Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia

OBJECTIVES: Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus. METHODS: From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined. RESULTS: All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%). CONCLUSIONS: H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.     

Antral gastritis in chronic alcoholism. Role of cirrhosis and Helicobacter pylori

OBJECTIVES: Antral gastritis is frequent in alcoholics. The role of H. pylori in the pathogenesis of gastritis in these patients is not well known. The aim of our study was to study the role of H. pylori and cirrhosis in the pathogenesis of antral gastritis in alcoholic patients. METHODS: Seventy-nine patients were included in the study. All underwent upper gastrointestinal tract endoscopy with antral biopsies, independently of the presence of abdominal pain, and had serological examination for H. pylori antibodies. RESULTS: Cirrhosis and gastritis were present in 50 and 40 patients respectively, H. pylori serological assay and histological identification of the bacterium were positive in 35 (44%) and 19 (24%) patients respectively. Discrepancy between the 2 tests were observed more frequently in cirrhotic patients. A positive serology with a negative histologic examination for H. pylori was present for 18 cirrhotic and 4 noncirrhotic patients (p < 0.05). A gastritis without evidence of H. pylori was more frequent in cirrhotic than in noncirrhotic patients. H. pylori was histologically present in 11 of 29 cirrhotic patients and in 8 of the 11 noncirrhotic patients with a gastritis (p < 0.05). CONCLUSIONS: Discrepancies between histological examination and H. pylori serology in patients with cirrhosis might be due to the inhospitable environment for H. pylori in case of portal hypertension; the positive serology could be in relation with a past infection.     

Construction and characterization of a Helicobacter pylori clpB mutant and role of the gene in the stress response

Antiserum raised against whole Helicobacter pylori cells identified a novel 94-kDa antigen. The nucleotide sequence of the gene encoding the 94-kDa antigen was determined, and analysis of the deduced amino acid sequence revealed structural features typical of the ClpB ATPase family of stress response proteins. An isogenic H. pylori clpB mutant showed increased sensitivity to high-temperature stress, indicating that the clpB gene product functions as a stress response protein in H. pylori.     

The morphological diagnosis of Helicobacter pylori in the gastric mucosa in chronic gastritis]

JC virus (JCV), a human polyomavirus, is the agent of the demyelinating disease progressive multifocal leukoencephalopathy (PML). JCV exists in four main genotypes in the USA. Type 1, including subtypes Type 1A and Type 1B, makes up about 64% of strains in the USA and is thought to be of European origin. Type 2 is found in Asia, and Type 3 in Africa. A fourth type is found only in the USA. In general, these genotypes differ in 1-2.5% of their DNA sequence. Thirty MS patients and 30 paired controls from Budapest were studied. The clinical course of MS was mainly secondary progressive, and patients were stable at the time of testing. Most of the controls were relatives of the probands: a spouse, parent, or child. Overall, 25 of 60 (42%) of the urines tested positive for JCV by PCR. These included 13 of 30 MS patients, and 12 of 30 controls. Genotyping in the VPI gene showed all 25 JCV strains to be Type 1. Among the MS patients, seven were Type 1A and six were Type 1B. Among the controls, nine were Type 1A and three were Type 1B. In five pairs of MS patients and controls, both were positive for JCV by PCR. Two of these were husband/wife pairs of which one pair was matched for subtype (both Type 1A), and the other was not. Two of them were mother/daughter pairs, and both were matched for subtype (both Type 1B). These findings demonstrate that JCV Type 1 predominates among Hungarians, and suggest that parent/child pairs can be used to trace JCV transmission within the MS family.     

Helicobacter pylori infection, gastritis, and the temperature of choice for hot drinks

A 44-year-old male presented with a solitary cerebellopontine angle (CPA) metastasis from lung cancer. His initial symptoms were vertigo and hearing loss beginning 5 months after the diagnosis of the primary cancer. Two months later, right facial paresis developed. His neurological deterioration was rapid. Magnetic resonance (MR) imaging with enhancement disclosed the CPA tumor. The tumor was partially removed through the retroauricular retromastoid approach. Histological examination of the specimen revealed adenocarcinoma. The characteristic rapidly progressive symptoms and MR imaging with enhancement are the most sensitive and essential examinations for this lesion.     

The prevalence of Helicobacter pylori gastritis in patients with reflux oesophagitis: a case-control study

Head and neck cancers (HNCs) are malignancies that can be induced by tobacco use, although host-specific factors such as the DNA repair capacity (DRC) may modulate individual susceptibility to tobacco carcinogenesis. To test the hypothesis that genetically determined DRC modulates HNC susceptibility, we measured the DRC in the peripheral blood lymphocytes of 55 patients with newly diagnosed, previously untreated HNC and 61 healthy controls by the host-cell reactivation assay using a reporter gene damaged by benzo(a)pyrene diol epoxide, an ultimate tobacco-related carcinogen. The mean DRC was significantly lower in cases (8.6%) than it was in controls (12.4%; P < 0.001). The DRC was an independent risk factor for HNC (P < 0.01); those in the middle and lowest tertiles of DRC had increased odds ratios [2.17 (95% confidence interval, 0.74-6.39) and 4.27 (confidence interval, 1.45-12.5), respectively] for HNC. These findings suggest that individuals with reduced DRC may be at increased risk of developing HNC.     

Gastric mucosal hepatocyte growth factor in Helicobacter pylori gastritis and peptic ulcer disease

OBJECTIVES: Hepatocyte growth factor (HGF) is increasingly recognized for its role in a variety of hepatic and systemic diseases. Its relationship to gastritis has not been studied. We aimed at measuring gastric mucosal HGF levels in the presence or absence of Helicobacter pylori gastritis, in peptic ulcers, and in response to H. pylori eradication. METHODS: Fifty one patients were studied. Patients were not entered if they had liver disease, malignancy, or any systemic illness. HGF was measured in gastric antral incubates using an enzyme-linked immunosorbent assay. Assessments were repeated 6 wk after a 2-wk course of anti-H. pylori triple therapy in 12 patients. Code numbers were used for blinding. RESULTS: The median gastric mucosal HGF level was 36 ng/gm/tissue in patients with H. pylori gastritis (n = 33) compared with 19 ng/gm in 18 negative controls (p = 0.0024), 18 ng/gm after the eradication of H. pylori (p = 0.021), 23 ng/gm in all patients with ulcers (n = 10), and 26 ng/gm/tissue in H. pylori-positive ulcers (n = 7). CONCLUSIONS: Gastric mucosal HGF levels were elevated in H. pylori gastritis and reduced by its eradication. These results are relevant to our understanding of the increased gastric cell proliferation in patients with H. pylori-related gastritis.     

Cure of autoimmune gastritis by Helicobacter pylori eradication in a 21-year-old male

BACKGROUND: More recent investigations have shown that in some patients Helicobacter pylori (Hp) antibodies can act as antigastric antibodies and lead to atrophic autoimmune gastritis of the oxyntic mucosa. The question thus arises as to whether this form of autoimmune gastritis can be healed by eradicating Hp. METHODS: Case history of a 21-year-old man with active autoimmune gastritis of the oxyntic mucosa with lymphocytic infiltration of the entire lamina propria, foci of lymphocytic destruction of a number of glands, and hypertrophy of the preserved parietal cells, but no signs of Hp in the Warthin Starry stain. The search for parietal cell antibodies and intrinsic factor antibodies proved negative, while the level of the gastrin in the serum was slightly elevated. Since the presence of Hp IgG antibodies (243 U/ml) was confirmed. Hp eradication therapy was carried out. RESULTS: 15 months after Hp treatment the Hp IgG antibody titre had decreased to 11 U/ml. The autoimmune gastritis had healed, and autoaggressive inflammatory infiltrates with focal destruction of corpus glands and hypertrophy of the parietal cells were no longer detectable. CONCLUSIONS: Autoimmune gastritis induced by Hp may possibly be cured with Hp eradication treatment; to confirm this, further controlled prospective studies are needed.     

Reactive oxygen species activity and lipid peroxidation in Helicobacter pylori associated gastritis: relation to gastric mucosal ascorbic acid concentrations and effect of H pylori eradication

BACKGROUND: Helicobacter pylori is an independent risk factor for gastric cancer, and this association may be due to the bacterium causing reactive oxygen species mediated damage to DNA in the gastric epithelium. High dietary ascorbic acid intake may protect against gastric cancer by scavenging reactive oxygen species. AIMS: To assess reactive oxygen species activity and damage in gastric mucosa in relation to gastric pathology and mucosal ascorbic acid level, and to determine the effect of H pylori eradication on these parameters. PATIENTS: Gastric biopsy specimens were obtained for analysis from 161 patients undergoing endoscopy for dyspepsia. METHODS: Reactive oxygen species activity and damage was assessed by luminol enhanced chemiluminescence and malondialdehyde equivalent estimation respectively. Ascorbic acid concentrations were measured using HPLC. RESULTS: Chemiluminescence and malondialdehyde levels in gastric mucosa were higher in patients with H pylori gastritis than in those with normal histology. Successful eradication of the bacterium led to decreases in both parameters four weeks after treatment was completed. Gastric mucosal ascorbic acid and total vitamin C concentrations were not related to mucosal histology, but correlated weakly with reactive oxygen species activity (chemiluminescence and malodialdehyde levels). CONCLUSIONS: Data suggest that reactive oxygen species play a pathological role in H pylori gastritis, but mucosal ascorbic acid is not depleted in this condition.     

Heterogeneity in susceptibility to metronidazole among Helicobacter pylori isolates from patients with gastritis or peptic ulcer disease

Combination therapies that include metronidazole (MTZ) are the most successful therapies used in eradicating Helicobacter pylori. In this study, the prevalence and the relevance of heterogeneity in susceptibility to MTZ among H. pylori populations of 156 patients were evaluated. The results of this study show that 37 patients (24%) were infected with MTZ-resistant H. pylori (MIC > or = 8 micrograms/ml). Furthermore, 33% (52 of 156) of the patients were found to be infected with H. pylori populations heterogeneous for their susceptibility to MTZ. The reassessment of the MICs of MTZ for these 52 H. pylori populations revealed MTZ resistance in 28 of them, increasing the number of MTZ-resistant H. pylori populations among the 156 patients to 65 (42%). Out of 20 isolates, 2 (10%) heterogeneous in their susceptibility to MTZ also appeared to be heterogeneous at the genome level as determined by randomly amplified polymorphic DNA fingerprinting. In conclusion, the results show the limitations and risk of possible misinterpretations when only a single colony, picked from the primary H. pylori populations isolated from patients, is analyzed for its susceptibility to MTZ.     

Experimental Helicobacter pylori infection induces antral gastritis and gastric mucosa-associated lymphoid tissue in guinea pigs

Humans infected with Helicobacter pylori have abnormally low levels of the antioxidant vitamin C, which protects against the formation of carcinogenic nitrosamines, in gastric juice. Guinea pigs, like humans and nonhuman primates, have a dietary requirement for vitamin C. As such, these species have gastrointestinal vitamin C transport systems not found in other animals. We have developed and characterized a guinea pig model of chronic gastric H. pylori infection with the rodent-adapted Sydney strain of H. pylori. At 4 weeks postinfection, five of six animals of the infected group and zero of two animals of the control group were positive for H. pylori as determined by culture or PCR. At 15 weeks, six of six animals of the infected group and zero of two animals of the control group were positive. H. pylori-specific seroconversion was observed among infected animals. There were no histologic abnormalities in the gastric antra or fundi of control guinea pigs. In contrast, there was multifocal, mild to moderate lymphohistiocytic antral gastritis and formation of antral lymphoid follicles in H. pylori-infected animals. The lesion distribution in the gastric antra paralleled that observed in H. pylori-infected humans. The H. pylori-infected guinea pig should prove useful in modeling the interaction of helicobacter and vitamin C in gastric carcinogenesis.     

Stimulated gastrinemia, parietal cell mass and stimulated acid secretion in autonomous chronic gastritis: Helicobacter pylori influence

BACKGROUND/AIMS: In the present experience, an evaluation has been carried out of stimulated gastrinemia, parietal cell mass, and acid secretion in the course of a paradigmatic condition, such as autonomous chronic gastritis, in order to reveal possible changes induced by the presence of Helicobacter Pylori (HP). MATERIALS AND METHODS: We evaluated 153 patients with chronic gastritis of the antrum and/or body fundus, in different combinations not associated with peptic pathology. RESULTS: In the group of subjects with antral superficial chronic gastritis associated with normal body-fundic mucosa or with body-fundic superficial chronic gastritis, about 40% of the subjects in the HP positive group show gastrinemia values which are higher than the norm. The evaluation of parietal cell and stimulated acid secretion yielded no differences between the HP positive and HP negative groups: it emerges that these parameters vary exclusively according to the histologic state of the body-fundic mucosa. In the patients group with hypergastrinemia, the study has revealed no variations in parietal cell mass and acid secretion. CONCLUSION: Evidently the increase in gastrinemia in these subjects was not important enough to induce an increase in parietal cell mass and acid secretion. It emerges how the presence of HP does not imply substantial changes on the gastric cyto-functional parameters: these variations depend mainly on the histologic state of the gastric mucosa.     

Dyspepsia in relation to Helicobacter pylori infection and psychosocial work stress in white collar employees

OBJECTIVE: We undertook an investigation of the relationship between psychosocial work stress and Helicobacter pylori (H. pylori) infection with dyspepsia. METHODS: We conducted a cross-sectional study among 189 employees of a health insurance company in the city of Ulm, Germany. RESULTS: A clear association between work-related psychosocial factors and the occurrence of dyspeptic symptoms during the past 3 months was evident. Persons who were considered to have a critical style of coping with work demands suffered more often from dyspeptic symptoms. Current infection with H. pylori was not associated with prevalence of dyspeptic symptoms. These results were also confirmed by adjustment for age, gender, smoking status, education, and use of antiinflammatory drugs within the past 3 months, by means of multivariate analysis. The odds ratio (OR) for having a dyspepsia symptom score in the upper tertile versus the 1st or 2nd was 3.22 (95% confidence interval [CI], 1.56-6.65), given that the employee was considered to have a critical style of coping with work demands. The OR for having a dyspepsia symptom score in the upper tertile given H. pylori infection was 1.23 (95% CI, 0.44-3.46), indicating no association of current H. pylori infection with dyspeptic symptoms. CONCLUSIONS: A critical style of coping with work demands may be an important determinant for dyspepsia-like symptoms. Therefore, in the absence of an underlying disease, specific intervention programs should be targeted at the behavior of the affected individual (e.g., stress-reduction programs) rather than on the treatment of specific symptoms or infection with H. pylori.     

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

BACKGROUND: Cancer of the skin may be difficult to diagnose clinically if there are minimal skin findings on examination. OBJECTIVE: To remind physicians that the symptoms of squamous cell carcinoma (SCC) may precede physical signs of the tumor. METHODS: Perineural invasion of SCC was confirmed by histologic examination of surgical specimens. RESULTS: We present two patients whose initial presentation of SCC was facial pain due to extensive perineural invasion. Their diagnoses were delayed until skin lesions eventually became evident months later. CONCLUSION: Early detection can be lifesaving, thus emphasizing the importance of including skin cancer in the differential for facial pain or paresthesia.     

A standardized mouse model of Helicobacter pylori infection: introducing the Sydney strain

BACKGROUND & AIMS: Currently available Helicobacter pylori models show variable and, in some instances, poor colonization. There is a need for a strain with high colonizing ability to act as a standard for animal studies. METHODS: After screening a range of fresh clinical isolates and long-term adaptation in mice, a strain of H. pylon has been isolated with a very good colonizing ability. RESULTS: This strain, named the Sydney strain of H. pylori (strain SS1), is cagA and vacA positive. High levels of colonization (10(6)-10(7) colony-forming units/g tissue) were achieved consistently in C57BL/6 mice. Colonization levels varied depending on the mouse strain used with BALB/c, DBA/2, and C3H/He, all being colonized but in lower numbers. In all strains of mice, bacteria were clearly visible at the junctional zone between the antrum and the body. The phenotype was stable with colonizing ability remaining after 20 subcultures in vitro. The bacterium attached firmly to gastric epithelium. During 8 months, a chronic active gastritis slowly developed, progressing to severe atrophy in both C57BL/6 and BALB/c mice. CONCLUSIONS: The Sydney strain of H. pylori is available to all and will provide a standardized mouse model for vaccine development, compound screening, and studies in pathogenesis.