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PubMed1999

Host response and vaccine development to Helicobacter pylori infection.

Studies in both humans and animals demonstrate that H. pylori is capable of illiciting an innate response that in part is regulated by the genetic makeup of the host. These innate responses includes stimulating immune effector mechanisms at the cellular and biochemical level resulting in the influx of neutrophils into the lamina propria and have even been shown to modify gastric acid secretion. The availability of good animal models of chronic Helicobacter infection has also allowed investigators to begin to examine how the adaptive host immune response prevents and/or exacerbates Helicobacter-induced gastroduodenal disease. The experimental H. felis/mouse model has been utilized by a number of laboratories to investigate mechanisms of host defense against chronic Helicobacter infection. This model and the more recently developed H. pylori rodent model has not only allowed investigators to confirm the feasibility of immunotherapy to prevent and/or cure Helicobacter infection but also to begin to examine how the host immune response prevents and/or exacerbates Helicobacter-induced gastroduodenal disease. Based on these studies a hypothesis is emerging that suggests that protection and/or cure from Helicobacter infection is mediated primarily by an upregulated cellular immune response which may act via an antibody independent mechanism. Paradoxically, following natural infection with H. pylori, a component of the cellular immune response also promotes chronic gastric inflammation without clearance of the organism. The recent development of reliable and reproducible H. pylori/rodent models of disease and the availability of numerous inbred strains, transgenic and knockout animals, will allow investigators to continue to explore the role the host cellular and humoral immune response plays in promoting or preventing this infection.

Adjuvants, Immunologic↗
PubMed1993

Prospective, randomized, investigator-blind trial of Helicobacter pylori infection treatment in patients with refractory duodenal ulcers. Healing and long-term relapse rates.

In this study, 26 patients with duodenal ulcers refractory to treatment with H2-receptor antagonists for 8-12 weeks were randomly assigned to eight weeks of treatment with colloidal bismuth subcitrate (120 mg four times a day) alone (N = 12) or in combination with tetracycline hydrochloride (500 mg four times a day, days 0-14) and metronidazole (500 mg three times a day, days 15-28). Symptoms were scored and endoscopy, histology, and CLO tests were performed before, on completion of treatment, and 3, 6, 12, and 18 months after treatment. Treatment was considered successful when Helicobacter pylori was not detected by CLO tests and Warthin-Starry stains on gastric biopsies taken from antrum, body, and fundus. On triple therapy, ulcers healed in 12/14 patients (85.71%) and 10/14 (71.42%) patients became Helicobacter pylori-negative. On bismuth, only one patient became Helicobacter pylori-negative (8.33%, P < 0.0001), but ulcers healed in 8/12 patients (67%, P = NS). Six patients on bismuth, whose ulcers remained unhealed or relapsed early after healing, were offered triple therapy, which resulted in ulcer healing in three and Helicobacter pylori clearance in two patients. At 18 months, none of the Helicobacter pylori-negative patients had ulcer relapse. On the contrary, ulcers relapsed in all but one patient, who remained Helicobacter pylori-positive. Smoking and drinking did not influence the therapeutic outcome. The data confirm previous reports that many duodenal ulcers are infectious and therefore curable.

Adolescent↗
PubMed1993

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion.

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.

Adult↗
PubMed1991

Severity of Helicobacter-induced gastric injury correlates with gastric juice ammonia.

We postulated that ammonia produced by Helicobacter pylori may contribute to gastric mucosal injury. This hypothesis was evaluated in Helicobacter-positive patients with chronic renal failure in whom a high urea concentration might amplify this phenomenon. Gastric urea and ammonia were measured, and the severity of gastritis was evaluated by counting mononuclear and polymorphonuclear cells. High gastric ammonia and low urea in Helicobacter-positive patients, and the converse in Helicobacter-negative subjects, were observed. There was a significant correlation between gastric ammonia and interstitial polymorphonuclear leukocytes infiltration (P less than 0.05), suggesting a causal link. Eradication of Helicobacter pylori was associated with a decrease of ammonia and an increase of urea (P less than 0.01). The significant correlation between the severity of gastric inflammation and the gastric juice ammonia concentration suggests that ammonia may play a pathogenic role in Helicobacter-associated gastric injury.

Ammonia↗
PubMed1996

Influence of oropharyngeal flora and specimen pretreatment on the recovery of Helicobacter pylori.

The recovery of Helicobacter pylori was studied in vitro in the presence of different concentrations of oropharyngeal flora. The effect on the bacterial yield of Helicobacter pylori and oropharyngeal flora of washing biopsies once, twice or thrice before culture was then studied in biopsies taken from 35 patients. A low rate of recovery of low Helicobacter pylori concentrations (< or = 10(3) cfu/ml) was related to the presence of relatively high oropharyngeal flora concentrations (> or = 10(4) cfu/ml). After three washings a decrease in oropharyngeal flora between 10-fold and 100-fold cfu/biopsy was observed in seven patient samples. In another three specimens a more than 100-fold reduction in cfu/biopsy was observed. In the case of Helicobacter pylori, a 60-fold decrease in log cfu/biopsy was observed in only one patient. Pretreatment of the specimens by washing of the biopsies improved the recovery of small amounts of Helicobacter pylori in 10 of 28 patients. For optimal detection of Helicobacter pylori in gastric mucosal biopsies, washing of the specimens in addition to the use of selective media is recommended.

Biopsy↗
PubMed1995

Presence of Helicobacter pylori in the oral cavity, oesophagus, stomach and faeces of patients with gastritis.

The presence of Helicobacter pylori in the oral cavity (6 sites), oesophagus, stomach and bowel of 20 dyspeptic patients was investigated. Samples were cultured on three selective media and analyzed by 16S rDNA polymerase chain reaction (PCR) and southern hybridization. Helicobacter pylori DNA was detected by PCR from oral-cavity samples of three (20%) and from faeces samples of only one (7%) of the patients whose stomach biopsies were positive for Helicobacter pylori. When culture was used, the microorganism's rate of recovery from the oral cavity and faeces was 13% and 7%, respectively. One patient had a Helicobacter pylori-like organism in samples collected from the tongue and palate. Both strains were urease, catalase and oxidase positive and grew microaerophilically but were negative on PCR analysis. This demonstrates the possibility of false identification of Helicobacter pylori by use of routine enzyme reactions. Interestingly, specimens collected from the cheeks of three patients were positive for Helicobacter pylori by PCR analysis. This is the first instance of detection of this microorganism in the cheek.

Adult↗
PubMedDate not supplied

Presentation and management of Helicobacter pylori infection in childhood.

Helicobacter pylori is responsible for one of the most frequently encountered infectious diseases worldwide. Helicobacter pylori infection can lead to the development of gastritis and peptic ulcer disease. The presence of Helicobacter pylori in the human stomach also represents an increased risk of gastric cancer and gastric lymphoma. Epidemiological data obtained in adults suggest that the actual colonization with Helicobacter pylori is in fact determined by childhood factors. Therefore, the pediatric age group represents the ideal target population for studies concerning the pathogenesis and epidemiology of Helicobacter pylori infection. The present work reflects our experience with regard to the diagnosis, epidemiology and pathogenesis of Helicobacter pylori infection in childhood.

Adolescent↗
PubMed2000

Current status of Helicobacter contamination of laboratory mice, rats, gerbils, and house musk shrews in Japan.

The current status of Helicobacter contamination of laboratory mice, rats, gerbils, and house musk shrews from 47, 10, 4, and 3 colonies, respectively, in Japan was studied. Helicobacter was detected by reverse transcription (RT)-nested polymerase chain reaction (PCR) with Helicobacter genus-specific primers by using feces obtained from the animals. H. hepaticus, H. muridarum, H. bilis, H. rodentium, "Flexispira rappini", and "H. suncus" were identified with species-specific primers. Other species of Helicobacter were identified by sequencing of PCR products amplified with genus-specific primers. For mice, H. hepaticus, H. bilis, H. rodentium including H. rodentium-like organism, "H. typhlonicus"-like organism, and H. westmeadii-like organism were detected from 12 (25.5%), 1 (2.1%), 18 (38.3%), 1 (2.1%), and 1 (2.1%) colonies, respectively. Forty-seven (5.7%) mice from six (12.8%) colonies were contaminated with both H. hepaticus and H. rodentium. H. rodentium was detected in rats from three (30.0%) colonies. In gerbils, H. hepaticus was detected in three (75.0%) colonies, but other species of Helicobacter were not detected. In house musk shrews, "H. suncus" was detected in animals from two (66.7%) colonies. Visible lesions in the liver, which showed multiple pale to white foci, were observed in 6/42, 5/174, and 1/21 mice infected with H. hepaticus, H. rodentium, and H. hepaticus/H. rodentium, respectively, and 1/14 gerbils infected with H. hepaticus. The results suggest the prevalence of these species of Helicobacter in mice, rats, gerbils, and house musk shrews in Japan.

Animals↗
PubMed1999

Eradication of Helicobacter pylori heals atrophic corpus gastritis caused by long-term treatment with omeprazole.

Long-term treatment with proton pump inhibitors in patients with Helicobacter pylori gastritis can lead to atrophic changes in the corpus mucosa. What is still unclear, however, is whether this atrophy can regress in response to Helicobacter pylori eradication. We report on a male patient with Helicobacter pylori gastritis receiving long-term treatment (4 years) with omeprazole for gastrooesophageal reflux disease, who developed autoaggressive gastritis with progressive atrophy, hypochlorhydria, hypergastrinaemia and nodular ECL-cell hyperplasia. To determine whether these changes might be induced to regress, Helicobacter pylori eradication therapy was administered. Ten months after Helicobacter pylori eradication autoaggressive lymphocytic infiltrates were no longer detectable, and the glands in the corpus mucosa had normalised despite continued treatment with omeprazole - a finding that was confirmed at two further follow-up surveys performed at 6-month intervals. This case report shows that atrophy of the corpus mucosa developing under long-term treatment with a proton pump inhibitor can be cured by eradicating Helicobacter pylori.

Adult↗
PubMed1999

Immune response to natural and recombinant antigens of Helicobacter pylori in patients with dyspeptic complaints.

Sera of 223 dyspeptic patients with endoscopic findings of nonulcer dyspepsia (72%), gastric ulcer (15%) and duodenal ulcer (13%) were tested for antibodies against Helicobacter pylori with an enzyme immunoassay and an immunoblot technique using lysates of Helicobacter pylori cells as antigen source. One hundred and fifty-one (68%) sera were found to be positive for Helicobacter pylori IgG with both methods; 5% of the positive results in the enzyme immunoassay were false-positive due to cross-reactions mainly of proteins with a molecular mass of 43-66 kDa. Since cross-reactivity not only reduces the diagnostic value of the immunoassay but also complicates evaluation of the immunoblot results, an attempt was made to overcome these problems by using specific purified recombinant proteins instead of the crude cell preparations as antigens. Of the commonly recognised immunogens of Helicobacter pylori, antibodies against a cell surface protein of 26 kDa, the small urease subunit (29 kDa) and the cytotoxin-associated protein (130 kDa) were identified as highly sensitive serological markers for inclusion in a recombinant antigen mixture for Helicobacter pylori screening. Only the cytotoxin-associated protein was confirmed to be an indicator immunogen for ulcerogenic strains. To assess the reliability of recombinant fragments of this protein in serological screening, the reactivity of antibody to purified fragments of the cytotoxin-associated protein was compared with that to the natural protein. A C-terminal recombinant fragment of 58 kDa showed results identical to those obtained with the natural protein and was thus considered to be an appropriate component of an antigen mixture for serological detection of Helicobacter pylori.

Adult↗
PubMed1992

Helicobacter (aka Campylobacter) pylori as the major causal factor in chronic hypochlorhydria.

Helicobacter (formerly known as Campylobacter) pylori, a recently discovered gastrointestinal bacterial pathogen, has been shown to be etiologic for Type B or antral gastritis, and usually has chronic active pathological changes associated with its presence. Acute Helicobacter infection in most cases induces reduced stomach acid secretion which usually returns to normal levels of secretion after a few months. Yet Helicobacter gastritis has never been known to spontaneously remit after it has been established, and there is evidence suggesting that it often progresses to cause atrophic changes in the gastric mucosa. Since chronic gastritis has been shown in past studies to lead to chronic persistent hypochlorhydria from atrophic damage to secretory tissue, and Helicobacter has been shown to cause most chronic gastritis, the reasonable conclusion is that Helicobacter infection is etiologic for most chronic persistent hypochlorhydria. The apparent exception of the hyperchlorhydria in duodenal ulcer disease associated with Helicobacter infection is explained. The possible clinical relevance of hypochlorhydria will be the subject of a subsequent paper.

Achlorhydria↗
PubMed2004

Fecal shedding of Helicobacter spp. by co-housed Australian sea lions (Neophoca cinerea) and Australian fur seals (Arctocephalus pusillus doriferus).

With the emergence of Helicobacter species as agents of gastrointestinal disease within a broad range of animal hosts, there is growing awareness of the need to identify such species and the potential role(s) they play within the intestine. Of interest in this study are captive seals and sea lions, where close proximity to one another may enhance the transmission of pathogens, in particular Helicobacter. The feces of several captive Australian sea lions and Australian fur seals were assessed for the occurrence of Helicobacter over 31 days. The presence of Helicobacter, detected by the polymerase chain reaction (PCR) varied over time and at times could not be detected. Helicobacter species were detected in five of the six animals examined of which two species were identified. This is the first report of Helicobacter species in captive seals and demonstrates the diversity and potential role(s) they may play in the gut of these animals.

Animals↗
PubMed2002

Helicobacter pylori seropositivity in patients with hyperemesis gravidarum.

OBJECTIVES: To test the hypothesis that infection with Helicobacter pylori is associated with hyperemesis gravidarum. METHODS: From November 1999 to February 2001, we enrolled 54 pregnant women with hyperemesis gravidarum and 53 asymptomatic pregnant women in a prospective study. Specific serum immunoglobulin G for Helicobacter pylori was assayed in the sera of the study group and compared with the asymptomatic group. Chi-square and Student's t-test were used accordingly for statistical analysis of the data. RESULTS: Serologically positive Helicobacter pylori infection was detected in 44 out of 54 patients with hyperemesis gravidarum (81.5%) whereas 29 out of 53 asymptomatic gravidas (54.7%) had positive antibody titers for Helicobacter pylori. The ratio of Helicobacter pylori seropositivity in pregnant women with hyperemesis gravidarum was significantly higher than asymptomatic pregnant women (P<0.01). The mean (+/-S.D.) of the IgG titer was 69.7 (+/-77.5) in the hyperemesis gravidarum group and 34.5 (+/-47.8) in the control group (P<0.01). CONCLUSIONS: There is a significant association between Helicobacter pylori infection and hyperemesis gravidarum in our hyperemetic pregnant patients.

Female↗
PubMed2002

[Helicobacter pylori: a new cardiovascular risk factor?].

There is increasing evidence that certain microbial agents may have an etiopathogenic role in the development of atherothrombosis. Helicobacter pylori, a bacterium that causes peptic ulcer disease, has been suggested as one of the microbes involved in the development of atherothrombosis. This hypothesis is based on the following observations: a) a higher prevalence of Helicobacter pylori infection in patients with coronary artery disease, myocardial infarction, or cerebrovascular disease; b) the coincidence of Helicobacter pylori infection and cardiovascular risk factors, such as serum cholesterol and triglyceride concentrations and plasma fibrinogen; c) Helicobacter pylori seropositivity correlates with acute-phase proteins associated with higher risk of coronary disease, such as C-reactive protein, and d) controversial PCR studies indicating the presence of Helicobacter pylori in atheromas. Analysis of the scientific evidence suggests that Helicobacter pylori infection could indirectly contribute to the development and severity of atherothrombosis and cardiovascular disease.

Arteriosclerosis↗
PubMed1997

Strategy for the detection of Helicobacter species by amplification of 16S rRNA genes and identification of H. felis in a human gastric biopsy.

The aim of the present work was to develop polymerase chain reactions (PCRs) based on the conserved nucleotide sequence of the 16S rRNA gene for detection of bacteria of the Helicobacter genus in human antral biopsy samples. The assay for Helicobacter spp was developed by amplifying a 399-bp 16S rRNA gene sequence specific to the genus Helicobacter. The identity of the amplicon was confirmed by hybridization with an internal probe and by restriction by endonuclease VspI showing two expected fragments of 295 and 104 base pairs. A total of 65 dyspeptic patients from France and New Caledonia were screened for Helicobacter spp infection through the use of the following diagnostic assays on biopsy specimens collected through endoscopy: direct detection of bacteria in histological sections by Giemsa and Warthin Starry staining, urease test and bacterial isolation, PCR for Helicobacter pylori ureC/glmM gene, and PCR targeted to 16S rRNA genes. The 16S rRNA gene PCR assay was able to detect down to 680 bacterial cells, as assessed by agarose gel electrophoresis, and down to 4 bacterial cells by hybridization of amplicon with the internal probe. The 16S rRNA PCR test was 100% specific and sensitive; results obtained with this test were in agreement with the visualization of bacteria by histology. Urease test and culture were 86.4% and 22.7% sensitive, and 96.5 and 100% specific, respectively. The H. pylori ureC/glmM gene-based PCR was 100% specific and only 95.4% sensitive, since one biopsy from a Melanesian patient contained a Helicobacter strain other than H. pylori. For this Melanesian patient, a branch-specific PCR targeting the epsilon branch of Proteobacteria was used to amplify a 967-bp amplicon. This amplicon was sequenced and matched with the H. felis sequence. This was confirmed using an H. felis-specific urease PCR test.

Biopsy↗
PubMed2000

Relationship between antral lymphocyte density and basal gastrin levels in patients with Helicobacter pylori infection.

BACKGROUND: The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood. AIM: To evaluate whether antral lymphocyte density could play a role in this alteration. METHODS: A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment. RESULTS: Antral lymphocyte density (5,464 +/- 1,328 and 5,635 +/- 1,186 vs 2,267 +/- 557 lymphocytes/mm2; p<0.001 and p<0.001, respectively) and gastrin levels (66.7 +/- 14.1 and 60.4 +/- 21.7 vs 40.7 +/- 7.8 pg/dl; p=0.004 and p=0.02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and non-ulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0.77; p=0.003) and in non-ulcer dyspepsia (r=0.75; p=0.03) patients, while no correlation was found in controls [r=0.12; p=0.8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0.027), but disappeared in those successfully cured. CONCLUSIONS: These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.

Adult↗
PubMed2000

Hypersecretory duodenal ulcer and Helicobacter pylori infection: a four-year follow-up study.

BACKGROUND: About 10% of duodenal ulcer patients are characterized by gastric acid hypersecretion with normal gastrin values. Relapsing duodenal ulcer after Helicobacter pylori cure has been related to high acid output and maintenance antisecretory therapy has been suggested in hypersecretory duodenal ulcer patients. The role of Helicobacter pylori infection and the effects of Helicobacter pylori cure in hypersecretory duodenal ulcer patients still remain to be fully studied. AIM: To study: a) whether gastric acid hypersecretion "per se" is a risk factor for duodenal ulcer recurrence; b) whether maintenance antisecretory therapy is necessary after eradication in hypersecretory duodenal ulcer patients. PATIENTS: The study population comprised 8 hypersecretory duodenal ulcer patients, selected from a population of 79 Helicobacter pylori-positive duodenal ulcer patients. METHODS: Hypersecretory duodenal ulcer patients were followed-up for at least 4 years after eradication. Gastric acid secretion was measured again 12 months after Helicobacter pylori eradication. Gastroscopy with histology was performed 3, 6, 12 and 36 months after treatment, 13C-urea breath test after 42 months; clinical questionnaires were completed every 6 months. RESULTS: After eradication, despite a not significantly reduced high acid output (median value of basal acid output and pentagastrin-stimulated acid output, respectively, 23.1 mEq/h and 64.1 mEq/h before treatment vs 16 mEq/h and 49.7 mEq/h 12 months after treatment), all patients were free from symptoms, none of them had duodenal ulcer relapse or complications (7/8 before treatment), or needed antisecretory maintenance therapy, except for one patient taking non-steroidal anti-inflammatory drugs. CONCLUSIONS: These findings, obtained in a selected population of hypersecretory duodenal ulcer patients with long-term follow-up, suggest that after successful Helicobacter pylori eradication gastric acid hypersecretion "per se" is not able to determine the recurrence of duodenal ulcer.

Adolescent↗
PubMedDate not supplied

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients.

BACKGROUND: Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients. AIMS: To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status. PATIENTS AND METHODS: A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination. RESULTS: There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum. CONCLUSION: Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.

Antigens, Bacterial↗