis represents a possible end stage of H. pylori infection, characterized by a progressive disappearance of the bacterium and a progressive deterioration of gastric functions.     

幽门螺杆菌感染对胃黏膜环氧合酶-2表达的影响

目的评估幽门螺杆菌(Hp)感染对慢性胃炎胃黏膜环氧合酶-2(COX-2)表达的影响.方法与10例正常对照者比较,用免疫组化方法半定量检测46例慢性胃炎患者Hp根除治疗前后胃窦黏膜COX-2蛋白的表达,用悉尼分类标准对胃黏膜炎症、活动性和Hp密度进行半定量测定.结果在胃黏膜表面上皮、腺上皮细胞和固有层间质细胞的胞浆中可见COX-2表达.与正常对照者比较,Hp感染胃黏膜的COX-2平均阳性细胞率明显增加[(18.0±14.1)%比(12.3±4.6)%,P＜0.05)];成功根除Hp后的胃黏膜COX-2平均阳性细胞率明显下降[(20.1±13.1)%比(13.8±5.9)%,P＜0.05)];COX-2表达与慢性炎症计分相关(r=0.78,P＜0.05).结论Hp感染导致胃黏膜COX-2表达增加,提示COX-2在Hp相关性胃炎发生中起作用.