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PubMed1997

Short-term eradication therapy for Helicobacter pylori does not reduce the incidence of gastric metaplasia in duodenal ulcer patients.

The presence of gastric metaplasia in the duodenal mucosa and Helicobacter pylori infection play an important role in the development of duodenal ulcers and the risk for ulcer relapses. The purpose of the present study was to identify the presence of gastric metaplasia in the duodenum and observation of changes in its extent during eradication therapy for Helicobacter pylori. The study population consisted of 40 patients, 15 women (aged from 29 to 65 years) and 25 men (aged from 22 to 62 years). At baseline and after 6 weeks all patients underwent endoscopic examinations of the upper alimentary tract during which two gastric antral and duodenal biopsies were obtained. The first endoscopy revealed the presence of duodenal ulcers in 22 patients, no ulcers in 11 cases, and postulceration scar in the duodenal bulb in 7 cases. The specimens were stained with hematoxylin and eosin, Giemsa and periodic acid Schiff/Alcian Blue. On first examination Helicobacter pylori infection in gastric antral specimens was detected in 40 patients. Therapy with amoxycillin, metronidazole, ventrisol and omeprazole for two weeks was administered in patients without duodenal ulcers and with omeprazole and ventrisol for additional 14 days in patients with duodenal ulcers. After therapy the presence of Helicobacter pylori was found in 10 cases, thus the degree of Hp eradication in the present study was 75%. Gastric metaplasia in duodenal samples was seen in 15 patients with duodenal ulcers and in 10 nonulcer patients. After therapy only in 4 cases gastric metaplasia was reduced along with Hp eradication, whereas in 9 cases gastric metaplasia in the duodenum was still present despite effective Hp eradication. The present findings indicate that gastric metaplasia is a reversible lesion, although this process is not dynamic and requires more time. The presence of gastric metaplasia in the duodenum after Hp eradication indicates an increased risk for the recurrence of duodenal ulcers, thus providing a useful information for a clinician.

Adult↗
PubMed1997

Alterations in gastric physiology in Helicobacter pylori infection: causes of different diseases or all epiphenomena?

Helicobacter pylori infection exerts variable effects on gastric acid secretion. It may increase acid secretion, decrease acid secretion or produce no overall change. The effect of the infection on acid secretion depends upon the relative extent to which the Helicobacter pylori gastritis affects the antral and body mucosa of the stomach. When there is antral predominant, body-sparing gastritis, there is increased gastrin release and this is accompanied by increased acid secretion. When there is a significant body gastritis, acid secretion is reduced and subjects may be completely achlorhydric. The majority of subjects have both antral gastritis and body gastritis and this results in no overall change in gastric acid secretion. There is now increasing evidence that the alteration which Helicobacter pylori infection exerts upon gastric acid secretion is a pivotal factor in determining the clinical outcome of the infection. Subjects in whom the infection produces acid hypersecretion develop duodenal ulcer disease due to the increased duodenal acid load. In subjects in whom the infection induces marked hypochlorhydria, there is an increased risk of gastric cancer. The hypochlorhydria probably plays an important role in the carcinogenic process as high intragastric pH markedly raises intragastric nitrite levels, profoundly lowers gastric juice ascorbic acid and allows colonization by nitrosating bacteria. The reason for the different functional responses to Helicobacter pylori infection is unclear but may be related to the host's pre-morbid acid secretory status.

Duodenal Ulcer↗
PubMed1998

[Gastroesophageal reflux combined with Helicobacter pylori infection].

AIM: Investigation of the role of Helicobacter pylori infection of the low esophagus in patients with duodenal ulcer (DU). MATERIALS AND METHODS: Endoscopic examination was performed in 40 DU patients. All the biopsies were examined for Helicobacter pylori and degree of relevant contamination. RESULTS: Helicobacter pylori was present in all the patients' antral stomachs. It contaminated the low part of the esophagus in 17 of 40 patients. Endoscopic changes were more severe in those patients who had the infection both in the stomach and in the esophagus. CONCLUSION: The presence of Helicobacter pylori in the lower esophagus and antral stomach in DU patients may entail negative changes in the stomach and esophagus.

Biopsy↗
PubMed1998

[Relevance of Helicobacter pylori infection in the development of gastric tumors].

Helicobacter pylori plays an important role in the pathogenesis of peptic ulcer disease. Besides, epidemiological studies indicate that helicobacter may be involved in the development of gastric cancer and MALT-lymphoma by inducing gastritis and accumulation of lymph follicles in the gastric mucosa. The carcinogenic effect of helicobacter pylori can be explained by various pathogenetic factors which are produced by the bacterium itself. Furthermore, influences of helicobacter pylori on the vitamin C content of gastric mucosa might play a role. Currently, Hp-eradication therapies for the treatment of gastric MALT lymphomas are already under investigation in controlled studies. Concerning gastric cancer prevention, however, the available data are not sufficient to warrant a general recommendation for eradication-therapies of all Hp-infected persons. However, further studies must show whether Hp-eradication of high-risk subjects, i.e. members of gastric cancer families, young patients with chronic-active gastritis or with chronic-atrophic gastritis and intestinal metaplasia, are effective in reducing gastric cancer risk.

Helicobacter Infections↗
PubMedDate not supplied

[Primary gastritis associated with Helicobacter pylori in children].

The aim of this paper was to investigate whether a correlation between dyspeptic symptoms and infection due to Helicobacter pylori could be established. We conducted a prospective study with 27 children who had Helicobacter pylori associated antral gastritis with endoscopic and histologic alterations, without any other peptic lesions. Helicobacter pylori was detected by rapid urease test and histology with hematoxylin and eosin and Giemsa stain. Endoscopy revealed antral nodularities in 20/27 (74%) and enantema in six cases (23%). During histological examination active chronic superficial gastritis was confirmed in 26 cases (96%). Twenty seven children were treated with antimicrobial therapy, eight of which presented infection eradication, six presented nodularities regression and symptoms remission in four. Of the 19 non-eradicated patients, eight (42%) became asymptomatic and 11 maintained symptoms. Statistical analysis to compare symptoms remission was not significant. Taking into account the results presented herewith, we concluded that antral nodularity was the most common endoscopic finding, and there was no sufficient evidence of a correlation between Helicobacter pylori infection and dyspeptic symptoms.

Adolescent↗
PubMed1998

[Role of cytokines in the pathogenesis of gastrointestinal diseases associated with Helicobacter pylori infection].

It is well known that Helicobacter pylori can cause gastritis, gastroduodenal ulcers and malignant diseases. The infiltration of polymorphonuclear leukocytes is recognized in the lesions of these diseases, and the infiltration disappears by antibiotic therapy. However, it is not yet clarified how Helicobacter pylori induces the formation of lesions including leukocyte infiltration. Recently, we have confirmed that several kinds of cytokines are expressed in the gastric biopsy specimens of gastroduodenal diseases. Especially, it is conjectured that chemokines such as interleukin-8 (IL-8) which are expressed in the specimens, induce leukocyte infiltration, gastric mucosal inflammation and gastroduodenal ulcers. It is possible that Helicobacter pylori CagA gene is closely related with IL-8 expression because this cytokine is more strongly expressed in the specimens from the patients infected with CagA-positive Helicobacter than those with CagA-negative one.

Anti-Bacterial Agents↗
PubMed1998

[Eradication of Helicobacter pylori by triple therapy in ulcerous patients: the role of endoscopy and antibiotic sensitivity].

BACKGROUND: A protocol was conducted to evaluate the compliance and results of Helicobacter pylori infection treatment in patients with ulcer disease. To know the metronidazole, clarithromycin and amoxicillin activities of Helicobacter pylori strains from such patients. PATIENTS AND METHODS: 35 patients with ulcer disease (27 duodenal ulcer and 8 gastric ulcer) were studied. Diagnosis of Helicobacter pylori infection was performed by urease test and culture of mucosal gastric samples from patients undergoing endoscopy. The patients received the following treatment during 7 days: omeprazole (20 mg bid), clarithromycin (500 mg bid) and amoxicillin (1 g bid), OCA x 7. Susceptibility was determined by E-test system on Wilkins-Chalgren blood agar and read after 5 days. RESULTS: 22/24 patients who had completed the protocol design eradicated Helicobacter pylori (91.7%), 11 patients (31.4%) refused second endoscopy to verify control of eradication. After treatment 10 patients presented with pyrosis "de novo" (28%). The overall metronidazol, claritromycin and amoxicillin resistance rate was 50%, 1.5% and 0% respectively. CONCLUSIONS: OCA x 7 treatment obtains a eradication rate higher than 90% in our patients with ulcer disease, despite smoking habit, but with a significative number of patients presenting pyrosis after treatment. We recommend a non-endoscopy method to verify eradication rate, because of its poor acceptance. 3. Metronidazol resistance rate is high in our series but clarithromycin susceptibility is maintained.

Adult↗
PubMed1992

Catalase negative mutants of Helicobacter pylori.

Nine strains of Helicobacter pylori have been isolated exhibiting spontaneous mutations with a loss of catalase activity. Growth characteristics in vitro were unaffected by the mutation showing that catalase is not essential for growth of Helicobacter pylori. Parent strains and mutants could not be distinguished morphologically from each other when compared by electron microscopy. Restriction endonuclease digestion with HindIII, separated in an 0.7% agarose gel in TBE buffer, showed each pair to be highly related to each other. SDS-PAGE separation of proteins from four mutants and parent strains showed that all mutants lacked a 57 kDa protein. The partial N-terminal sequence of this protein shows homology with maize catalase and may be the subunit of the Helicobacter pylori catalase tetramer. It is concluded that catalase negative mutants of Helicobacter pylori occur spontaneously in vitro, but have not yet been observed in vivo. The paucity of such catalase negative strains in clinical specimens could mean that catalase is a virulence factor in vivo that puts mutants at a selective disadvantage.

Amino Acid Sequence↗
PubMed1991

Transport conditions and number of biopsies necessary for culture of Helicobacter pylori.

Stuart's transport medium with a charcoal impregnated swab was tested for transport of biopsies from the gastric antrum for culture of Helicobacter pylori. Biopsies were cultured under microaerophilic conditions either within 2 h or after a delay of 24 h at 4 degrees C. In 65 patients referred for gastroscopy two biopsies were taken. Helicobacter pylori was found in 39 patients. The rate of survival of Helicobacter pylori was found to be as high in Stuart's transport medium after 24 h at 4 degrees C as in the paired biopsy which was cultured immediately after transportation in normal saline. In five (13%) of 39 patients positive for Helicobacter pylori, the organism was cultured from only one of the biopsies. It is therefore recommended that two biopsies be taken for culture.

Bacteriological Techniques↗
PubMed1994

Culture of Helicobacter pylori under aerobic conditions on solid media.

The aim of the present study was to culture Helicobacter pylori under aerobic conditions and to investigate the characteristics of the organism when cultured aerobically. Most (22 of 23) of the Helicobacter pylori isolates grew under aerobic conditions, but with reduced viable cell counts. Blood agar was more suitable than chocolate agar. The morphological and enzymatic characteristics as well as the protein profiles of each organism were identical under aerobic and microaerophilic conditions. However, haemolysis of Helicobacter pylori was delayed under aerobic conditions. The MIC of metronidazole was slightly lower for some strains under aerobic conditions. These findings indicate that Helicobacter pylori is not only a microaerophilic organism but also adapts to aerobic conditions, which may have some important implications in microbiological and epidemiological studies.

Anaerobiosis↗
PubMed1990

Antigenicity of fractions of Helicobacter pylori prepared by fast protein liquid chromatography and urease captured by monoclonal antibodies.

The antigenicity of Helicobacter pylori protein fractions separated by fast protein liquid chromatography size exclusion was investigated by EIA with sera from patients of well defined Helicobacter pylori status. The antigenic material of Helicobacter pylori was confined to fractions 8 and 14 to 21. Urease containing fractions (14/15) and flagella containing fractions (17/18) were identified. Fraction 8 non-specifically bound human immunoglobulin as demonstrated by the binding of Helicobacter pylori negative sera. The remaining fractions 14 to 21 when used individually as EIA antigens were 91-100% specific, however fractions 16 to 19 showed a reduced sensitivity (78%) compared with the acid extract (95%). The urease fractions were 91% sensitive. Purified urease antigen captured by antiurease monoclonal antibodies was 83% sensitive and 93.3% specific.

Adult↗
PubMed1995

Detection and partial sequence analysis of Helicobacter pylori DNA in the bile samples.

The existence of Helicobacter pylori in the biliary tract was investigated. Seven bile samples were included in this study. Among them, six bile samples were collected by percutaneous transhepatic cholangiodrainage and the other by needle aspiration during cholecystectomy. Using nested PCR with two sets of primers homologous to the urease A gene, Helicobacter pylori DNA was detected. Three samples, one from a patient with advanced gastric cancer involving the pancreatic head and two from patients with pancreatic head tumor, were found to be positive for Helicobacter pylori DNA. On the other hand, three samples from patients with cholangiocarcinoma and one from a patient with chronic cholecystitis were all negative. To further verify the specificity of our PCR analysis, partial sequences of the PCR products from the three positive samples were analyzed by direct sequencing. Several silent mutations and a missense mutation (AAA to AGA; Lys-164 to Arg-164) were identified in the urease A gene. We conclude that Helicobacter pylori DNA can be easily detected in the bile samples. The possibility of asymptomatic cholangitis caused by this organism requires further investigation.

Adult↗
PubMed1999

Growth characteristics and influence of antibiotics on rough/smooth phenotypic variants of Helicobacter pylori.

Helicobacter pylori shows a rather high variability of several biochemical markers including lipopolysaccharide structures. This study aimed to determine whether Helicobacter pylori has a potential for phenotypic variability and to describe its effects on bacterial pathogenesis. From colonies of three clinical strains of Helicobacter pylori with rough (R) colony morphology, spontaneous phenotypic variants with smooth (S) colony morphology were isolated that occurred with a frequency of 10(-2) to 10(-3), irrespective of growth conditions. R-variant bacteria produced exclusively low-molecular-mass lipopolysaccharide. They exhibited increased lysis in the presence of plain air. In contrast, the S variants produced low- and high-molecular-mass lipopolysaccharide and did not exhibit increased lysis in the presence of plain air. Cocultivation of bacterial cells with AGS stomach cancer cells revealed that R-variant bacteria but not S-variant bacteria effected an inhibition of high molecular-weight glycoprotein biosynthesis and secretion by the host cells. Skirrow supplement added as selective agent to liquid and/or solid media was tolerated to a similar extent among R- and S-variant bacteria, while all variants proved sensitive to metronidazole, amoxicillin and clarithromycin except for the R and S isolates of strain Hp57, which showed resistance to the latter compound. It was concluded that R- and S-variants of Helicobacter pylori may have distinct roles in pathogenesis; nevertheless, these bacteria may be isolated by traditional methods and eradicated by conventional anti-infective therapy.

Anti-Bacterial Agents↗
PubMed1992

Alcohol dehydrogenase mediated acetaldehyde production by Helicobacter pylori--a possible mechanism behind gastric injury.

Two standard Helicobacter pylori strains showed significant cytosolic alcohol dehydrogenase activity and produced considerable amounts of acetaldehyde when incubated with an ethanol containing solution in vitro. The alcohol dehydrogenase activity of the Helicobacter pylori strains was almost as high as that found in Klebsiella pneumoniae and far greater than that in Escherichia coli or Campylobacter jejuni. The amount of acetaldehyde produced by cytosol prepared from Helicobacter pylori exceeded that by any of the other bacteria studied. The bacterial production of acetaldehyde--a highly toxic and reactive substance--could be an important factor in the pathogenesis of Helicobacter pylori associated gastric injury and increased risk of gastric cancer.

Acetaldehyde↗
PubMed2026

Molecular characterisation and mutational analysis of antimicrobial resistance genes in Helicobacter pylori isolates in Erbil, Iraq.

BACKGROUND: Antibiotic resistance in Helicobacter pylori poses a significant challenge to the effective eradication of infection worldwide. Understanding molecular mechanisms of resistance is essential for guiding treatment strategies. This study aimed to investigate the molecular basis of antimicrobial resistance in Helicobacter pylori isolates and their associated mutation frequencies. METHODS: In this cross-sectional study, gastric biopsy specimens were collected from 203 patients at Rizgary Hospital in Erbil, Kurdistan Region, Iraq, who underwent endoscopy for dyspepsia-related symptoms. Of the 137 positive patients, 91 Helicobacter pylori isolates were confirmed by colony morphology, Gram staining, and biochemical tests; 63 were successfully subcultured for antimicrobial susceptibility testing (culture success rate: 69.2%). Antimicrobial susceptibility testing was performed by the agar dilution method to determine the minimum inhibitory concentrations. The sequences of specific genes were examined and analysed by next-generation sequencing. Multiple sequence comparisons were performed to identify resistance-related genes and mutations, using 26695 (NC_000915.1) as the reference genome. RESULTS: Only two isolates (3.17%) were susceptible to all antibiotics examined. The frequency of metronidazole resistance was highest (85.71%), followed by levofloxacin (55.55%), clarithromycin (52.38%), amoxicillin (26.98%), tetracycline (6.35%), and rifabutin (4.76%). Mutations in the rdxA and frxA genes correlated with metronidazole resistance, while GyrA protein mutations at positions 87 and 91 were linked to levofloxacin resistance. Clarithromycin resistance was mainly associated with A2142G and A2143G mutations in 23S rRNA. Amoxicillin resistance (26.98%) was associated with mutations in the pbp1A gene, whereas resistance to tetracycline and rifabutin was infrequent. CONCLUSIONS: This study provides the first molecular surveillance data on antimicrobial resistance in Helicobacter pylori in northern Iraq, offering valuable regional evidence to guide local eradication strategies. The relatively high amoxicillin resistance, together with the elevated resistance to metronidazole, levofloxacin, and clarithromycin, underscores the need for susceptibility-guided therapy and continuous local antimicrobial resistance surveillance.

Antibiotic resistance↗
PubMed2005

Helicobacter spp. from captive bottlenose dolphins (Tursiops spp.) and polar bears (Ursus maritimus).

The gastric fluid of six bottlenose dolphins and the faeces of four polar bears from the same oceanarium were examined for the presence of Helicobacter. As detected by PCR, all dolphins and 8/12 samples collected from polar bears were positive for Helicobacter. Novel sequence types were identified in samples collected from these animals of which several were unique to either the dolphins or the polar bears. At least one sequence type was, however, detected in both animal taxa. In addition, a sequence type from a dolphin shared a 98.2-100% identity to sequences from other Helicobacter species from harp seals, sea otters and sea lions. This study reports on the occurrence of novel Helicobacter sequence types in polar bears and dolphins and demonstrates the broad-host range of some species within these animals.

Animals↗
PubMed2000

Synergistic interaction between hypergastrinemia and Helicobacter infection in a mouse model of gastric cancer.

BACKGROUND & AIMS: Hypergastrinemia occurs frequently in association with acid suppression and Helicobacter infection, but its role in the progression to gastric atrophy and gastric cancer has not been well defined. METHODS: The effects of hypergastrinemia, and possible synergy with Helicobacter felis infection, were investigated in insulin-gastrin (INS-GAS) transgenic mice. RESULTS: INS-GAS mice initially showed mild hypergastrinemia, increased maximal gastric acid secretion, and increased parietal cell number but later progressed to decreased parietal cell number and hypochlorhydria. Development of gastric atrophy was associated with increased expression of growth factors, heparin-binding epidermal growth factor and transforming growth factor alpha. At 20 months of age, INS-GAS mice showed no evidence of increased enterochromaffin-like cell number, but instead exhibited gastric metaplasia, dysplasia, carcinoma in situ, and gastric cancer with vascular invasion. Invasive gastric carcinoma was observed in 6 of 8 INS-GAS mice that were >20 months old. Helicobacter felis infection of INS-GAS mice led to accelerated (< or = 8 mo) development of intramucosal carcinoma (85%), with submucosal invasion (54%) and intravascular invasion (46%; P < or = 0.05). CONCLUSIONS: These findings support the unexpected conclusion that chronic hypergastrinemia in mice can synergize with Helicobacter infection and contribute to eventual parietal cell loss and progression to gastric cancer.

Animals↗
PubMed1997

Morphological diversity of cultured canine gastric Helicobacter spp.

The cell morphology, the number of flagella, the occurrence of periplasmic fibrils and ultrastructural structures of five groups of cultured canine gastric Helicobacter spp. were compared. The study included four strains of Helicobacter felis, four strains of Helicobacter bizzozeronii, one strain of 'Flexispira', six strains of an unnamed spiral organism 2 and one strain of an unnamed spiral organism 3 which were isolated from gastric biopsies. Cultures were studied with negative staining, transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Bacterial dimensions were measured from the negative staining samples and values were tested with ANOVA and Bonferroni tests. The organisms studied differed from each other morphologically. H. felis was a slightly spiraled organism with periplasmic fibrils. 'Flexispira' was a thin and straight organism with periplasmic fibrils. H. bizzozeronii was a tightly spiraled organism. Spiral organism 2 was loosely spiraled and thicker than the other organisms. Spiral organism 3 was a short curved rod having a single bipolar flagellum. The other species had multiple flagella. As a conclusion the canine gastric Helicobacter spp. can be differentiated from each other morphologically with an electron microscope. The morphological differences were mainly found in the structures involved in motility. The importance of the differences may lie in their impact on the colonization in a gastric mucous environment.

Animals↗