Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Effects of Helicobacter pylori eradication on the natural history of lymphocytic gastritis

BACKGROUND: Lymphocytic gastritis is characterised by an accumulation of lymphocytes in the surface epithelium of the stomach. Lymphocytic gastritis has been linked to coeliac disease and Helicobacter pylori infection. AIMS: To determine whether H pylori eradication leads to resolution of the lymphocytic infiltrate and clinical improvement in patients with lymphocytic gastritis, and to determine their HLA status. METHODS: The Leeds Dyspepsia Questionnaire (LDQ) was administered to 13 patients with lymphocytic gastritis. H pylori serology, (13)C urea breath test (UBT), and upper gastrointestinal endoscopy with sampling of the duodenum, antrum, and corpus were done in all cases and the HLA status was determined. Eleven patients had at least one positive test for H pylori. Patients with lymphocytic gastritis and H pylori infection were treated with a one week course of omeprazole, clarithromycin, and metronidazole. Gastric and duodenal intraepithelial lymphocyte (IEL) counts were performed, along with histological assessment of gastric and duodenal biopsies before and after H pylori eradication. RESULTS: Two months after treatment there was a significant reduction in gastric IEL counts in both antrum and corpus. There was no significant change in duodenal IEL counts before and after eradication. According to the Sydney grading there was significant improvement in corpus inflammation after eradication. The patients histologically H pylori positive before treatment became H pylori negative. Dyspepsia scores also improved significantly after treatment. CONCLUSIONS: H pylori eradication treatment in patients with lymphocytic gastritis causes significant improvement in the gastric IEL infiltrate, corpus inflammation, and dyspeptic symptoms. H pylori serology is frequently positive when histology and UBT are negative. Lymphocytic gastritis may represent a specific immune response to H pylori infection.     

Noninvasive tests as a substitute for histology in the diagnosis of Helicobacter pylori infection

BACKGROUND: Rapid urease tests for Helicobacter pylori have a sensitivity of 80% to 90%. Therefore histologic examination of gastric biopsies is recommended as a "backup" diagnostic test in rapid urease test-negative patients. However, noninvasive tests (urea breath test, serology, whole blood antibody tests) may provide a more rapid diagnosis and be less expensive but offer similar accuracy. METHODS: Sixty-seven patients (no prior treatment for H pylori, no proton pump inhibitors, antibiotics, or bismuth within 4 weeks) undergoing endoscopy for evaluation of dyspepsia symptoms and testing rapid urease test-negative by antral biopsy were enrolled. All had the following tests: gastric biopsies (2 antral, 1 fundus; H&E and Alcian Yellow stain) examined for gastritis and H pylori; (13)C-UBT; capillary blood for whole blood rapid antibody tests: FlexSure HP, QuickVue, AccuStat, and Stat-Simple Pylori; serum for FlexSure HP; HM-CAP enzyme-linked immunoassay. H pylori infection was diagnosed (reference standard) if chronic gastritis was present on histology and at least 2 of the 3 following tests were positive: urea breath test, H pylori organisms unequivocally demonstrated in biopsies on special stain, and/or enzyme-linked immunoassay. The test and treatment costs per patient were calculated. RESULTS: Of 67 patients with a negative rapid urease test, 4 were positive for H pylori. None had active peptic ulcer disease. Histology only identified 1 patient with organisms visible on special stain. Using chronic active gastritis (neutrophilic and mononuclear infiltrate) as a diagnostic criterion for H pylori, 6 patients would have been judged positive. However, only 2 of these were truly positive by the reference standard (positive predictive value 33%). Negative predictive value for presence of organisms and chronic active gastritis was 95% and 97%, respectively. All of the noninvasive tests identified all 4 truly positive patients correctly. Urea breath test and FlexSure whole blood assay yielded a substantial number of false-positive results (positive predictive value 31% and 36%, respectively); positive predictive value for the other tests ranged from 50% to 80%. All tests except histology had a negative predictive value of 100%. Histology was the most costly test (p < 0. 001 compared with all other tests), followed by urea breath test and HM-CAP serology (p < 0.001 compared with all rapid antibody tests). CONCLUSIONS: Whole blood or serum antibody testing is a rapid, accurate, and cost-effective means for establishing H pylori status in rapid urease test-negative patients. Whole blood or serology rapid antibody testing should substitute for histology when the patient has not been previously treated for H pylori.     

Histological analysis of gastritis and Helicobacter pylori infection in patients with early gastric cancer: a case-control study

BACKGROUND AND AIMS: Infection with Helicobacter pylori is associated with an increased risk of gastric adenocarcinoma. However, most patients with H. pylori infection will not develop gastric cancer. The aims of the present study were to examine which histological features, including H. pylori infection, would increase the risk of gastric cancer using a case-control study. METHODS: Three gastric biopsy specimens were taken from 72 patients with early gastric cancer and 72 age- and sex-matched control subjects. The grade of gastritis was examined according to the updated Sydney System. The presence of H. pylori infection was determined by serology and histology. Odds ratio (OR) of developing gastric cancer was calculated for H. pylori positivity and histological features using conditional logistic regression. For patients with H. pylori infection, histological features in cancer patients and control subjects were compared. RESULTS: The OR of the presence of mononuclear cell infiltration in the corpus and intestinal metaplasia in the angulus were significantly elevated. The grade of mononuclear cell infiltration in the corpus and antrum was significantly higher in both types of cancer patients than controls. Glandular atrophy and intestinal metaplasia were increased in patients with intestinal-type cancer in the angulus and antrum. Bacterial density in the corpus and polymorphonuclear cell infiltration in the antrum were increased in patients with diffuse-type cancer. CONCLUSIONS: Severe chronic gastritis induced by H. pylori infection seems to be associated with diffuse-type gastric cancer. Glandular atrophy and intestinal metaplasia, which occur in gastric mucosa with chronic inflammation, are significantly associated with intestinal-type cancer.     

Non-endoscopic diagnosis of multifocal atrophic gastritis; efficacy of serum gastrin-17, pepsinogens and Helicobacter pylori antibodies

BACKGROUND/AIMS: Infection with H. pylori is an important risk factor for the development of gastric cancer and glandular atrophy is an intermediate stage in gastric carcinogenesis. While screening the patients with atrophic gastritis by endoscopy is unrealistic, a concept of "serological gastric biopsy" based on measurement of gastric secretory proteins and peptides should be further validated. We sought to determine if the laboratory panel composed of serum PGI and protein stimulated gastrin-17 might select patients with MAG, and what is diagnostic significance of H. pylori serology in population of high prevalence of H. pylori infection. MATERIAL AND METHODS: 55 consecutive patients of both sexes (M/F 25/30; range of age 55 -81 years) were referred for gastroscopy with antrum and corpus mucosal biopsies. Patients with histological signs of glandular atrophy at any site of the stomach were considered to have multifocal atrophic gastritis. A first blood sample was collected for measurement of basal gastrin-17, pepsinogens and H. pylori IgG-antibodies, and second was taken 20 minutes after use of protein-rich drink to measure stimulated gastrin-17. RESULTS: Signs of mucosal atrophy were found in 19 patients, while 29 patients showed non-atrophic gastritis and seven H. pylori-negative patients had no histological pathology. Low serum level of stimulated gastrin-17 (< 5 pmol/l) and/or pepsinogen I (< 50 microg/l), were found in 16 of 19 patients (84.2%) with and in 7 of 36 patients (19.4%) without atrophy in the histological study. Combining of H. pylori serology with serum levels of secretory peptides had no significant effect on diagnostic sensitivity of the test panel. CONCLUSION: The test panel composed of pepsinogen I and protein stimulated gastrin-17 may be used as the "serological gastric biopsy" detecting multifocal atrophic gastritis. The diagnostic sensitivity of this test panel is not increased by knowledge of H. pylori status.     

Serum anti-Lewis X antibody is associated with VacA seropositivity but not atrophic gastritis in patients with Helicobacter pylori infection

OBJECTIVES: Lipopolysaccharides of Helicobacter pylori have an antigenic structure that mimics Lewis X occurring in gastric mucosa. The pathogenic role of antigenic mimicry in H. pylori-induced gastritis has been of recent interest. The aim of this study was to examine the relevance of anti-Lewis X antibody in the development of atrophic gastritis in H. pylori infection. METHODS: A total of 72 patients were studied. Serum samples were collected to measure IgG antibodies to H. pylori, CagA, VacA and Lewis X. Biopsy specimens were obtained from the antrum and the corpus to examine the grade and the type of atrophic gastritis. RESULTS: Mean anti-Lewis X antibody titres were higher in 38 VacA-seropositive patients than in 13 seronegative patients (P < 0.05). The difference was not significant between patients with diffuse-type atrophic gastritis and those with multi-focal type. No significant correlation was observed between the titre of anti-Lewis X antibody and the grade of glandular atrophy, whereas CagA seropositivity was associated with glandular atrophy. CONCLUSIONS: Anti-Lewis X antibody may play a role in persistent gastric inflammation, particularly in VacA-seropositive H. pylori infection. However, anti-Lewis X antibody does not seem itself to be associated with atrophic gastritis in patients with H. pylori infection.     

Atrophic Gastritis Serum Levels of Amidated Gastrin-17 and Pepsinogen I in Atrophic Gastritis: An Observational Case-Control Study

Background: Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed nonendoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing. Methods: The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method. Results: A low S-PGI (<25 μg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori -associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori -related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; CI 95%: 81%-97%) had a low SPGI and/or a low S-G-17prand with positive H. pylori serology. Such low values were found in 3 of the 44 control patients (7%; CI 95%: 0%-14%). Conclusions: Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori .     

Diagnosis of Helicobacter pylori gastritis in children using the 13C urea breath test

The clinical recognition of Helicobacter pylori gastritis in children with recurrent abdominal pain is difficult. We assessed the value of a simplified 13C urea breath test (13C-UBT) in a selected group of children with nocturnal waking and disruptive recurrent abdominal pain who fulfilled criteria for endoscopy. Gastric antral biopsies were examined histologically and by the quick urease test and were compared with H. pylori serology and the 13C-UBT in a prospective study of 50 children referred to a tertiary center. Thirty-two patients had gastritis and of these, 19 had histologically proven H. pylori gastritis. Seventeen of these 19 patients had a positive 13C-UBT. The sensitivity and specificity of the 13C-UBT compared with the histologic diagnosis of H. pylori was 89 and 90% respectively. The 13C-UBT was more specific than the H. pylori serology. The 13C-UBT using two breath collections is a reliable and noninvasive diagnostic test for H. pylori infection in children.     

Detecting Helicobacter pylori infection in hospitalized frail older patients: the challenge

OBJECTIVES: Helicobacter pylori infection has not been well studied in older people, especially in hospitalized, frail patients. The aim of our study was to evaluate the prevalence of the infection in this population using five H. pylori diagnostic tests. DESIGN: Prospective observational study. SETTING: Geriatric acute care unit of the Department of Geriatrics (H?pital Xavier Arnozan, Pessac, France). PARTICIPANTS: One hundred seven consecutively hospitalized patients with a diagnostic indication for upper gastrointestinal endoscopy. MEASUREMENTS: Geriatric assessment, information on drug intake, indication/results of gastric endoscopy, and results of H. pylori infection diagnostic tests (culture and histological analysis on biopsy specimens, serology, 13carbon-urea breath test (13C-UBT), detection of H. pylori stool antigens (HpSA)) were assessed for each included patient. RESULTS: Fifty-one patients (47.7%) were H. pylori positive with at least one test. 13C-UBT was more frequently positive than the other four tests, with a significant difference from culture, histological analysis, and HpSA (P <.05). Positive 13C-UBT results were significantly associated with H. pylori presence using histological analysis and neutrophil activity of the antrum and corpus. Antibiotic treatments significantly decreased the positivity rate of all of the tests performed, and severe corpus atrophy decreased the positivity rate of culture, histological analysis, and HpSA. CONCLUSIONS: Almost one-third of the H. pylori-positive patients would have remained undetected without performing the 13C-UBT. The low prevalence of H. pylori detection in these hospitalized, frail patients may be explained by the high frequency of current and previous antibiotic treatments.     

Prevalence of Helicobacter pylori infection and gastric cancer precursor lesions in patients with dyspepsia

BACKGROUND: Helicobacter pylori infection has been considered to play significant role in gastric carcinogenesis, but only a minority of people who harbor this organism will develop gastric cancer. H. pylori infection first causes chronic non atrophic gastritis. Chronic non atrophic gastritis may evolve to atrophic gastritis and intestinal metaplasia and finally to dysplasia and adenocarcinoma. AIMS: To estimate the prevalence of H. pylori infection and the precancerous gastric lesions and their relationship, in patients with dyspeptic symptoms who underwent upper gastrointestinal endoscopy at a reference center in the central region of Rio Grande do Sul state, Brazil. METHODS: We analyzed gastric biopsies taken from corpus and antrum of patients who underwent upper gastrointestinal endoscopy for H. pylori detection, between 1994 and 2003. According to Sydney system, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed by histological examination (H-E stain). The histological diagnoses were related to H. pylori infection status. RESULTS: Biopsies from 2,019 patients were included in the study. Patients mean age was 52 (+/-15) and 59% were female. Seventy six percent had H. pylori infection. Normal mucosa, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed in 5%, 77%, 3% and 15%, respectively. The OR for any degree of gastric mucosa lesion in infected patients was 10 (CI95% 6.50 - 17%). The OR for infected patients had chronic non atrophic gastritis was 3 (CI95% 2,2 - 3,4). The OR for infected patients had atrophic gastritis or intestinal metaplasia was less than 1. CONCLUSIONS: The prevalence of H. pylori infection in this population was high (76%) and infected individuals had the probability 10 folds greater than non infected individuals to have any lesion of gastric mucosa. The prevalence of precancerous lesions was 77% for non atrophic chronic gastritis, 3% for atrophic gastritis and 15% for intestinal metaplasia. Infected patients had risk 3 folds greater than non-infected for the occurrence of non atrophic chronic gastritis. H. pylori infection did not show risk for occurrence of atrophic gastritis and intestinal metaplasia, suggesting that other risk factors should be involved in the carcinogenesis process.     

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and Hpylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylon positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.     

High frequency of helicobacter negative gastritis in patients with Crohn's disease.

The frequency of gastric Crohn''s disease has been considered low. This study was undertaken to determine the prevalence of chronic gastritis and Helicobacter pylori infection in patients with Crohn''s disease. Oesophagogastroduodenoscopy was performed on 62 consecutive patients suffering from ileocolonic Crohn''s disease. Biopsy specimens from the antrum and corpus were processed for both histological and bacteriological examinations. H pylori antibodies of IgG and IgA classes were measured in serum samples by enzyme immunoassay. Six patients (9.7%) were infected with H pylori, as shown by histology, and in five of them the infection was also verified by serology. Twenty one patients (32%) had chronic H pylori negative gastritis (negative by both histology and serology) and one of them also had atrophy in the antrum and corpus. Granulomas were found in four patients. The characteristic appearance of H pylori negative gastritis was focal and mostly mild inflammation resembling the inflammatory changes seen in the gut in Crohn''s disease. Patients with H pylori negative chronic gastritis had a significantly more active disease in their gut than those with normal gastric mucosa (p < 0.01). It is concluded that H pylori positive gastritis is rare, while H pylori negative gastritis is relatively common in patients with Crohn''s disease. H pylori negative ''Crohn''s gastritis'' seems to be associated with active Crohn''s disease.     

How to determine the diagnosis of Helicobacter pylori infection in the elderly?

PURPOSE: The real prevalence of Helicobacter pylori (H. pylori) infection is difficult to determine in the elderly because of the frequency of drug intake (antibiotics or anti-secretory drugs). The aim of this study was to evaluate the diagnostic performance of five tests in the elderly. METHODS: The study population consisted of consecutive patients undergoing a routine endoscopy between August 1998 and December 1999. We evaluated the diagnostic performance of four tests in all of the included patients: culture and histology of biopsy specimens, serology (ELISA) and urea breath test (13C-UBT). Detection of H. pylori antigens in stool samples (HpSA) was realized in a subgroup. Patients were considered H. pylori + when result for culture was positive or when two tests were positive. RESULTS: One hundred and sixty-seven patients were included in this study (55 men, 112 women; mean age: 85.6 +/- 5.1 years). Only 38 (22.8%) patients were H. pylori+. Test performances showed the following results: serology sensitivity: 90.9% (IC 95%: 75.6-98.1) versus 86.9% (IC 95%: 63.6-96.9) for culture versus 77.8% (IC 95%: 60.8-89.9) for histology and 74.3% (IC 95%: 56.7-87.5) for 13C-UBT. Eighty-nine (53.3%) took antibiotics or anti-secretory drugs, only 13C-UBT performances decreased significantly (sensitivity: 94.4% [72.7-99.8] versus 52.9% [27.8-77]; P < 10(-6)). When gastric or duodenal ulcer were endoscopically diagnosed in older patients, both histology and 13C-UBT could not improve the diagnosis of H. pylori infection. HpSA was realized in 107 patients (sensitivity: 74.1%, specificity: 98.7%). We showed no statistical difference between HpSA performances and drug intake. CONCLUSION: Diagnostic performances decreased in older patients especially because of drug intake.     

Apparent Reversal of Early Gastric Mucosal Atrophy after Triple Therapy for Helicobacter pylori

Helicobacter pylori may be difficult to detect in individuals with intestinal metaplasia or atrophic gastritis, even though bacteria may persist in the mucosa in low numbers, maintaining elevated serum H. pylori antibody levels. We report a patient with marked, endoscopically visible gastric mucosal changes and focal changes of histological atrophic gastritis, who was negative for H. pylori on urease test, culture, and histology, but had positive H. pylori serology. When treated with triple therapy and reassessed at 6 months, his H. pylori antibody titer fell to low/negative levels, abnormal mucosa was replaced by a velvety, normal lining, and the previous evidence of histological atrophic gastritis was no longer detectable.     

Role of Helicobacter pylori and autoimmunity in serological atrophic corpus gastritis in a Dutch primary care community

BACKGROUND: Atrophic corpus gastritis predisposes to vitamin B12 deficiency and gastric cancer. Little is known about the seroprevalence of atrophic corpus gastritis in the general population of Western Europe. AIM: To investigate the seroprevalence of atrophic corpus gastritis in a West-European primary care community in relation to Helicobacter pylori infection and autoimmunity. METHODS: Nine hundred and ninety-seven consecutive persons attending one general practice were asked to participate in the study by completing a questionnaire and donating fasting blood. Gastrin, pepsinogen A and C, and antibodies to H. pylori and parietal cells were measured by well-validated immunological methods. Criteria for serological atrophic corpus gastritis were pepsinogen A < 17 microg/l, pepsinogen A/C ratio <1.6, and gastrin >100 ng/l. RESULTS: Thirty-four participants (3.4%) fulfilled the serological criteria of atrophic corpus gastritis. Twenty-one of them (62%) and 17 of 34 (50%) age-matched and sex-matched nested controls were H. pylori positive [NS; odds ratio, 1.62 (0.62-4.24)], while 15 of them (44%) and one of 34 controls had antibodies to parietal cells [P < 0.005; odds ratio, 24.0 (3.00-201)]. CONCLUSIONS: The seroprevalence of atrophic corpus gastritis in this primary care community is 3.4%. When compared with controls, the approximate relative risk of having atrophic corpus gastritis was significantly higher (P < 0.025) for antibodies to parietal cells (24.0) than to H. pylori (1.62). In view of the decreasing risk of H. pylori infection in the western world, it is likely that the impact of H. pylori on the development of atrophic corpus gastritis will further diminish.     

Anti Helicobacter pylori IgG and IgA response in patients with gastric cancer and chronic gastritis

BACKGROUND/AIMS: Immune response against Helicobacter pylori is important for the course and outcome of infection. We conducted study looking for the difference in anti H. pylori IgG and IgA between patients with intestinal type of gastric cancer, superficial and atrophic gastritis. METHODOLOGY: For this study, 133 patients infected with H. pylori were enrolled: 50 with superficial gastritis, 42 with atrophic gastritis and 41 with gastric cancer. Anti H. pylori IgG and IgA ELISA tests were performed. The difference in antibody titers of IgG and IgA, frequency of IgA > IgG ratio and combination of low IgG and IgA > IgG ratio were analyzed. RESULTS: The patients with gastritis had higher titer of IgG that the patients with gastric cancer (p < 0.01). The patients with superficial gastritis had higher titer of IgA than the patients with gastric cancer (p < 0.05). IgA > IgG ratio is more frequent in patients with gastric cancer than in the patients with superficial gastritis (p < 0.01). Low IgG and IgA > IgG is more frequent in the patients with gastric cancer than in the patients with gastritis (p < 0.01). CONCLUSIONS: The patients with gastric cancer elicit different anti H. pylori IgG and IgA response than the patients with superficial and atrophic gastritis. Low IgG and IgA predominance seems characteristic for gastric cancer.     

Helicobacter pylori Infection and Gastric Neoplasia: Correlations With Histological Gastritis and Tumor Histology

Objective: Several authors have reported an association between Helicobacter pylori ( H. pylori ) and gastric carcinoma, but the data are conflicting. Atrophic gastritis and intestinal metaplasia (IM) have also been linked to gastric carcinoma, especially the intestinal tumor type. We investigated the relationship between H. pylori infection, gastric neoplasms, and histological gastritis.
Methods: A total of 105 patients with gastric carcinoma, 36 patients with gastric adenoma, and 105 age- and sex-matched control subjects were examined for H. pylori infection and histological gastritis. H. pylori status was evaluated by Giemsa staining and IgG serology. Mucosal inflammation, atrophy, and IM were evaluated in biopsy specimens from antrum and corpus.
Results: H. pylori seroprevalence was higher in patients with gastric carcinoma (98 of 105, 93%) and adenoma (34 of 36, 94%) than in control subjects (82 of 105, 71%,   p < 0.05  ). H. pylori was more prevalent in patients with noncardia (OR, 5.67; 95% CI, 2.25–14.44) than cardia (OR, 5.20; 95% CI, 0.65–41.68) tumors. Histologic types and tumor stage (early; OR, 6.60; 95% CI, 2.23–19.69, advanced; OR, 4.27; 95% CI, 1.21–15.03) showed no difference in H. pylori prevalence. Atrophy and IM scores were higher in patients with the intestinal- but not diffuse-type of carcinoma and adenoma than in H. pylori -positive control subjects. Smoking was associated with gastric carcinoma (OR, 3.05; 95% CI, 1.58–5.93) but not alcohol or coffee use, blood group A, or a family history of gastric cancer.
Conclusions: Our results confirm a strong association between H. pylori and gastric carcinoma and adenoma. The intestinal-type gastric carcinoma is associated with atrophic gastritis and IM.     

Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy

BACKGROUND: Atrophic gastritis has been shown to be one of the long term sequelae of Helicobacter pylori infection. AIMS: To determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological methods for revealing atrophy, and to define the association of H pylori infection with atrophic gastritis in these patients. PATIENTS/METHODS: A total of 207 consecutive outpatients referred for gastroscopy were included. Biopsy specimens from the antrum and corpus were assessed histologically according to the Sydney system. Serum samples were studied for H pylori IgG and IgA antibodies by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence. RESULTS: Histological examination revealed atrophic gastritis in 52 (25%) of 207 patients. H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with atrophic corpus gastritis. Low serum pepsinogen I was the most sensitive and specific indicator of moderate and severe atrophic corpus gastritis. All six patients with moderate atrophic corpus gastritis had H pylori infection but eight of 10 patients with severe atrophic corpus had increased parietal cell antibodies and nine had no signs of H pylori infection. CONCLUSIONS: Atrophic antral gastritis was strongly associated with CagA positive H pylori infection. Severe atrophic corpus gastritis was not determined by H pylori tests but low serum pepsinogen I, high gastrin, and parietal cell antibodies may be valuable in detecting these changes.     

Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis

OBJECTIVE: Although it is widely accepted that Helicobacter pylori (H. pylori) infection is an important cause of atrophic gastritis, few studies have examined the relationship between H. pylori-induced atrophic gastritis and the occurrence of reflux esophagitis. The present study was aimed to examine the relationship between H. pylori infection, atrophic gastritis, and reflux esophagitis in Japan. METHODS: A total of 175 patients with reflux esophagitis were compared with sex- and age-matched 175 control subjects. Diagnosis of H. pylori infection was made by gastric mucosal biopsy, rapid urease test, and serum IgG antibodies. Severity of atrophic gastritis was assessed by histology and serum pepsinogen I/II ratio. RESULTS: H. pylori infection was found in 59 (33.7%) patients with reflux esophagitis, whereas it was found in 126 (72.0%) control subjects. The grade of atrophic gastritis was significantly lower in the former than in the latter. Among the H. pylori-positive patients, atrophic gastritis was milder in the patients with reflux esophagitis than in the patients without it. CONCLUSIONS: These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.     

Simplified single sample 13Carbon urea breath test for Helicobacter pylori: comparison with histology, culture, and ELISA serology.

There is no ideal method for detecting Helicobacter pylori. The 'standard' 13Carbon urea breath test (13C-UBT), which involves collecting eight to 15 breath samples and subsequent costly analysis, was modified by pooling 21 samples of expired breath taken at five minute intervals for 40 minutes into a collecting bag, from which a single 20 ml aliquot was taken and analysed by mass spectrometry. This test was evaluated on 50 patients after routine upper gastrointestinal endoscopy, and results were compared with those from the standard 13C-UBT, bacteriology, ELISA serology, and histology--the latter being taken as the gold standard. H pylori were seen in 34 of 50 (68%) patients (in three it was detected in biopsy specimens from the corpus alone). The modified 13C-UBT was positive (pooled excretion delta 13CO2 greater than 5 per mil) in 31 patients and negative in 19 (three false negative results), specificity was 100% (standard 13C-UBT 94%) and sensitivity 92% (standard 13C-UBT 93%). The modified 13C-UBT had a coefficient of variation within subjects of 3.7%. For the ELISA serology and culture the specificities were both 100%, but the sensitivities were 82% and 68% respectively. The 13C-UBT results correlated with the grade of histological gastritis. The modified 13C-UBT is simpler, cheaper, more reproducible, and provides an easy non-invasive method for the detection of H pylori.