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At least 631 records · Page 35Linked to original sources
PubMed2005

Experimental induction of bacterial gastritis and gastric ulcer disease in gnotobiotic swine inoculated with porcine Helicobacter-like species.

OBJECTIVE: To determine whether 2 isolates of recently isolated swine-origin Helicobacter pylori-like bacteria are pathogenic in pigs and compare the signs of gastric disease induced by these isolates with those detected in H pylori- and Helicobacter heilmannii-infected pigs. ANIMALS: 36 neonatal gnotobiotic pigs. PROCEDURE: Groups of separately housed pigs were inoculated orally with swine-origin Helicobacter-like isolates 2662 or 1268, H pylori (human gastric pathogen), or a gastric homogenate from gnotobiotic swine containing H heilmannii. Noninoculated pigs were used as control animals. Clinical signs and development of homologous and heterologous antibodies against Helicobacter organisms were assessed. After euthanasia, gastric tissues were examined grossly and microscopically; Helicobacter organisms were detected by use of Warthin-Starry and immunohistochemical stains. RESULTS: Both porcine Helicobacter-like isolates colonized the stomachs of swine. Isolate 2662 was highly pathogenic; in 13 isolate 2662-inoculated pigs, gastroesophageal ulcerations developed in 9 and ulceration of the gastric glandular mucosa was detected in 5. Histologically, inflammatory gastritis consisting of multifocal to diffuse lymphocytic and plasmacytic cellular infiltrates and lymphoid follicle formation in the gastric lamina propria accompanied bacterial colonization of the gastric compartment. In contrast, H heilmannii was minimally pathogenic in that only modest inflammatory cell infiltrates were seen. Gastroesophageal or mucosal ulcers were not evident in pigs inoculated with H heilmannii. CONCLUSIONS AND CLINICAL RELEVANCE: These data indicate that swine-origin H pylori-like bacteria can be pathogenic in pigs and suggest that porcine gastric disease may be mediated, in part, by colonization of the stomach by swine-origin H pylori-like bacteria.

Animals↗
PubMed1995

Helicobacter infections in laboratory animals: a model for gastric neoplasias?

Evidence is rapidly accumulating that Helicobacter pylori is a major risk factor for human gastric adenocarcinomas and all low-grade B-cell gastric lymphomas. Given this, there is a need to develop animal models with a view to discovering not only how carcinogenesis is initiated, but also how the process can be prevented. The lack of H. pylori animal models suitable for long-term studies means that alternatives are needed. The most productive models are likely to be the Helicobacter mustelae-infected ferret or the mouse infected with either Helicobacter felis or 'Helicobacter heilmannii'. The first evidence that helicobacter infection induces a chronic inflammation that progresses to gastric atrophy, the precursor lesion to gastric adenocarcinoma in humans, has come from the mouse model. The severity of inflammation is dependent on the type of mouse strain used, highlighting the importance of host factors in the development of gastritis. Carcinogenesis studies should only be done with mouse strains known to cause atrophy. The H. mustaelae-infected ferret appears very susceptible to the development of adenocarcinoma following ingestion of chemical carcinogens. Long-term infection of mice with H. felis results in the development of low-grade B-cell gastric lymphomas indistinguishable to those found in H. pylori-infected humans. Helicobacter-infected animals, rodents in particular are going to provide exciting opportunities to investigate not only important aspects of gastric cancer and lymphoma but also fundamental issues of carcinogenesis in general.

Animals↗
PubMed1994

Age-related prevalence of Helicobacter pylori antibodies in Indian subjects.

OBJECTIVE: To determine the age-related prevalence of Helicobacter pylori antibodies in Indian subjects without upper gastrointestinal symptoms. MATERIAL AND METHODS: Sera of 340 subjects without any upper gastrointestinal complaints were screened for IgG and IgA Helicobacter pylori antibodies by the ELISA technique. RESULTS: The prevalence of IgG and IgA antibodies was 22%, 56% and 87% and 48%, 58% and 83% in 0-4, 5-9 and 10-19 year age groups respectively; thereafter it remained almost constant upto fifth decade. A significant fall in IgG and IgA prevalence was observed from fifth to seventh decades. CONCLUSION: Our data indicate that in India exposure to Helicobacter pylori occurs early in life and is widespread; about 83% of the population is exposed to Helicobacter pylori during the first two decades of life. The comparable prevalence rates of IgG antibodies to Helicobacter pylori and hepatitis A virus, in different age groups, in India and in the West, suggest a feco-oral mode of transmission for Helicobacter pylori.

Adolescent↗
PubMed1995

Morphological and immunohistochemical examinations of the dynamic changes of gastric mucosa associated with the treatment of helicobacter pylori infection in children.

The aim of this study was to investigate the consequence of Helicobacter pylori eradication on gastric mucosa and antral G and D-cells. Forty children, aged 5-17 years with Helicobacter pylori infection were assessed. Helicobacter pylori was detected by a urease test and identified by serological and microbiological methods. Twenty children were again assessed after the therapy (the combination of colloid bismuth subcitrate, amoxycillin and metronidazole). Gastroscopic examination was performed and at least six bioptic specimens were taken from the antrum, body and fundus. Tissue samples, processed with the paraffin method and stained with hematoxyllin and eosin, were assessed. Monoclonal antiserum Gastrin PAP kit 516 and somatostatin PAP kit 512 (DAKO) in the peroxidase-antiperoxidase technique (PAP) have been used to detect G and D-cells. Helicobacter pylori in the gastric mucosa was demonstrated with the Giemsa method. The results show the coincidence of Helicobacter pylori infection and the count of antral G and D-cells and active chronic gastritis in children. After the treatment Helicobacter pylori was eradicated in 70% of children. In 34% of these cases the eradication was followed by a diminution of activity of gastric antral mucosa inflammation and in 20% of these children the resolution of the inflammatory infiltration in the gastric mucosa was seen. A decrease of the antral G and D-cells count and also a diminution of G/D index in these cases were observed.

Adolescent↗
PubMed1997

Should Helicobacter pylori be eradicated before starting long-term proton pump inhibitors?

Symptomatic gastro-oesophageal reflux disease is a common disorder characterized by pathological exposure of the distal oesophagus to acid. The management requires the control of symptoms, prevention of relapse and complications. Proton pump inhibitors are without doubt the most effective agents in the management of gastro-oesophageal reflux disease. In Helicobacter pylori-negative individuals the efficacy of ranitidine, but more pronounced of omeprazole, on the nocturnal intragastric acidity, is less than in Helicobacter pylori-positive patients. Curing the Helicobacter pylori infection in gastro-oesophageal reflux disease patients might, therefore, have the disadvantage of losing efficacy of antisecretory therapy. Conversely, several studies have shown that long-term use of proton pump inhibitors is associated with progression and worsening of body gastritis exclusively in Helicobacter pylori-positives. This observation makes Helicobacter pylori eradication indicated before starting long-term treatment with proton pump inhibitors for gastro-oesophageal reflux disease and other acid-related diseases. The data reported, so far, however, are not conclusive. The Federal Drugs Administration Advisory Committee concluded on available data, that there is no evidence that longterm proton pump inhibitors treatment leads to gastric atrophy, intestinal metaplasia or gastric cancer. Eradication of Helicobacter pylori infection might lead to reduction in the efficacy of antisecretory agents, but might prevent worsening of the gastric corpus gastritis. More data are needed to really answer these clinically relevant questions.

Anti-Ulcer Agents↗
PubMedDate not supplied

[Low-grade gastric MALT lymphoma and helicobacter heilmannii (Gastrospirillum hominis].

We report the fourth case of low-grade gastric MALT lymphoma associated to Helicobacter heilmannii. This spiral organism may be present in the gastric mucosa of animals where it is non pathogenic while, in humans, its presence is always associated with chronic gastritis. In this case, Helicobacter heilmannii was observed in the absence of Helicobacter pylori. Regression of endoscopic and histological lesions after Helicobacter heilmannii eradication suggests its role in gastric lymphoma. This observation underlines the need for searching for Helicobacter heilmannii by careful histological examination, in the absence of Helicobacter pylori, and the importance of its eradication in the treatment of gastric lymphoma.

Helicobacter Infections↗
PubMed1994

Helicobacter infection and gastric ethanol metabolism.

The organism frequently colonizing the stomach of patients suffering from chronic active gastritis and peptic ulcer disease--Helicobacter pylori--possesses marked alcohol dehydrogenase (ADH) activity. Consequently, Helicobacter infection may contribute to the capacity of the stomach to metabolize ethanol and lead to increased acetaldehyde production. To study this hypothesis, we first determined ADH activity in a variety of H. pylori strains originally isolated from human gastric mucosal biopsies. ADH activity was also measured in endoscopic gastric mucosal specimens obtained from H. pylori-positive and -negative patients. Furthermore, we used a mouse model of Helicobacter infection to determine whether infected animals exhibit more gastric ethanol metabolism than noninfected controls. Most of the 32 H. pylori strains studied possessed clear ADH activity and produced acetaldehyde. In humans, gastric ADH activity of corpus mucosa did not differ between H. pylori-positive and -negative subjects, whereas in antral biopsies ADH activity was significantly lower in infected patients. In mice, gastric ADH activity was similar or even lower in infected animals than in controls, depending on the duration of infection, despite the fact that the infectious agent used--Helicobacter felis--showed ADH activity in vitro. In accordance with this, Helicobacter infection tended to decrease rather than increase gastric ethanol metabolism in mice. In humans, it remains to be established whether the observed decrease in antral ADH activity associated with H. pylori infection can lead to reduced gastric first-pass metabolism of ethanol.

Acetaldehyde↗
PubMed2004

Multiplex PCR assay for differentiation of Helicobacter felis, H. bizzozeronii, and H. salomonis.

Helicobacter felis, Helicobacter bizzozeronii, and Helicobacter salomonis are frequently found in the gastric mucous membrane of dogs and cats. These large spiral organisms are phylogenetically highly related to each other. Their fastidious nature makes it difficult to cultivate them in vitro, hampering traditional identification methods. We describe here a multiplex PCR test based on the tRNA intergenic spacers and on the urease gene, combined with capillary electrophoresis, that allows discrimination of these three species. In combination with previously described 16S ribosomal DNA-based primers specific for the nonculturable "Candidatus Helicobacter suis," our procedure was shown to be very useful in determining the species identity of "Helicobacter heilmannii"-like organisms observed in human stomachs and will facilitate research concerning their possible zoonotic importance.

Animals↗
PubMed1999

Extragastroduodenal conditions associated with Helicobacter pylori infection.

Helicobacter pylori is a Gram-negative bacterium that is considered a causative agent of peptic ulcer disease, gastric lymphoma, and gastric carcinoma. Helicobacter pylori triggers an intense leucocyte infiltration of the gastric submucosa, an action which is mediated by pro-inflammatory cytokines. This pathogenetic mechanism is common to many other diseases and consequently, Helicobacter pylori seroprevalence has also been investigated in other diseases. It is now known that Helicobacter pylori seropositivity is associated with various cardiovascular, respiratory, extragastroduodenal digestive, neurological, dermatological, autoimmune, and growth disorders. Although the precise role of Helicobacter pylori is unknown in these diseases, the organism can be eradicated using simple and reliable drug regimens. The conditions associated with Helicobacter pylori seropositivity are highlighted in this article.

Journal Article↗
PubMed1999

Physicians' practice patterns of treating Helicobacter pylori-associated peptic ulceration in public hospitals in Hong Kong: questionnaire survey. Coordinator Group of the Quality Assurance Subcommittee (Medicine), Hospital Authority, Hong Kong.

To survey the practice patterns of physicians in public hospitals in Hong Kong when treating Helicobacter pylori-associated peptic ulceration, the records of all patients from 22 medical units who had new peptic ulcers that had been diagnosed endoscopically during August 1996 were examined systematically. Patient data were entered on a one-page questionnaire. Five hundred and twelve patients with peptic ulceration were studied; 173 (34%) of whom had presented with gastro-intestinal bleeding. The Helicobacter pylori status had been determined in 449 (88%) patients, 280 (62%) of whom had subsequently tested positive for Helicobacter pylori. The biopsy urease test or histological examination had been performed for more than 95% of patients. Of 260 patients who had tested positive for Helicobacter pylori, 244 (94%) had received eradication therapy to eliminate this organism; a total of 291 patients, however, were receiving eradication therapy. The most commonly used regimen was proton pump inhibitor triple therapy (151 [52%] of 291 patients). Confirmation of the eradication of Helicobacter pylori had been planned for 152 (52%) of the 291 patients, whereas ulcer-healing drugs--mainly H2-receptor antagonists--had been prescribed for 87 (30%) patients after eradication. Curing Helicobacter pylori infection is therefore widely accepted in the management of peptic ulcer disease among physicians working in Hong Kong public hospitals.

Journal Article↗
PubMed2002

The relationship between Helicobacter pylori intensity and histopathological findings in cases with chronic gastritis and duodenal ulcer.

BACKGROUND/AIMS: Helicobacter pylori infection affects many people in developing countries. The inflammation it induces can cause malignant gastric lymphoma and also gastric carcinoma, depending on the intensity of inflammatory reaction, specific properties related to the strain and the host response. METHODS: Fifty patients (35 cases with gastritis and 15 with duodenal ulcer) were included in the study. Hematoxylin-eosin paraffin sections were prepared from their endoscopic biopsies and Helicobacter pylori presence, activity of the infection, lymphoplasmacytoid cell infiltration and the degree of atrophy were determined semiquantitatively. Toludin O stain was applied to determine Helicobacter pylori intensity. RESULTS: We found a statistically significant positive correlation of Helicobacter pylori intensity and activity of infection, lymphoplasmacytoid cell infiltration and atrophy in the 35 cases with gastritis and the relationship between Helicobacter pylori intensity and inflammatory activity was statistically significant in the 15 cases with duodenal ulcer. CONCLUSION: As morphological characteristics are crucial for the early diagnosis and treatment of gastric malignities; histopathological confirmation of helicobacter intensity is important.

Journal Article↗
PubMed2002

Eradication of Helicobacter pylori may be beneficial in the management of chronic open-angle glaucoma.

BACKGROUND: We have documented a high prevalence of Helicobacter pylori infection in patients with glaucoma. OBJECTIVE: To evaluate the effect of H pylori eradication on the 2 most commonly used glaucoma parameters: intraocular pressure and visual field. METHODS: A total of 41 patients with glaucoma and 30 age-matched anemic controls underwent upper gastrointestinal endoscopies and gastric mucosal biopsies to detect the presence of H. pylori infection by histologic analysis and rapid urease test (CLOtest; Delta West, Draper, Utah). Saliva samples were also tested by CLOtest. Serum anti-H pylori-specific IgG was analyzed by enzyme-linked immunosorbent assay. Helicobacter pylori-positive patients received a triple eradication regimen (omeprazole, clarithromycin, and amoxicillin treatment), and all patients were observed for 2 years while remaining under the same antiglaucoma therapy. RESULTS: Helicobacter pylori was detected in 88% of glaucoma cases and in 47% of controls (P<.001). Helicobacter pylori eradication was successful in 83% of treated patients. At the 2-year clinical end point, glaucoma parameters (mean intraocular pressure and mean visual field parameters) were improved in the subgroup of patients where H. pylori eradication was successful (P<.001 for intraocular pressure; P< or =.01 for visual field parameters), but not in the other patients. CONCLUSION: Helicobacter pylori eradication may positively influence glaucoma parameters, suggesting a possible causal link between H pylori and glaucoma.

Aged↗
PubMed1999

Antibody-independent protective mucosal immunity to gastric helicobacter infection in mice.

Helicobacter pylori infection of the gastric mucosa can result in gastritis and peptic ulcer disease. Although vaccination can induce protective immunity in animal models of Helicobacter infection, the mechanism(s) of protective immunity has not been fully elucidated. This study was designed to determine whether humoral immune responses are required for protective Helicobacter immunity. IgA-deficient or immunoglobulin-deficient mice were orally immunized against Helicobacter felis and then challenged with live H. felis. Both groups were protected at levels comparable to that of wild-type mice. Additionally, inflammation was equivalent in extent and character between wild-type and antibody-deficient mice. Therefore antibody-independent mechanisms of immunity can protect mice against gastric Helicobacter infection.

Animals↗
PubMed1997

Quantitative polymerase chain reaction for the detection of Helicobacter pylori in gastric biopsy specimens.

A variety of methods, including the polymerase chain reaction (PCR), are available for the detection of Helicobacter pylori in clinical samples, but none of them can adequately quantify the organism. In the present study, the competitive PCR, a rapid and simple method for quantification of Helicobacter pylori DNA in gastric biopsies, was used to measure the amount of DNA present in Helicobacter pylori-positive biopsies. This method is based on coamplification of an internal standard and a target DNA sequence with one set of primers. The internal standard was prepared using a nonhomologous fragment of DNA ligated to specific primers used to amplify the target DNA. This competitive DNA fragment of a desired size and containing primer templates is called a PCR MIMIC. To perform a quantitative PCR, PCR amplification reactions were spiked with known quantities of PCR MIMICs containing unknown amounts of DNA from Helicobacter pylori-positive biopsies. The amount of target DNA was determined by visual comparison of the PCR products after establishment of the correlation between the internal control concentration and the DNA concentration in a competitive amplification reaction. The results were confirmed by a radioactive method. Quantitative PCR can be a reliable method for determining the extent of Helicobacter pylori infection.

Biopsy↗
PubMed1992

Effect of antimicrobial therapy on the specific serological response to Helicobacter pylori infection.

The systemic immune response to Helicobacter pylori was studied in 247 infected adult patients before antimicrobial therapy and at different intervals following therapy. Endoscopy with simultaneous collection of biopsies was performed in all patients immediately before treatment, 4 to 6 weeks after the end of therapy and 6 to 12 months later. A 14C-urea breath test was performed 3 to 6 months after the end of treatment. Biopsy specimens were cultured and examined histologically using Giemsa stain. Sera were tested for Helicobacter pylori IgG antibodies with a commercial enzyme immunoassay using species-specific antigens. Overall, Helicobacter pylori was eradicated in 120 patients while the other 127 remained infected with the organism. The follow-up period ranged from 4 weeks to 33 months (mean 10.2 months). Pretreatment IgG levels did not differ significantly between the two groups of patients. Six weeks after the end of treatment a slight but definite decrease in the IgG antibody levels was seen irrespective of treatment success. In the 127 patients who remained Helicobacter pylori-positive, the level of IgG antibodies remained stable or increased with time. A continuous fall in antibody levels was observed following bacterial eradication in the other 120 patients, but the difference in antibody levels between treatment responders and nonresponders became significant only more than six months after the end of treatment (p = 0.001). Serological testing may be useful for monitoring the outcome of long-term treatment of Helicobacter pylori infection and obviate the need for endoscopy.

Adult↗
PubMed1992

Use of a urea breath test versus invasive methods to determine the prevalence of Helicobacter pylori in Zaire.

The prevalence of Helicobacter pylori infection in Zaire was determined by means of a [14C] urea breath test in 133 asymptomatic subjects, by culture and histological examination of biopsies in 324 consecutive endoscopy patients with chronic epigastric complaints, and by both the breath test and culture/histology in a subset of 92 patients. Sixty healthy Belgian students or hospital laboratory workers were also included for comparison. The prevalence of Helicobacter pylori was significantly higher in asymptomatic Zairian subjects (77.4%) than in the Belgians (30%; p less than 10(-6)). Infection was also acquired much earlier in life in Africans, 66% of the children aged 5 to 9 years already being infected versus none of the Belgian subjects below the age of 20 years. In Zaire, however, the prevalence of Helicobacter pylori in patients with gastroduodenal disorders (87.5%) was similar to that in the group of asymptomatic subjects (77.5%) after adjustment for age and other epidemiological parameters (gender, place of residency, education level, smoking and drinking habits) in a multivariate analysis. The high rate of acquisition of Helicobacter pylori infection in Zaire emphasizes the need to consider the baseline prevalence of Helicobacter pylori in a defined population when studying its association with various diseases.

Adult↗
PubMed1996

Helicobacter pylori in promotion of gastric carcinogenesis.

Gastric atrophy and intestinal metaplasia are considered the earliest phenotypic changes in the cascade of events leading from normal mucosa to intestinal-type gastric cancer, and epidemiological evidence links Helicobacter pylori to gastric epithelial malignancies. To evaluate any causal relationship between bacterial infection and atrophic metaplastic lesions, gastric pathology was histologically and histochemically evaluated in 267 consecutive, nonulcerous, untreated subjects, with attention given the phenotypes of intestinal metaplasia. The prevalence of Helicobacter pylori infection was 61%. Intestinal metaplasia (particularly types II and III) was significantly associated with both Helicobacter pylori detection (chi 2 LR: P < 0.002) and increasing age (chi 2 LR: P < 0.002). Using logistic regression analysis, the development of intestinal metaplasia proved more significantly linked with Helicobacter pylori infection [odds ratio = 4.55 (95% confidence interval: 1.51-13.7)], than with age [odds ratio = 1.03 (95% CI: 1.01-1.06)], with no interaction. In conclusion, Helicobacter pylori can be considered among the major causal agents of mucosal lesions involved in the multistep process of gastric carcinogenesis, justifying any attempt to eradicate this bacterial infection.

Adolescent↗
PubMed1995

Transport and storage of Helicobacter pylori from gastric mucosal biopsies and clinical isolates.

Various transport and storage conditions for the recovery of Helicobacter pylori from gastric biopsies were evaluated. Gastric mucosal biopsies from 16 Helicobacter pylori-infected patients were stored in cysteine-Albimi medium containing 20% glycerol in a refrigerator (4 degrees C) for 1 and 2 weeks and in a -20 degrees C laboratory freezer for 4 and 12 weeks. Two clinical isolates were stored in saline, Stuart's transport media, cysteine-Albimi broth with 20% glycerol, brucella broth with 20% glycerol and skim milk with 17% glycerol at room temperature, 4 degrees C, -20 degrees C and -70 degrees C. Storage at 4 degrees C for 1 and 2 weeks resulted in Helicobacter pylori recovery from 81% and 19% of biopsies, respectively. Storage at -20 degrees C yielded Helicobacter pylori recovery in 100% and 57% after 4 and 12 weeks, respectively. At room temperature after 6 h, the Helicobacter pylori titer was reduced. The best storage media for frozen isolates were skim milk/glycerol, brucella broth/glycerol and cysteine-Albimi/glycerol (in descending order). Recovery was better at -70 degrees C than -20 degrees C.

Biopsy↗