Frequency of Helicobacter pylori and gastritis in healthy subjects without gastrointestinal symptoms.

To investigate the frequency of Helicobacter pylori and gastritis in asymptomatic adults, 30 healthy volunteers underwent upper endoscopy. Biopsy specimens were obtained from the corporeal and antral mucosa of the stomach. The specimens were examined by light microscopy for gastritis and the occurrence of H. pylori. In 12 subjects signs of gastritis were noted at endoscopy, but only in 7 of them was this diagnosis confirmed histologically. No other abnormalities were observed by the endoscopist. Histologic examination was normal in 17 subjects, but in 13 subjects (43%) inflammation was found in the gastric specimens. Ten had inflammation both in the corpus and in the prepyloric specimens, and in six of these subjects H. pylori was discovered. H. pylori was only found in subjects with inflammation in both the corpus and the antrum. Subjects with gastritis were slightly older than subjects with normal gastric mucosa (median age, 47 versus 37 years; not significant). In the group of subjects with gastritis, persons with H. pylori were older than those without (median age, 53.5 versus 36 years; p = 0.05). The results of our study indicate that gastritis is present before colonization with H. pylori occurs. This could imply that H. pylori is not the cause of gastritis but that the presence of gastritis is a prerequisite for colonization of the bacterium in the stomach.     

A 12-Year Follow-up Study of Chronic Gastritis and Helicobacter pylori in a Population-Based Random Sample

Background: The study is a 12-year endoscopic follow-up investigation on the course of chronic gastritis and Helicobacter pylori infection in a sample of 81 Estonian people. Methods: The series is a subset from a random sample of 227 subjects in whom a gastroduodenal endoscopy had been done. The grade of superficial gastritis (SG), atrophy, and colonization of the mucosa by H. pylori was evaluated in biopsy specimens from both antrum and corpus in accordance with the principles of the Sydney System. Resufrs: The healing rate of the H. pylori and gastritis was 0.3% (3 of 81); H. pylori colonization with gastritis developed in 5 of 81 during the follow-up. The mean prevalence of atrophic gastritis (AG) was three times more common in the corpus than in the antrum on the average. The formation of new cases of AG and the disappearance of AG were quite equal during the follow-up, and the overall changes in the grade of SG and atrophy were slow. The mean life span of corpus AG was nearly three times as long as that of antrum AG. In the antrum the grade of chronic inflammation correlated positively with the grade of H. pylori colonization. In cases of SG a low grade of colonization of H. pylori in the antral mucosa in connection with moderate inflammation predicted a reduction or even a healing of gastritis in the long term. Conclusions: New H. pylori infections with subsequent gastritis may occur in adulthood; a healing of gastritis occurs but is a quite rare event in the course of the 12-year follow-up. Further, in the present random sample of Estonian people atrophic corpus gastritis did not show an overall progression, in contrast to our earlier findings.     

Risk of Recurrence of Gastric Ulcer,Chronic Gastritis,and Grade of Helicobacter pylori Colonization: A Long-Term Follow-up Study of 25 Patients

Maaroos H-I, Kekki M, Vorobjova T, Salupere V, Sipponen P. Risk of recurrence of gastric ulcer, chronic gastritis, and grade of Helicobacter pylori colonization. A long-term follow-up study of 25 patients. Scand J Gastroenterol 1994;29:532-536.

Background: We describe here our observations on colonization of the gastric mucosa by Helicobacter pylori in a long-term follow-up of 25 patients with gastric ulcer (GU).

Methods: All patients were followed-up endoscopically for more than 10 years (mean, 16 years) and endoscopically verified to have GU in the angular or corpus area of the stomach. None had received treatment with H₂ blockers or omeprazole or had undergone any maintenance therapy or surgery. On the basis of the endoscopic findings on the activity of GU at follow-up endoscopies, the patients were divided into a group of subjects with 'low risk' of recurrence (15 patients who either had no (7 patients) or only a single recurrence (8 patients) at the first follow-up endoscopy but not thereafter) and into those with a 'high risk' of recurrence (10 patients who had at least 2 episodes of recurrence at follow-up endoscopies).

Results: A severe bilateral (antrum and corpus) colonization of the gastric mucosa by H. pylori at the first re-examination (1-6 years after the initial diagnosis of GU) was the most important characteristic feature in the patients with high risk of recurrence as compared with those with low risk. In the course of the follow-up, colonization of the corpus mucosa by H. pylori remained rather unchanged in both high- and low-risk subjects but decreased in grade in antrum particularly in those with low risk (no bacteria at the last endoscopy in 13 of 16 low-risk patients and in 2 of 8 high-risk patients). In both low-and high-risk groups corpus gastritis developed progressively into atrophic gastritis (11 of 25 patients had severe corpus atrophy at the last endoscopy). On the other hand, antral gastritis showed a tendency to heal (13 of 24 patients had normal or only slightly gastritic antrum at the last endoscopy).

Conclusions: The observations indicate that the H. pylori plays a role in and associates closely with the long-term course of angular or corpus GU disease and is related to the tendency of these ulcers to recur.     

Apoptosis in Different Compartments of Antrum and Corpus Mucosa in Chronic Helicobacter pylori Gastritis. An 18-Year Follow-up Study

Background: The association of apoptosis was analysed in three different compartments (foveolar cells- FC, proliferating zone-PZ and glandular part-GP) of antrum and corpus mucosa specimens with development of atrophy and the extent of apoptosis as depending on grade of chronic inflammation, activity of gastritis and Helicobacter pylori colonization at two time points of an 18-year follow-up in an adult population from Saaremaa, Estonia, with a high prevalence of H. pylori infection were compared. Methods: A total of 68 persons (31 men, 37 women; median age, 39 years in 1979) from a primary sample of 304 subjects, endoscoped in 1979 and reinvestigated by endoscopy and biopsy in 1997, were included in the study. The state of the gastric mucosa and the presence of H. pylori in the antrum and corpus mucosa were assessed in accordance with the Sydney system. The dynamics of apoptotic index (AI) between two time points in 1979 and 1997 was evaluated in antrum biopsies of 49 persons and in corpus biopsies of 64 persons. Apoptosis was measured using terminal deoxyuridine nucleotide nick end labelling (TUNEL) histochemistry. Results: The antrum as well as the corpus of 2/68 persons were H. pylori negative at both time points. Atrophy developed in 9/68 persons in the antrum and in 23/68 in the corpus. In PZ and GP of the corpus mucosa as well as in GP of the antrum mucosa, AI decreased significantly during 18 years compared with initial values (P < 0.05), which was not associated with development of atrophy. In all compartments of the antrum and corpus mucosa, studied at the initial and end points of observation, AI did not reveal a difference in persons with and without development of atrophy (P > 0.05). In the samples of 1979 the highest independent effect on the value of AI in the FC compartment for the antrum was exerted by grade of activity of gastritis (P = 0.01) and in GP by degree of chronic inflammation (P = 0.03), while in the samples of 1997 the highest effect was exerted by grade of H. pylori colonization (P = 0.02 and 0.03 in FC and GP, respectively). For the corpus mucosa AI was most strongly affected also by grade of activity of gastritis in FC compartment (P = 0.02) and by degree of chronic inflammation in PZ (P = 0.04), but not by grade of H. pylori colonization. Conclusion: AI was not associated with development of atrophy, but was largely dependent on grade of activity of gastritis and degree of chronic inflammation; in the antrum mucosa AI depended also on grade of H. pylori colonization.     

High acid secretion may protect the gastric mucosa from injury caused by ammonia produced by Helicobacter pylori in duodenal ulcer patients

The aim of the present study was to investigate the mechanism by which gastric atrophy does not tend to occur in patients with duodenal ulcer despite frequent Helicobacter pylori infection. This investigation was performed in 60 patients with duodenal ulcer and 63 age-matched gastritis patients. Endoscopic findings in the antrum and corpus were classified as normal, atrophic and superficial changes. Biopsy specimens were taken from the antrum and corpus. Ninety per cent of patients with duodenal ulcer and 63.5% of patients with gastritis had H. pylori infection (P<0.01). The incidence of normal findings in duodenal patients was 30% in antral regions and 50% in the corpus (P<0.05). Atrophic change was observed in 21.7% of patients in the antrum and 3.3% of patients in the corpus (P<0.01). The grade of inflammation in duodenal ulcer specimens was significantly higher in the antrum than in the corpus (P<0.01). >H. pylori density was significantly higher in the antrum than in the corpus in ulcer patients (P<0.01). No significant difference in endoscopic findings, >H. pylori density or the grade of inflammation was found between the antrum and corpus in patients with gastritis. The mean intragastric ammonia concentration was 10.3 mg/dL in duodenal ulcer patients and 6.2 mg/dL in gastritis patients (P<0.01). The mean pH was 3.5 and 4.6 in ulcer and gastritis specimens, respectively (P<0.01). Our data suggest that gastric mucosa injury is less frequently associated with duodenal ulcers than with gastritis due to the low >H. pylori density in the corpus and to the higher acid output that neutralizes the ammonia produced by H. pylori.     

Stem Cell Factor Expressed in Human Gastric Mucosa in Relation to Mast Cell Increase in Helicobacter pylori-Infected Gastritis

We previously reported mast cell increases in H. pylori gastritis. To determine the mechanism, we investigated the kinetics of mast cells and mast cell growth factor (stem cell factor, SCF) in H. pylori-positive and -negative gastric mucosa. Biopsy specimens from 12 H. pylori-negative and 28 positive subjects were examined. Sections were stained for mast cells, proliferating cell nuclear antigen (PCNA), and SCF. Densities of mast cells, PCNA-positive mast cells, and SCF-positive cells were significantly greater in H. pylori-positive than -negative subjects. SCF was expressed in mast cells and fibroblasts. The density of SCF-positive fibroblasts increased in H. pylori-positive gastritis and decreased after cure of infection. SCF mRNA was detected in H. pylori-positive gastric mucosa. Fibroblasts isolated from the normal gastric mucosa expressed SCF mRNA after incubation with H. pylori water extract. SCF may be one of the factors for mast cell increase. Fibroblasts may participate in mast cell increase and inflammation in H. pylori infection.     

Characterization of the Gastric Cardia in Volunteers from the General Population

The aim of this research was to characterize the mucosa of the gastric cardia in relation to infection with Helicobacter pylori and the occurrence of chronic gastritis in other parts of the stomach in a sample of the general population. In this study, 80 adult volunteers underwent esophagogastroscopy with biopsies from the gastric cardia, corpus, and antrum. Gastritis was classified according to the Sydney system. Chronic gastritis (cardia excepted) was diagnosed in 35 subjects, 30 with H. pylori infection. Epithelial proliferative activity (Ki-67), p53- and p21 expression were examined quantitatively with cell counting after immunohistochemical stainings. Esophagitis was diagnosed macroscopically. Fourty eight subjects had cardia-type and 32 corpus-type mucosa in the anatomical cardia. The prevalence of esophagitis (nine cases) did not differ between these groups. Carditis was more prevalent among subjects with cardia-type mucosa (73 vs. 28%, P < 0.0001). H. pylori was present in 48% of those with cardia-type and 25% of those with corpus-type mucosa (P = 0.06). Of the 44 subjects with carditis, 31 had H. pylori in this location. The group with H. pylori infection had significantly higher mucosal proliferative activity when compared to uninfected subjects. Among the subjects with H. pylori-associated carditis, more p53-positive epithelial cells were detected compared to both the non-infected group (P = 0.0004) and to subjects with non-H. pylori-associated carditis (P = 0.03). In subjects with cardia-type mucosa, and both carditis and gastritis, the degree of chronic inflammation was higher in the cardia compared to the corpus and antrum and the p53 expression was significantly higher in the cardia compared to the corpus, but similar to that in the antrum. The proliferative activity was significantly higher in the antrum compared to the cardia and corpus, respectively. In conclusion, H. pylori infection, carditis, and increased p53 expression are more common in subjects with cardia- than corpus-type mucosa in the gastric cardia. Carditis is mainly related to H. pylori infection. There are some differences regarding inflammation, proliferative activity, and p53 expression between the cardia and other regions of the stomach, yet the significance of these differences remains to be clarified.     

Helicobacter pylori Infection,Pattern of Gastritis,and Symptoms in Erosive and Nonerosive Gastroesophageal Reflux Disease

Background: The aim of this study was to evaluate the prevalence of Helicobacter pylori infection and the characteristics of gastritis and symptoms of patients with erosive and nonerosive gastroesophageal reflux disease (GERD). Methods: We studied 202 consecutive patients with a diagnosis of GERD (symptoms score and endoscopy): group A (n = 110), erosive GERD; group B (n = 92), nonerosive GERD; 200 patients with upper abdominal complaints without abnormalities at endoscopy (functional dyspepsia, group C); and 200 asymptomatic controls tested for H. pylori serum antibody (group D). Antral and body biopsy specimens were taken for histology and the rapid urease test in groups A, B, and C. Results: The prevalence of H. pylori infection was higher in groups B and C (62% and 55%, respectively) than in A and D (36% and 40%) (P &lt; 0.05). In positive patients H. pylori colonization and gastritis grade scores in the gastric body were higher in nonerosive than in erosive GERD and functional dyspepsia (P &lt; 0.05). No differences in H. pylori colonization or gastritis grades were found in the antrum. Fifty-nine patients with nonerosive GERD (64%) and 42 with erosive GERD (38%) showed other dyspeptic symptoms associated with reflux symptoms (P &lt; 0.05). Conclusions: H. pylori prevalence is higher in patients with nonerosive GERD than in normal subjects and in patients with erosive GERD and similar to that of patients with dyspepsia. Patients with nonerosive GERD often show dyspeptic symptoms and higher H. pylori colonization and inflammation grades in the proximal stomach. Our data support the hypothesis that in GERD H. pylori gastritis may, on the one hand, protect against the development of esophageal erosions and, on the other, contribute to the esophageal hypersensitivity to acid which is a feature of GERD.     

Serum Gastrin and Mucosal Somatostatin in Helicobacter pylori-Associated Gastritis

Aims: The aims were to study serum gastrin concentrations and gastric mucosal somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter pylori infection. Methods: We measured basal serum gastrin concentrations and somatostatin and gastrin concentrations in antral mucosal biopsy specimens and somatostatin concentrations in corpus biopsy specimens in 88 consecutive dyspeptic subjects undergoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pangastritis, H. pylori-positive antral gastritis with normal body histology, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test. Results: Basal serum gastrin concentrations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with controls (mean ± SEM: 72 ± 7, 46 ± 10, and 42 ± 7ng/l, respectively). Subjects with pangastritis or antral gastritis had significantly lower antral somatostatin concentrations than controls (mean ± SEM: 0.80 ± 0.07, 1.03 ± 0.15, and 2.40 ± 0.31 μg/g(protein), respectively). We also found significantly lower antral mucosal gastrin concentrations in subjects with pangastritis and in those with antral gastritis only as compared with controls (mean ± SEM: 62 ± 13, 78 ± 16, and 165 ± 25 μg/g(protein), respectively). In subjects with pangastritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis only and controls. Conclusion: These results suggest that hypergastrinemia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a key role in the origin of hypergastrinemia. Furthermore, in patients with pangastritis a corpus mucosal somatostatin deficiency was found.     

Pathogenetic role of the tyrosine-phosphorylated CagA EPIYA sequence of Helicobacter pylori in histological gastritis in Japanese patients

Background   Helicobacter pylori (H. pylori) CagA protein plays an important role in the clinical outcome of gastritis treatment. Tyrosine phosphorylated Glu-Pro-Ile-Tyr-Ala motif in CagA (CagA-P) plays a critical role in the morphological transformation of cells. Aim  We examine the relationship between serum titer of anti-CagA-P antibody and gastric inflammation as well as the status of the CagA-P expression in gastric mucosa. Methods  Fasting sera from 127 dyspeptic patients were collected, and anti-CagA-P antibody was evaluated. Gastric biopsy specimens were collected and histological gastritis was evaluated. We investigate the expression of CagA-P in human gastric mucosa by Western blotting and immunohistochemistry. Results  The titers of anti-CagA-P antibodies in the sera of H. pylori (+) patients were significantly higher than those of H. pylori (–) patients (P < 0.001). In 107 H. pylori (+) patients, anti-CagA-P titer was statistically higher in patients with high gastritis scores in the corpus than in those with low scores (P < 0.05). CagA-P expression was detected in the foveolar epithelium of the H. pylori infected gastric mucosa. Conclusion  CagA-P is an antigen-peptide against the host, and serum titer of anti-CagA-P antibody may be a new marker for gastritis in the corpus. Grant support: Tsuchiya Medical Foundation.     

Enhanced levels of C-X-C chemokine,human GROα, in Helicobacter pylori-associated gastric disease*

C-X-C Chemokines play an important role for neutrophil extravasation through microvessels. Although the level of interleukin (IL)-8 is known to increase in the Helicobacter pylori-infected gastric mucosa, another C-X-C chemokine, GROα, has not been evaluated in the H. pylori-associated gastric mucosal injury. The present study was designed to investigate gastric contents of GROα in relation to those of IL-8 in the gastric mucosa of H. pylori-infected peptic ulcer patients. Thirty-eight patients with gastric ulcer and 41 with gastritis underwent endoscopy with informed consent and 49 were found to be H. pylori positive and 30 H. pylori negative. Biopsies from the gastric corpus were performed in each patient to examine the H. pylori colonization by bacterial culture, the rapid urease test and histological specimens as well as measurement of the contents of human GROα and IL-8. Helicobacter pylori infection was eradicated in 21 patients by triple therapy (lansoprazole 30mg, amoxycillin 2.0g, clarithromycin 600 mg; 2 weeks). The samples for GROα and IL-8 assay were homogenized in 0.02% aprotinin containing phosphate-buffered solution and the mucosal contents of GROα and IL-8 in the supernatants were quantified by sandwich enzyme immunoassay methods. The levels of GROα and IL-8 in H. pylori-positive gastric mucosa were significantly higher than those in the H. pylori-negative mucosa. There was a significant linear correlation between the levels of GROα and IL-8 (r= 0.798, P < 0.01). After the eradication of H. pylori by the triple therapy, the levels of GROα and IL-8 were significantly decreased. The GROα showed an increase in the H. pylori-positive gastric mucosa in a similar fashion as IL-8 contents, suggesting a pathogenetic role for GROα in H. pylori-associated gastric mucosal injury.     

Gastric mucosal plasminogen activators inHelicobacter pylori infection

Long-termH. pylori associated gastritis is recognized as a pathogenic factor in gastric carcinogenesis. In gastric carcinomas the amount and activity of the tissue-type plasminogen activator (t-PA) have been reported to be decreased, whereas those of the urokinase-type plasminogen activator (u-PA) were increased, contributing to the neoplastic and invasive process. The present study was performed to determine t-PA and u-PA levels and activity in gastric mucosa from 102 patients and to investigate whether these levels are influenced byH. pylori infection. The antigen concentration and activity of t-PA and u-PA in corpus mucosa were low (P<0.001) compared with those in antral mucosa, although for the u-PA activity this did not reach statistical significance. InH. pylori-associated antral gastritis the mucosal t-PA antigen concentration and activity were found to be decreased (P<0.001) compared with normal mucosa, whereas inH. pylori-associated pangastritis the corpus t-PA levels were not affected. The antigen concentration and activity of u-PA were found to be significantly (P<0.005) increased, both inH. pylori-associated gastritis of antrum and corpus mucosa. Levels of u-PA in histologically normal corpus mucosa of patients with anH. pylori-associated antral gastritis were also found to be increased (P<0.05). In conclusion, the alterations in the plasminogen activator profile found inH. pylori-associated gastritis, ie, a decrease in t-PA and an increase in u-PA, show a similar tendency as the previously found alterations in gastric carcinomas, which provides additional support for the possible involvement ofH. pylori-associated gastritis in the pathogenesis of gastric carcinoma.     

The Clinical Course and Prognostic Determinants of Non-Ulcer Dyspepsia: A Literature Review

Background: The long-term course of Helicobacter pylori gastritis is not well known because there are few follow-up studies available, and the follow-up time has been short. Methods: The progression of H. pylori infection and chronic gastritis was retrospectively examined in 102 patients followed up for 32 years. In all patients a blind suction biopsy from the corpus mucosa was taken in 1952, and an endoscopic re-examination with biopsy specimens from the antrum and corpus was performed in 1983. Results: In the first examination 85 patients (83%) were H. pylori-positive as assessed from Giemsa-stained corpus mucosa specimens as compared with 70 H. pylori-positive patients (69%) at the end of the follow-up (1983). Two of the 17 patients who were initially H. pylori-negative became positive in 1983, implying an infection rate of 0.4% per patient-year. On the other hand, 17 of the 85 patients who were initially H. pylori-positive became negative in 1983, representing a disappearance rate of 0.6%. However, the stomach became completely normal in only eight cases, which represents a healing rate of 0.3% per patient-year. All patients with duodenal ulcer disease were H. pylori-positive at the first examination and remained so during the follow-up. In these patients chronic gastritis affected predominantly the antral mucosa, and corpus atrophy did not develop. Parietal cell antibodies appeared during the follow-up in six cases, and five of them were H. pylori-positive at the first examination. In most of these cases gastritis progressed into severe grades of corpus atrophy accompanied by the disappearance of H. pylori infection and normalization of the antral mucosa. Conclusions: New H. pylori infection and complete healing of infected mucosa may occur in adult life, but this is rare. Duodenal ulcer disease is associated with persistent H. pylori infection and absence of corpus atrophy. The appearance of parietal cell antibodies leads to progression of corpus atrophy and disappearance of H. pylori.     

Association Between Gastric Atrophy and Helicobacter pylori Infection in Japanese Children: A Retrospective Multicenter Study

The purpose of this study was to determine whether Helicobacter pylori infection and mucosal inflammation result in gastric atrophy in Japanese children. A total of 196 patients ages 1–16 years were retrospectively studied: 131 patients were infected with H. pylori and 65 patients were uninfected. Antral (n = 196) and corpus biopsy specimens (n = 70) were investigated based on the Updated Sydney system. In both the antrum and corpus, H. pylori-infected patients showed significantly higher degrees of inflammation and activity of gastritis, compared with noninfected patients. The prevalence of grade 2 or 3 atrophy in the antrum was 10.7% in H. pylori-infected patients and 0% in the noninfected patients (P < .01) and in corpus 4.3% and 0%, respectively (P = .20). The frequency of intestinal metaplasia in the 2 study groups was 4.6% and 4.6% in the antrum and 0% and 4.2% in the corpus, respectively. Among H. pylori-infected patients, the antrum showed significantly higher degrees of H. pylori density, inflammation and activity of gastritis, and atrophy than the corpus. In the antrum, atrophy was significantly correlated with activity, whereas in the corpus, atrophy correlated with H. pylori density, inflammation, and activity. H. pylori-induced gastric inflammation can cause atrophy in Japanese children, predominantly in the antrum. It remains to be determined whether H. pylori-infected children with gastric atrophy are at increased risk for gastric cancer.     

Gastric epithelial proliferation and p53 and p21 expression in a general population sample: relations to age,sex, and mucosal changes associated with H. pylori infection

Helicobacter pylori infection is the main cause of chronic gastritis. The infection has been linked to altered proliferative activity and changes in various cell cycle regulating proteins. To determine, in a general population sample, the proliferative activity and expression of p53 and p21 in males and females of different age groups with and without H. pylori-associated chronic gastritis, gastric biopsies from 273 subjects (188 with and 85 without H. pylori infection) randomly selected from a general population were examined immunohistochemically for Ki-67, p53, and p21. One thousand epithelial cells, including the surface, neck, and glandular areas, were counted in both the corpus and the antrum. Results are expressed as the percentage of positive cells. Subjects with H. pylori infection showed significantly increased proliferative activity and expression of p53 compared to uninfected individuals. Regarding the expression of p21, no difference was detected. Multiple linear regression analysis showed significant associations between chronic inflammation or inflammatory activity, on the one hand, and the degree of proliferation in both the corpus and the antrum, on the other hand. In the antrum, the degree of H. pylori colonization was related to the expression of p53. H. pylori seems to cause increased proliferation and increased expression of p53 (but not p21) in the gastric mucosa, neither of which is age or sex dependent. The proliferative activity is related mainly to events associated with inflammation, while the expression of p53 in the antrum is associated with the degree of H. pylori infection. The action of p53 appears to be independent of p21 activity.     

Omeprazole Therapy for Helicobacter pylori Infection

To determine whether omeprazole eradicates Helicobacter pylori infection of the gastric antrum, six adolescents and one adult with H. pylori colonization of the antrum were entered into a clinical, open trial of medical therapy. Histologic evidence of antral gastritis and three complementary methods to document H. pylori colonization of the stomach (silver stain, urease testing, and culture of antrum) were obtained before and after an 8-week course of omeprazole. In vitro susceptibility to omeprazole and restriction endonuclease analysis were performed on H. pylori isolates obtained from patients before and after omeprazole therapy. Each of the seven patients treated with omeprazole had continued active inflammation in the antrum and one or more features indicative of persisting H. pylori colonization. Minimum inhibitory concentrations and DNA fingerprints of H. pylori isolated after therapy were identical to those of the pre-treatment bacterial isolates in each of the four subjects examined. We conclude that omeprazole therapy alone did not eradicate H. pylori infection of the human antrum. Continued bacterial colonization was not related to either acquired bacterial resistance to the drug or reinfection of the stomach with a different H. pylori strain.     

Gastric mucosa in Mongolian and Japanese patients with gastric cancer and Helicobacter pylori infection

AIM: To investigate the characteristics of gastric cancer and gastric mucosa in a Mongolian populationby comparison with a Japanese population.METHODS: A total of 484 Mongolian patients with gastric cancer were enrolled to study gastric cancer characteristics in Mongolians. In addition, a total of 208 Mongolian and 3205 Japanese consecutive outpatients who underwent endoscopy, had abdominal complaints, no history of gastric operation or Helicobacter pylori eradication treatment, and no use of gastric secretion inhibitors such as histamine H2-receptor antagonists or proton pump inhibitors were enrolled. This study was conducted with the approval of the ethics committees of all hospitals. The triple-site biopsy method was used for the histologic diagnosis of gastritis and H. pylori infection in all Mongolian and Japanese cases. The infection rate of H. pylori and the status of gastric mucosa in H. pylori-infected patients were compared between Mongolian and Japanese subjects. Age(± 5 years), sex, and endoscopic diagnosis were matched between the two countries.RESULTS: Approximately 70% of Mongolian patients with gastric cancer were 50-79 years of age, and approximately half of the cancers were located in the upper part of the stomach. Histologically, 65.7% of early cancers exhibited differentiated adenocarcinoma, where as 73.9 % of advanced can cersdisplayed undifferentiated adenocarcinoma. The infection rate of H. pylori was higher in Mongolian than Japanese patients(75.9% vs 4 8. 3 %, P0.0001). When stratified by age, the prevalence was highest among young patients, and tended to decrease in patients aged 50 years or older. The anti-East-Asian Cag Aspecific antibody was negative in 99.4% of H. pyloripositive Mongolian patients. Chronic inflammation, neutrophil activity, glandular atrophy, and intestinal metaplasia scores were significantly lower in Mongolian compared to Japanese H. pylori-positive patients(P 0.0001), with the exception of the intestinal metaplasia score of specimen from the greater curvature of the upper body. The type of gastritis changed from antrumpredominant gastritis to corpus-predominant gastritis with age in both populations.CONCLUSION: Gastric cancer was located in the upper part of the stomach in half of the Mongolian patients; Mongolian patients were infected with non-East-Asiantype H. pylori.     

Helicobacter pylori infection accelerates human gastric mucosal cell proliferation

Helicobacter pylori causes chronic atrophic gastritis and intestinal type gastric cancer arises against a background of atrophic gastritis. Increased proliferation of epithelial cells is an important indicator of increased risk for gastric adenocarcinoma. We investigated gastric mucosal cell proliferation inH. pylori-associated gastritis and the effect of eradication therapy on this proliferation in 45 patients endoscopically diagnosed (31 with persistent eradication and 14 in whomH. pylori) recurred.H. pylori status was determined by culture and histology in biopsied specimens from the gastric antrum and corpus. Eradication of the infection was defined as reversal to negative on both tests. In vitro Ki-67 immunostaining of endoscopic biopsy specimens was used to measure mucosal cell proliferation inH. pylori-associated gastritis before and after therapy. The proliferative zone was defined as the distance of Ki-67-positive gastric epithelial cells between the highest and the lowest cells. In patients in whomH. pylori was eradicated, cell proliferation in both the antral and corpus mucosa had decreased 4 weeks after completion of the eradication therapy (P<0.01,P<0.001), and 6 months later, it had markedly decreased (P<0.05,P<0.05) and returned to normal. In patients in whomH. pylori recurred, only antral epithelial cell proliferation was reduced 4 weeks after eradication therapy, but whenH. pylori recurred, determined by culture and histology, cell proliferation level was the same as that before eradication. These results suggest thatH. pylori infection accelerates cell proliferation in gastric mucosa and may play a causal role in the chain of events leading to gastric carcinoma.     

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.     

Helicobacter pylori infection induces a decrease in immunoreactive-somatostatin concentrations of human stomach

Immunoreactive-somatostatin (ir-somatostatin) concentrations of the gastric mucosa and gastric juice withHelicobacter pylori infection were measured in the human stomach. One hundred seventy-one patients (106 males, 65 females;, mean age, 52.0; range, 19–84 years) were registered. Gastric juice and mucosa were obtained with the usual endoscopy procedure. Somatostatin concentration was measured by radioimmunoassay. The irsomatostatin concentrations in theH. pylori-negative group were significantly higher than in the positive group gastric mucosa, whereas its levels in gastric juice tended to decrease withH. pylori infection. There was an inverse correlation between luminal ammonia levels and ir-somatostatin concentrations of the gastric mucosa. On the other hand, ir-somatostatin concentrations of the gastric mucosa significantly decreased with chronic and active inflammatory change. This decrease was not correlated with the grade of active inflammation, which was in close relation, toH. pylori infection, but with the grade of chronic inflammation. These results indicate thatH. pylori may reduce ir-somatostatin concentrations of the human stomach and that its effect is partly mediated via luminal ammonia produced byH. pylori.