Campylobacter associated gastritis in patients with non-ulcer dyspepsia.

Gastric biopsy specimens from 109 patients with non-ulcer dyspepsia were retrospectively examined. Sixty one patients had gastritis and there was a strong correlation with the presence of Campylobacter pyloridis. Ninety eight per cent were positive in large numbers for C pyloridis by histological examination or by culture, or both. Of 48 patients with normal histological results, 21 had evidence of C pyloridis by histological examination or culture, or both, but in small numbers. It is concluded that there is a quantitative rather than a qualitative association between C pyloridis and gastritis.     

Prevalence of lymphoid follicles and aggregates in Helicobacter pylori gastritis in antral and body mucosa.

AIMS--To evaluate the prevalence of lymphoid follicles and aggregates in the antral and body mucosa in Helicobacter pylori gastritis and to assess if there were correlations with ulcers in the duodenum, pylorus, or stomach, and with chronic antral erosions. METHODS--Patients (n = 2692) with histologically confirmed H pylori antral gastritis were investigated. These comprised five groups: those with duodenal ulcers; those with pyloric ulcers; those with gastric ulcers; those with chronic erosions; and those with no associated lesions. In 1446 cases at least two additional biopsy specimens from the oxyntic mucosa were available. RESULTS--Lymphoid follicles and aggregates were found in 53.8% of cases in the antral mucosa compared with 14.8% in the oxyntic mucosa (p < 0.001). The various diseases showed significant differences in terms of the prevalence of follicles and aggregates: The highest numbers in the antral mucosa as well as the lowest in the oxyntic mucosa were found in patients with duodenal ulcers (60.5% and 9.2%, respectively). The highest numbers of follicles and aggregates in the oxyntic mucosa occurred in patients with gastric ulcers. CONCLUSIONS--The detection of lymphoid follicles and aggregates in oxyntic mucosa and the higher prevalence in antral mucosa fits well with the distribution of primary gastric lymphomas. This adds further weight to the notion that the development of follicles and aggregates, triggered by H pylori, might be an early precursor to gastric lymphoma. The differences between the groups investigated might be due to different strains of H pylori or differences in the respective sizes of antral and oxyntic mucosa.     

Duodenal bulb biopsy findings for patients with non-ulcer dyspepsia with or without Campylobacter pylori gastritis

Duodenal bulb biopsy specimens from 85 patients with non-ulcer dyspepsia (30 of whom had normal stomachs and 52 of whom had Campylobacter pylori gastritis) were examined for the presence and amount of gastric surface epithelial metaplasia (using both the hematoxylin and eosin stain and the Alcian blue-periodic acid-Schiff method), acute inflammation, and C. pylori (using the Giemsa stain). Gastric metaplasia occurred in the duodenal bulb in 61% of patients with gastric C. pylori and in an identical percentage for those who lacked C. pylori gastritis. For patients with gastric metaplasia, foci of metaplastic cells were seen in 70% of their bulb biopsy fragments. The Alcian blue-periodic acid-Schiff stain was superior to the hematoxylin and eosin stain for detecting gastric metaplasia. Only one of 33 patients without gastric C. pylori had gastritis and duodenitis. Fourteen of 52 (27%) patients with C. pylori gastritis had duodenitis; C. pylori was seen in the duodenal biopsy specimens from 13 of these patients. The organisms were often few, requiring oil immersion microscopy for detection. Each patient with duodenitis had gastric metaplasia, but some of these metaplastic foci were not inflamed. When present in the duodenum of patients with C. pylori gastritis, gastric metaplasia, acute inflammation, and C. pylori are typically patchy. Hence, several biopsy fragments of the duodenal bulb would be required for studies designed to determine the effectiveness of compounds used to treat C. pylori duodenitis.     

Long-term follow up of patients with gastritis associated with Helicobacter pylori infection.

The aim of this study was to evaluate the long-term prognosis for patients suffering from gastritis associated with Helicobacter pylori infection, and in particular the proportion of cases progressing to peptic ulcer. The study was carried out in one urban general practice. One hundred and three patients who had presented with dyspepsia over the 1973-80 period and who were found to have a macroscopically normal endoscopy were reassessed between seven and 14 years later. Gastric antral biopsies had been taken routinely at endoscopy and were subsequently re-examined for the presence of H pylori. The patients' medical records were examined to establish their consulting rates over the follow-up period and whether they suffered from any other medical conditions. Patients were interviewed to assess the course of their dyspeptic symptoms. Comparison of patients who were unequivocally H pylori positive with those who were negative revealed no significant differences in the consultation rate for gastroenterological symptoms, in the proportion of patients referred to a hospital consultant or for further gastroenterological investigations or in the proportion reporting that their symptoms had improved. However, a statistically highly significant relationship was found between H pylori infection and hypertension. The results of this study have shown that there is a good prognosis for non-ulcer dyspepsia whether or not H pylori infection is present. The association between H pylori gastritis and hypertension clearly merits further investigation.     

Distinct B-cell clonal bands in Helicobacter pylori gastritis with lymphoid hyperplasia

Helicobacter pylori (Hp)-associated gastritis is a risk factor for gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Clonal B-cell populations are present in both reactive and neoplastic MALT tissue, thus limiting their usefulness in the evaluation of gastric lymphoid infiltrates in endoscopic biopsy specimens. The aim of this study was to identify the presence of clonal B-cell populations in Hp-gastritis with MALT and to assess their usefulness in distinguishing reactive from malignant infiltrates. Routinely fixed paraffin-embedded blocks from 20 patients with Hp-gastritis with lymphoid hyperplasia were analysed for B-cell clonality by a semi-nested polymerase chain reaction (PCR) using FRIII/LJH and FRIII/VLJH primers for amplification of the VDJ region of the immunoglobulin heavy chain gene. The histopathological findings were evaluated according to a previously published scoring system. Immunohistochemistry was performed by the labelled streptavidin-biotin technique using the following primary antibodies: CD45, CD45RO, CD3, CD20, and cytokeratin. The histopathological findings were diagnostic of Hp-chronic active gastritis (grade 2, n=17; grade 3, n=3). Scattered intraepithelial B-cells were present in all cases and non-destructive lymphoepithelial lesions in one grade 3 case. Amplifiable DNA was obtained from all samples. Clonal bands were observed in ten (7/17 grade 2 and 3/3 grade 3 lesions) and polyclonal smears in ten cases (all grade 2). The clonal bands were often (n=6) associated with a background polyclonal smear and were not reproducible from deeper sections (n=10) or another paraffin block (n=1), while the clonal bands in control low-grade MALT lymphomas were not associated with a background smear and were reproducible from deeper sections. None of the patients has developed lymphoma to date (follow-up 21-44 months). In conclusion, B-cell clonal bands are common in H. pylori-gastritis with lymphoid hyperplasia. The irreproducibility of these bands is a useful feature in favouring a reactive process.     

Serological response to Helicobacter pylori recombinant antigens in Chilean infected patients with duodenal ulcer, non-ulcer dyspepsia and gastric cancer

We have previously cloned 10 Helicobacter pylori antigen genes from a Chilean strain including: cytotoxin VacA, a truncated region of CagA (called A17), a species-specific protein (Ag26), urease subunits (UreA, UreB), a flagellin, (FlaB), heat shock proteins (HspA and HspB), an adhesin (HpaA) and a lipoprotein (Lpp20). Immunogenicity of these antigens was tested by immunoblot with sera of Chilean infected patients, revealing that HpaA, A17, HspB and VacA were more frequently recognized (86%, 82%, 68% and 68%, respectively). According to the clinical condition, it was determined that Lpp20 was preferentially recognized by sera from non-ulcer dyspepsia patients (80%), A17 and VacA by patients with duodenal ulcer (92% and 83% respectively), and HspB by patients with duodenal ulcer (83%) and gastric cancer (90%). An ELISA was developed with a purified mixture of A17 and VacA antigens to test the different groups of patients. It was found that sera from duodenal ulcer patients showed higher values than those from non-ulcer dyspepsia patients, but this difference was not significant (p<0.2). Moreover, sera from gastric cancer patients showed values lower than those from non-ulcer dyspepsia patients (p<0.019). These results indicate that, in the Chilean population, antibodies raised against VacA and A 7 are not markers either for duodenal ulcer or for gastric cancer.     

High prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic Hispanics.

In this study, we estimated the prevalence of Helicobacter pylori infection and histologic gastritis in 58 asymptomatic Hispanic adult volunteers (mean age, 41 years; 59% male) by endoscopic biopsy of the upper gastrointestinal tract. Forty-six subjects (79%) were found to harbor H. pylori in gastric biopsies, and all had histologic gastritis. Four other subjects were found to have gastritis in the absence of H. pylori. Similar prevalences of H. pylori and gastritis were noted in all age groups and also in American-born and immigrant Hispanics. Biopsy data and serologic studies of H. pylori antibodies correlated well. We conclude that H. pylori infection is an almost universal finding in the gastric mucosa of asymptomatic adult Hispanics, regardless of age. The clinical significance of these findings is unknown, but we speculate that H. pylori and its associated gastritis could have a role in the high incidence of gastric carcinoma in Hispanic populations.     

Mast cells in Helicobacter pylori associated antral gastritis

Mast cells are known to be effector cells in various inflammatory reactions, but their role in gastritis is unclear. The present study was undertaken to investigate the extent of mast cell involvement in antral gastritis with and without Helicobacter pylori (H. pylori) infection and thus evaluate the possible role of mast cells in the pathogenesis of H. pylori-associated gastritis. Antral mucosal biopsies were taken from 212 subjects with symptoms suggestive of acid peptic disease. Sections were assessed for inflammation. Modified Giemsa stain was used to detect H. pylori infection and 1% toluidine blue to count mast cells. Mast cell counts were significantly higher in the antral mucosa even in H. pylori-negative gastritis (68.4 +/- 6.7/mm2), as compared to normal non-inflamed mucosa (45.7 +/- 5.8/mm2) (P < 0.05). However, with H. pylori infection, the mucosal mast cell count were markedly increased (123.8 +/- 4.7/mm2) as compared to normal mucosa (P < 0.01). and H. pylori-negative gastritis (P < 0.01) this increase was noticed uniformly in patients with H. pylori-positivity, irrespective of the presence or absence of a peptic ulcer. After cure of H. pylori infection, the mast cell density decreased significantly (44.9 +/- 4.6/mm2) to reach levels that were similar to those in normal mucosa. There was a positive correlation between the antral mucosal mast cell density and polymorphonuclear and mononuclear cell infiltration (rs = 0.61). H. pylori infection, and 0.73 respy. It was concluded that could be responsible for increasing the mast cell density in the gastric antrum. Probably by inducing castain mucosal cytokine.     

Distribution of vacA alleles and cagA status of Helicobacter pylori in peptic ulcer disease and non-ulcer dyspepsia

The occurrence of cagA and vacA alleles among Helicobacter pylori isolates from Turkish patients and their relationship with ulcer disease outcome was investigated. Among isolates from 47 patients with peptic ulcer disease and 51 patients with non-ulcer dyspepsia, 72.3% and 44.4%, respectively, were cagA-positive (p 0.019). Most (88.8%) isolates were typed as vacA s1, and all of these were subtype s1a. The commonest (51.0%) vacA genotype was s1a m1. The results of multivariate analysis indicated that infection with cagA-positive H. pylori was the only variable associated with an increased risk of peptic ulcer disease (odds ratio, 3.01; 95% confidence interval, 1.27-7.10; p 0.012).     

Absence of benefit of eradicating Helicobacter pylori in patients with nonulcer dyspepsia.

BACKGROUND: The relation between Helicobacter pylori infection and nonulcer dyspepsia is uncertain. We tested the hypothesis that curing the infection will relieve symptoms of dyspepsia. METHODS: We randomly assigned 170 H. pylori-infected patients with nonulcer dyspepsia to receive twice-daily treatment with 20 mg of omeprazole, 1000 mg of amoxicillin, and 500 mg of clarithromycin for 14 days and 167 such patients to receive identical-appearing placebos; all patients were then followed through regular visits for 12 months. Symptoms were scored on diary cards for seven days before each visit. A carbon-13 urea breath test was performed at base line and repeated at 1 and 12 months, and endoscopic biopsy was performed at 12 months to determine H. pylori status. Treatment was considered successful if the patient had only mild pain or discomfort or none at all. RESULTS: The rate of eradication of H. pylori infection was 90 percent in the active-treatment group and 2 percent in the placebo group at four to six weeks (P<0.001). At 12 months, there was no significant difference between groups in the rate of successful treatment (46 percent in the active-treatment group and 50 percent in the placebo group; relative likelihood of success with active treatment, 0.93; 95 percent confidence interval, 0.73 to 1.18; P=0.56). There was also no significant difference in the rate of successful treatment at 12 months between patients who were H. pylori-negative and those who were H. pylori-positive (48 percent vs. 49 percent). The rates of successful treatment were also similar when patients were analyzed according to the type of dyspepsia (ulcer-like, reflux-like, or dysmotility-like) and changes in the quality of life. There was no significant association between treatment success and histologic improvement in chronic gastritis at 12 months (P=0.68). CONCLUSIONS: We found no evidence that curing H. pylori infection in patients with nonulcer dyspepsia leads to relief of symptoms.     

Helicobacter heilmannii gastritis: association with acid peptic diseases and comparison with Helicobacter pylori gastritis.

We analyzed 2 antral and 1 corpus full-thickness random endoscopic gastric mucosal samples obtained from 946 patients with duodenal ulcers (6077 biopsies) and from 281 patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (1794 biopsies). We stained tissue sections with hematoxylin and eosin and Warthin-Starry silver stain and immunostained them with polyclonal antibodies against Helicobacter pylori. Hematoxylin- and eosin-stained sections from 6 patients with Helicobacter heilmannii (18 biopsies) and 23 randomly selected patients with H. pylori (68 biopsies) were evaluated and semiquantitated for the presence of acute inflammation, chronic inflammation, glandular atrophy, intestinal metaplasia, H. pylori, H. heilmannii, lymphoid follicles, or vasodilatation. Additional specimens were obtained for H. pylori culture, a CLO test, and serologic examination. H. heilmannii was detected in 6 (0.49%) of 1227 patients (14 [0.18%] of 7871 biopsies). Of these, 4 (0.42%) of 946 were patients with duodenal ulcers (9 [0.15%] of 6077 biopsies), and 2 (0.71%) of 281 were patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (5 [0.28%] of 1794 biopsies). We found H. heilmannii with hematoxylin and eosin stain, Warthin-Starry stain, and immunoperoxidase stain for H. pylori. Culture for H. pylori was negative in the four patients with duodenal ulcers. The CLO and serologic tests were positive in three of five and five of five patients, respectively. Our results indicate that H. heilmannii, like H. pylori, is associated with peptic ulcer disease (both active and inactive gastritis) and that it preferentially colonizes the gastric antrum. The severity of the H. heilmannii-associated gastritis is less intense and lymphoid aggregates are less common than in H. pylori-associated gastritis. Morphologic detection seems to be the method of choice for detecting H. heilmanni. Immunoperoxidase stain specific for H. pylori also stains H. heilmannii, indicating cross-reacting antigenic epitopes between H. heilmannii and H. pylori.     

Increased gastric epithelial cell proliferation in Helicobacter pylori associated follicular gastritis.

AIMS: An increase in the proliferative state of the gastric epithelium has been attributed to infection with Helicobacter pylori. In order to obtain a more precise estimate of the magnitude of this change, the proliferative state of 17 cases of florid H pylori associated follicular gastritis was examined using the antibody MIB-1. METHODS: Comparable results were produced from control and gastritis cases by using a combination of two reproducible measures of the labelled cells. Dividing cells in the gastric mucosa are concentrated within a proliferating compartment, situated at the base of the crypts. This compartment was measured and expressed as a proportion of the total crypt length. The proportion of positively labelled cells within the compartment was also counted. RESULTS: The proliferation compartment in the gastritis cases occupied 45.6% of the gastric crypt compared with 15.4% in the control group. Of the cells in the proliferating compartment, 79.5% were positively labelled in the gastritis cases and 33.4% in the control group. CONCLUSIONS: The convoluted nature of the gastric crypt does not make it a forgiving experimental model. The use of long lengths of mucosa obtained from gastrectomy specimens permitted the production of consistent results, using a morphometric method. The greater than 100% difference in the proportion of proliferating cells between the two groups suggests that further investigation is warranted.     

Histology of chronic gastritis with and without duodenitis in patients with Helicobacter pylori infection.

AIM: To compare the histological characteristics of Helicobacter pylori positive chronic gastritis in patients with and without associated duodenitis. METHODS: Gastric mucosal biopsy specimens were obtained from patients undergoing endoscopy for dyspepsia. Severity of gastritis and density of H pylori infection were graded according to the Sydney system. RESULTS: Of the 69 patients studied, 15 had normal histology, 22 had chronic gastritis only (77.3% H pylori positive), 21 had duodenitis (90.5% H pylori positive), and 11 had other diagnoses. In the H pylori positive patients, the median gastritis score was higher in the duodenitis group (6, range 3-9) than in the chronic gastritis only group (5, range 2-8), because of greater neutrophil activity scores in patients with duodenitis (median score 2 v 1). There were no differences in the density of H pylori infection, inflammation, atrophy, or intestinal metaplasia between patients with chronic gastritis only and those with duodenitis. CONCLUSIONS: These results suggest that H pylori positive patients with duodenitis have a more severe form of gastritis than those without associated duodenal inflammation. This is because of increased neutrophil activity, which seems to be independent of the density of H pylori infection.     

In patients with Helicobacter pylori gastritis and functional dyspepsia, a biopsy from the incisura angularis provides useful diagnostic information

The aim of this study was to assess whether the taking of an additional biopsy from the incisura angularis increases the chance of detecting maximal degrees of atrophy and intestinal metaplasia (IM) in patients with Helicobacter pylori gastritis and functional dyspepsia. At entry into a randomised trial, biopsies were taken from 328 patients (mean age 48 years), two from both the gastric antrum and corpus, and one from the incisura angularis, and comparative grading of gastritis variables was carried out. Biopsy material from the gastric antrum, corpus, and the incisura angularis revealed no notable differences in atrophy or an incidence of IM and mucosa-associated lymphatic tissue. However, when the incisura biopsies were classified histologically, 58% contained antral mucosa (AM), 18% corpus mucosa (CM), and 24% intermediate zone mucosa. AM at the incisura was associated with considerably more severe gastritis in both the incisura and antrum (14% atrophy, 20% IM) than in CM of incisura (2% atrophy, 6% IM). Corpus atrophy and IM were rare in the AM group and absent from the CM group. Incisura angularis biopsy in patients with H. pylori gastritis and functional dyspepsia does give additional information regarding the severity of gastritis expected in the corpus and antrum. Antral-type mucosa in the incisura angularis region seems to indicate an increased risk for the development of atrophy and/or IM.     

Polymorphism of IL-1RA and TNF-alpha genes in patients with Helicobacter pylori associated gastritis and duodenal ulcer

The goal of this work was to determine the frequency of major types of polymorphism in the genes of interleukin-1 receptor antagonist (IL-1RA) and TNF-alpha in patients with Helicobacter pylori-associated gastritis and duodenal ulcer and elucidate its correlation with clinical manifestation of the disease. A total of 126 patients were selected for the study with different gastroduodenal pathologies and H. pylori detected in biopsy material. The obtained data indicate a possible correlation between the risk of developing duodenal ulcer and the presence of the allele A in the TNF-alpha gene at the ?308 position in the patients. Polymorphism analysis of the IL-1RA gene revealed a statistically significant difference in the availability of the 2/L genotype in the studied groups of patients. The conducted research demonstrates that a parallel typing of the H. pylori virulence genes and determination of the cytokine gene polymorphism in the biopsy material taken from the patient is required for characterization of the bacterium-host interaction.     

Helicobacter felis gastritis in gnotobiotic rats: an animal model of Helicobacter pylori gastritis.

The gastric spirillum Helicobacter felis, originally isolated from the cat stomach, colonizes the stomachs of germfree rats. Studies were designed to examine the pathological and serological responses of germfree rats inoculated orally with H. felis. At 2 weeks postinoculation, the gastric mucosa of germfree rats had lymphocytes and eosinophils scattered in small foci throughout the subglandular region of the antrum. Small numbers of lymphocytes were present in the subglandular portion of the antral mucosa that focally extended through the lamina propria towards the luminal surface. Eight weeks postinoculation, the inflammation was confined to the antrum. It was characterized by increased numbers of lymphocytes and eosinophils in the subglandular areas, with focal aggregates of lymphocytes in the submucosa. Some lymphoid aggregates extended from the submucosa through the muscularis mucosa and lamina propria to the luminal surface. H. felis was demonstrated with the Warthin-Starry stain, bacterial culture, and urease assay, particularly in the antrum. H. felis also produced a significant immunoglobulin G antibody titer at 2, 4, and 8 weeks postinoculation as well as a transitory immunoglobulin M response at 2 to 4 weeks postinoculation. Contact control rats were not infected, inferring that fecal-oral spread of H. felis did not occur.     

Russell body gastritis associated with Helicobacter pylori infection: a case report

An unusual and rare gastric mucosal lesion histologically consisting of a localised accumulation of Russell bodies and Russell body-containing plasma cells, the so-called Mott cells, has been recognised only recently and termed as "Russell body gastritis". This lesion, despite its densely monomorphous appearance is easily confirmed to be non-neoplastic by its polyclonal immunoreactive pattern to immunoglobulin light chains. However, the aetiology of Russell body gastritis is controversial and hence the optimal treatment for this disease has not been established. Two cases of Russell body gastritis associated with Helicobacter pylori infection are reported, and the possible role of H pylori infection in the pathogenesis is discussed.