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PubMed2001

Molecular resistance testing of Helicobacter pylori in gastric biopsies.

OBJECTIVE: To evaluate simultaneous diagnosis of infection and molecular resistance testing of Helicobacter pylori. METHODS: Gastric biopsies were obtained from 26 rapid urease-positive and 51 rapid urease-negative test kits used to diagnose H pylori infection. Following glass bead-assisted DNA isolation, amplification of H pylori 16S ribosomal DNA (rDNA), glmM, and 23S rDNA target genes was performed. RESULTS: Helicobacter pylori DNA was successfully amplified from 100% (26/26) of urease-positive and 3.9% (2/51) of urease-negative gastric biopsies. Subsequent restriction enzyme-mediated digestion of 23S rDNA amplification products revealed that 17% (4/24) of urease-positive and H pylori DNA-positive biopsy specimens contained point mutations (A2142G or A2143G) associated with clarithromycin resistance. Helicobacter pylori DNA from gastric biopsies was successfully amplified 8 weeks following rapid urease testing. CONCLUSION: Helicobacter pylori genotyping may be used to detect macrolide-resistant H pylori in individuals prior to initiation of therapy or in patients refractory to anti-H pylori therapy. Two urease-negative specimens yielded Helicobacter DNA distinct from that of H pylori and indicated the need for further investigations of Helicobacter species present in the human stomach.

Anti-Bacterial Agents↗
PubMed1998

Enterohepatic Helicobacters: natural and experimental models.

The genus Helicobacter now includes at least 18 formally named species as well as several novel helicobacters that have not been formally named. Eleven Helicobacter spp. colonize the intestinal tract of mammals and birds. In addition, a number of the intestinal helicobacters can colonize the biliary tract and liver, induce hepatitis and one in particular, Helicobacter hepaticus, can cause liver cancer in susceptible strains of mice. Further studies are needed to ascertain whether these helicobacters are also responsible for enterohepatic diseases in humans.

Animals↗
PubMed1998

Routes of transmission of Helicobacter pylori infection.

Helicobacter pylori is an important gastroduodenal pathogen, which has been recognized as a Class I carcinogen factor for gastric cancer and gastric mucosa associated lymphoid tissue lymphomas. In spite of the world-wide spread of the infection, the route of transmission is still not known. We reviewed data from several sero-epidemiological studies and aimed to identify potential sources of Helicobacter pylori infection. Available evidence strongly suggests an inverse correlation between socio-economic status and prevalence of Helicobacter pylori. The infection is acquired mostly during childhood in the third world, but is rare in children in developed countries, where the prevalence of Helicobacter pylori increases with age. Following the detection of the bacterium in saliva, faeces, and gastric juice, oral-oral or faecal-oral transmission and iatrogenic spread, through the use of unsterile endoscopes, have been proposed as possible routes of infection. Helicobacter pylori has also been found in some domestic cats, but at present, the risk of infection from these animals appears slight. The mode of transmission of Helicobacter pylori, as is yet, not known. Available information support the hypothesis of spread through close personal contact, considering humans as the only significant reservoir of infection.

Age Factors↗
PubMed1998

Gastro-oesophageal reflux and Helicobacter pylori.

The nature of the relationship between Helicobacter pylori infection and reflux oesophagitis is still not completely understood. To review the available evidence from the literature concerning the relationship between Helicobacter pylori infection and reflux oesophagitis with or without Barrett's metaplasia, we performed a Medline search to discover all published reports available in this field since the first description of Helicobacter pylori (1984) to April 1998. A total of 37 papers were found addressing the issue. From the available data, it can be concluded that Hp infection has probably only a minor protective role against the development of reflux oesophagitis. The related mechanisms are, however, still to be clarified. The presence of Helicobacter pylori infection is also likely to increase the efficacy of PPI drugs and, conversely, the eradication of the bacterium decreases the drug effect. The bacterial production of ammonia is the most likely factor explaining this observation. Furthermore, it is now sufficiently clear that patients placed on long-term PPI therapy develop atrophic gastritis only if Helicobacter pylori infection is not eradicated. Finally, both the development of metaplastic changes and the progression to severe dysplasia and adenocarcinoma in Barrett's oesophagus patients are phenomena not related to the presence of Helicobacter pylori antral or oesophageal colonization.

Adenocarcinoma↗
PubMed1999

Helicobacter pylori increases the risk of peptic ulcer bleeding: a case-control study.

AIM: Aim of the present case-control study was to establish whether Helicobacter pylori increases the risk of ulcer bleeding. PATIENTS AND METHODS: All patients presenting with upper gastrointestinal bleeding between November 1994 and November 1995 were prospectively investigated and compared with hospital controls matched for age, sex, and race. We evaluated the frequency of Helicobacter pylori infection, intake of aspirin or non-steroidal anti-inflammatory drugs, use of alcohol, and smoking habits in patients and controls. RESULTS: Included in the study were 128 patients. In 72 patients, the source of bleeding was a peptic ulcer (duodenal ulcer: n = 33; gastric ulcer: n = 39). Ulcer patients were more frequently infected by Helicobacter pylori than controls (72% vs 42%; p < 0.001) while the incidence of infection was similar in patients with non-ulcer bleeding and controls (52% vs 46%; p = 0.59). Conditional multiple logistic regression analysis showed that Helicobacter pylori infection (odds ratio, 3.3 [Confidence interval, 1.5 to 7.0]; p = 0.002) and regular use of alcohol (odds ratio, 3.1 [Confidence interval, 1.0 to 9.0]; p = 0.041) increased the risk of peptic ulcer bleeding while previous intake of aspirin (> 100 mg) or non-steroidal anti-inflammatory drugs independently increased the risk of bleeding only in the case of gastric ulcer (odds ratio, 8.1 [Confidence interval 1.2 to 56.6]; p = 0.034). CONCLUSIONS: Helicobacter pylori infection increases the risk of peptic ulcer bleeding. Our results suggest that Helicobacter pylori and non-steroidal anti-inflammatory drugs are independent risk factors for peptic ulcer bleeding.

Adult↗
PubMedDate not supplied

[The evaluation of a new immunoenzyme analysis for the detection of Helicobacter pylori infection in stool samples].

BACKGROUND: Detection of bacterial antigen in stool specimens (HpSAT) is a new promising tool for diagnosing Helicobacter pylori infection. OBJECTIVE: To evaluate diagnostic accuracy of HpSAT in the diagnosis of Helicobacter pylori infection. PATIENTS AND METHODS: We evaluate the presence of Helicobacter pylori infection by the rapid urease test and the 13C-urea breath test in endoscopic biopsies. Patients who were positive for both tests were considered to have Helicobacter pylori infection. Patients negative for both tests were considered free of infection. The presence of Helicobacter pylori infection was also determined in stool specimens by means of HpSAT. RESULTS: The sensitivity of HpSAT was 92.8%, the specificity 92.3%, the positive predictive value 98.1% and the negative predictive value 75%. CONCLUSIONS: HpSAT is a reliable tool for diagnosing Helicobacter pylori infection.

Adult↗
PubMed1999

Cellular immune responses are essential for the development of Helicobacter felis-associated gastric pathology.

The bacteria Helicobacter pylori is a major human pathogen that infects over half of the world's population. Infection initiates a series of changes in the gastric mucosa, beginning with atrophic gastritis and leading in some patients to peptic ulcer disease, mucosa-associated lymphomas, and gastric adenocarcinoma. Although this cascade of events clearly occurs, little is known about the role of the host immune response in disease progression. We have utilized the C57BL/6 Helicobacter felis mouse model to critically analyze the role of the adaptive immune response in the development of Helicobacter-associated gastric pathology. Infection of B and T cell-deficient RAG-1-/- mice or T cell-deficient TCRbetadelta-/- mice with H. felis resulted in high levels of colonization, but no detectable gastric pathology. Conversely, infection of B cell-deficient microMT mice resulted in severe gastric alterations identical with those seen in immunocompetent C57BL/6-infected mice, including gastric mucosal hyperplasia and intestinal metaplasia. These results demonstrate that the host T cell response is a critical mediator of Helicobacter-associated gastric pathology, and that B cells and their secreted Abs are not the effectors of the immune-mediated gastric pathology seen after H. felis infection. These results indicate that in addition to specific Helicobacter virulence factors, the host immune response is an important determinant of Helicobacter-associated disease.

Animals↗
PubMedDate not supplied

[The effects of eradication therapy in patients with chronic atrophic gastritis and seropositivity for anti-HP antibodies and histological negativity for Helicobacter pylori].

PURPOSE: The present study was undertaken to analyze both whether the elevated Helicobacter pylori levels in patients with atrophic gastritis without histologic evidence of Helicobacter pylori would be a sign of an ongoing infection and the effects of eradication on gastric atrophy. PATIENTS AND METHODS: Twenty patients (10 M e 10 F; mean age 57.25 SD 12.19) with atrophic gastritis and elevated Helicobacter pylori titers without histological evidence for Helicobacter-like organisms were included in the study. Ten patients were randomized into eradication group (Group 1) (amoxicillin at 500 mg twice a day for 14 days, metronidazole at 500 mg twice a day for 10 days and omeprazole at 20 mg twice a day for 20 days) and 10 patients were randomized into the control group (Group 2). For all subjects, serum samples and duplicate biopsy specimens (obtained endoscopically) were collected prior the study period and approximately 6 months after the therapy or the follow-up for serum samples and 8 weeks for biopsy specimens. RESULTS: In the Group 1, the Helicobacter pylori antibody titers dropped significantly in 73.39% of the patients (p < 0.0001), while in the Group 2, the antibody titers declined only in a patient who received antibiotics during the study period (p < 0.00006). In both groups, no significant improvement of atrophic gastritis was observed. CONCLUSIONS: In conclusion, in patients with atrophic gastritis, the only histological evaluation of Helicobacter-like organisms colonization in gastric biopsy specimens, appeared in our study to underestimate the true prevalence of current HP infection and the importance of the bacterium in the pathogenesis and progression of such disease. Since HP infection is often associated with an increase of proliferative index, the eradication of HP could induce a mucosal protective effect against the other carcinogen factors, although it is extremely unlikely that it can promote the regeneration of a normal gastric mucosa.

Adult↗
PubMed1999

Relationship of Helicobacter pylori infection with gastrointestinal motility.

The interest of gastroenterologists in the relationship between Helicobacter pylori and gastrointestinal motility emerges from the observation that Helicobacter pylori may be involved in the pathogenesis of functional dyspepsia and that a relatively large percentage of patients with dyspepsia may show impaired gastrointestinal motility. A number of studies have been published on the interaction between Helicobacter pylori infection and gastrointestinal motility with controversial results, and, therefore, there are no definite conclusions, as yet, as to whether Helicobacter pylori is able, at all, or in which degree, to influence the motility of the upper gastrointestinal tract. Motility of the upper gastrointestinal tract has been studied in Helicobacter pylori positive and negative individuals by means of manometry, scintigraphy, radio-opaque markers or by other, recently developed, procedures such as breath tests, ultrasonography, and barostat. The vast majority of studies do not support the hypothesis that Helicobacter pylori may influence gastrointestinal motility. Nearly all these studies are, however, affected by methodological problems related to the small numbers of patients, different methodological approaches, and to the well-known difficulties in studying both gastrointestinal motility and functional dyspepsia.

Dyspepsia↗
PubMed2000

Monitoring sentinel mice for Helicobacter hepaticus, H rodentium, and H bilis infection by use of polymerase chain reaction analysis and serologic testing.

BACKGROUND AND PURPOSE: Natural infection of research mice with enterohepatic Helicobacter spp. is common and may confound experimental studies from intercurrent disease. We evaluated a protocol of dirty bedding exposure for transmission of Helicobacter infection from colony mice to female Tac:(SW)fBR sentinel mice over 6 months. METHODS: Cecal scrapings from culled colony mice and associated sentinel mice were tested for H. hepaticus, H. rodentium, and H. bilis using polymerase chain reaction analysis (PCR). These results were correlated with the results of sentinel serum IgG responses measured by ELISA. RESULTS: In 9 colony rooms, 43 of 45 mice were infected with H. hepaticus; in 14 rooms, 58 of 70 mice were infected with H. rodentium; and in 2 rooms, 2 of 10 mice were infected with H. bilis. Concurrence of Helicobacter infection between colony and sentinel mice was 82% for H. hepaticus, 88% for H. rodentium, and 94% for H. bilis. Concurrence of Helicobacter infection status of sentinel cagemates was 98% for H. hepaticus, 86% for H. rodentium, and 95% for H. bilis. Fecal samples pooled by sentinel cage had positive PCR results for H. hepaticus and H. rodentium at 1 month in 60 and 44%, respectively, of the cages that contained test-positive mice at necropsy (6 months). By 3 months, detection rates were 100 and 81% for H. hepaticus and H. rodentium, respectively, and H. bilis was not detected until 4 months. Newly acquired infections with H. rodentium and H. bilis were evident throughout the 6-month study period. Seroconversion was coincident with positive PCR results in sentinel mice, and serum IgG values continued to increase until necropsy. The serum IgG ELISA was 98 to 100% sensitive, but was low in specificity (34 to 44%), most likely attributable to common coinfection with H. hepaticus and H. rodentium. CONCLUSION: Sentinel mice acquire infection with Helicobacter spp. through dirty bedding exposure. Combined use of PCR analysis and serologic testing of sentinel mice was predictive of Helicobacter infection status of mouse colonies used for biomedical research.

Animals↗
PubMed2002

The current status of Helicobacter pylori.

We present a review of the current status of Helicobacter pylori infection, and focus on the clinical issues facing physicians with regards to its pathogenicity, diagnosis and treatment. We have attempted to address the important clinical issues relevant to the subject, and summarize the currently accepted concepts concerning Helicobacter pylori. Our knowledge regarding Helicobacter pylori biology is enormous, but detailed knowledge on its transmission is still far from clear. Helicobacter pylori is mainly involved in gastrointestinal and possibly in other extra-intestinal disorders. There are differences in the clinical presentation in various geographical regions resulting from variations in the genetic make-up of Helicobacter pylori. There is still need for more simple, cost-effective, accurate and less invasive diagnostic techniques. The gold standard treatment is the one-week proton pump inhibitor-based triple regimen as first line, with quadruple therapy as a 2nd line. Helicobacter pylori resistance to the main antimicrobials needs to be defined in particular geographical areas.

Gastroesophageal Reflux↗
PubMed2002

Frequency of Helicobacter pylori infection in dyspeptic patients in Libya.

OBJECTIVE: Helicobacter pylori infection is a very common infection worldwide particularly in the developing countries. The organism plays an important role in peptic ulcer diseases. The aim of the study was to detect and correlate the prevalence of Helicobacter pylori with such diseases and to evaluate the histopathological grading of gastritis. METHODS: One hundred thirty two patients of 15-83 years of age (average 38) attending the endoscopy unit at the El-Jamahiria Hospital, Binghazi, Libya, mainly complaining from epigastric pain were randomly selected. Three antral biopsies for rapid urease test, direct smear stain and histology together with serum samples were obtained from each patient. Grading of gastritis and the presence of Helicobacter pylori was scored according to the Sydney system. RESULTS: Patients were considered infected when 2 of the biopsy-based tests were positive. Helicobacter pylori was detected in 108 (82%) of 132 patients examined (86% by rapid urease test, 77% by direct smear stain, 95% by histology). The endoscopic findings revealed that 77 (77%) of 100 patients with non-ulcer dyspepsia, 26 (96%) of 27 with duodenal ulcer, 4 (100%) of 4 with gastric ulcer and in one patient with gastric cancer were Helicobacter pylori positive. The enzyme-linked immunosorbent assay test showed 94% sensitivity and 88% specificity. Histopathological sections from the majority of duodenal ulcer and gastric ulcer patients revealed higher grade (II and III) of gastritis than non-ulcer dyspepsia patients. CONCLUSION: Helicobacter pylori infection is significantly correlated with peptic ulcer diseases than with non-ulcer dyspepsia. Patients with duodenal ulcer and gastric ulcer had a significantly higher grade of gastritis than patients with non-ulcer dyspepsia.

Adolescent↗
PubMed2002

[Non-ulcer dyspepsia and Helicobacter pylori infection].

In this article we reviewed experiences in approach and procedure with dyspepsia, with special accent on non-ulcer dyspepsia and Helicobacter pylori infection. Dyspepsia makes around 50% of gastroenterology cases. In 20% of cases it is caused by peptic ulcer disease and in 50% of cases non-ulcer dyspepsia. Around 50% of non-ulcer dyspepsia is followed by coexistent Helicobacter pylori positive gastritis. Dyspepsia followed by alarming symptoms in patients who are over 55 years old or in patients who are using NSAID indicated urgent endoscopic procedure--gastroscopy. In other patients non-invasive testing on Helicobacter pylori infection is recommended where eradication therapy should be applied in Helicobacter pylori positive and empirical cure by antisecreting drugs or prokinetics in Helicobacter pylori negative patients. Final gastroscopic evaluation is indicated after unsuccessful therapy. Ceasing of non-ulcer dyspeptic symptoms could be predicted in 20% of patients with cured Helicobacter pylori infection.

Adult↗
PubMed2002

[A vaccine against Helicobacter pylori infection].

Oral immunization with the urease of Helicobacter pylori was shown to induce protection against Helicobacter felis in mice. The first identification of a protective antigen (urease) was followed by the identification of the protective antigens, such as the heat-shock protein (HspA) and the vacuolating cytotoxin VacA. The final selection of the antigens to be used in a vaccine depends on the conservation of these antigens among Helicobacter pylori strains, their role as virulence factors and conservation of their immunogenic properties when expressed as recombinant proteins. Furthermore, therapeutic immunizations were also effective in eradication of Helicobacter from chronically infected animals. These encouraging results imply that immunization may also be useful in the therapy of Helicobacter pylori infection in humans. In this review, preliminary data and directions for future research on Helicobacter vaccines are described.

Animals↗
PubMed2002

UreC PCR based diagnosis of Helicobacter pylori infection and detection of cag A gene in gastric biopsies.

Polymerase chain reaction assay using ureC gene specific primers for the detection of Helicobacter pylori in gastric biopsy specimens from 116 dyspeptic patients was compared with other routine invasive diagnostic methods (culture, rapid urease test [RUT] and histology). In parallel, gastric biospy specimens from 54 patients and their corresponding Helicobacter pylori isolates were subjected to PCR with cagA targeting primers using standard protocols. Helicobacter pylori were detected in 53%, 43%, 48% and 50% of patients by PCR, RUT, culture and histological examination respectively. Based on histology and culture positive and at least three test positive result, 44 (37%), 46 (39%) and 26 (22%), and 56 (48%), 52 (44%) and 8 (6%) patients were classified as Helicobacter pylori positive, negative and indeterminate respectively. The sensitivity and specificity of PCR assay was the highest-95% and 100% when compared with both culture and histology positive, and at least any three positive results respectively. The result of cagA positivity in 54 gastric biopsy specimens and their corresponding Helicobacter pylori isolates were identical; 18 of 20 (90%) duodenal ulcer patients and 23 of 28 (82%) patients with chronic gastritis and 2 (40%) of 5 patients with portal hypertension and one gastric biopsy specimens from gastric cancer patients were found to be cagA positive. PCR-based method to detect Helicobacter pylori and the virulence gene cag A directly from gastric biopsy specimens appears to be promising and can curtail the lengthy process of culture-based approaches. The procedure proved to be rapid and reliable and could be utilized for diagnostic purposes.

Adult↗
PubMed2002

Helicobacter pylori-negative peptic ulcer. What is its aetiopathogenesis and treatment?

Although the vast majority of peptic ulcers are widely considered as related to the germ Helicobacter pylori, ulcers exhibiting absence of this infection are increasingly seen in recent years. This fact has been partly related to a decreased prevalence of Helicobacter pylori among the population, a consequence of improved hygiene and housing conditions. Causes in relation to Helicobacter pylori-negative ulcers are: 1. Falsely negative infection diagnostic tests. They represent 25% of ulcers considered as Helicobacter pylori-negative in health-care practice (falsely negative diagnostic test 5%, previous or concomitant therapy with antibiotics, bismuth or proton pump inhibitors 20%). 2. Aspirin (ASA) or non-steroidal anti-inflammatory drug (NSAID) therapy. This is no doubt the most common cause, representing 50 to 60% of all infection-free ulcers. 3. Other causes (Zollinger-Ellison syndrome, Helicobacter heilmannii, generalised gut disease such as Crohn's disease, amyloidosis, eosinophilic gastroenteritis, etc.) may be responsible for less than 5% of all Helicobacter pylori-negative ulcers. 4. "Idiopathic" peptic ulcers. Thus are considered ulcers for which no potential cause may be found, representing 5-15% of all infection-free ulcers. Acid hyper-secretion is probably an important factor in them.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2003

Optimal age at fostering for derivation of Helicobacter hepaticus-free mice.

Helicobacter hepaticus is well established as an unwanted variable in laboratory rodent colonies. Historically, cesarean section and embryo transfer have been used to derive Helicobacter-free mouse colonies. Neonatal transfer of newborn mice onto Helicobacter-free foster dams was recently reported as an alternative method of deriving Helicobacter-free mice, but until now, the age by which pups must be fostered to remain Helicobacter-free was unknown. The purpose of the study reported here was to determine the age by which mouse pups must be fostered to remain free of H. hepaticus. Beginning on the day of birth, 20 C57BL/6 mice were fostered from H. hepaticus-positive parents onto Helicobacter-free BALB/c dams each day for 14 days for a total of 280 pups fostered. Fecal specimens collected at weaning, and fecal, liver, and cecal specimens collected at euthanasia were analyzed by use of polymerase chain reaction (PCR) analysis. No pup fostered within 24 h of birth became infected with H. hepaticus; however, many of those fostered after 24 h became infected. These results were supported by those of a large field trial, in which 201 litters representing 71 strains of mice were fostered within 24 h of birth. Follow-up fecal PCR analysis was performed on 52 mice or their progeny that were randomly sampled from the 201 fostered litters. All mice tested remained free of H. hepaticus approximately 100 days after fostering. The results indicate that mouse pups must be fostered within 24 h of birth to remain free of H. hepaticus. In addition, cecal and fecal PCR analyses detected more infections, than did liver PCR analysis, thus indicating that those specimens are preferred for detection of H. hepaticus infection.

Age Factors↗
PubMed2003

Serum Helicobacter pylori IgG and IgA levels in patients with gastric cancer.

The association between Helicobacter pylori and gastric cancer has been debated in the last decade and evidence for such a causal relationship has been claimed. This study aimed to detect the seroprevalence of Helicobacter pylori in patients with gastric cancer and compare it to the other cancer patients. In addition, the value of IgG and IgA in Helicobacter pylori detection was compared in patients with gastric cancer. Consecutive gastric and other cancer patients treated between 1999-2001 were prospectively studied. Serum Helicobacter pylori IgG and IgA levels were determined. Serological tests revealed IgA and IgG positivity as 53.9% and 50.9%, respectively, while 74.5% had positive results for either IgA or IgG. Serum IgA positivity was significantly higher in gastric cancer group compared to control group (p=0.02). In contrast, serum IgG positivity did not show a significant difference in both groups and either IgG or IgA seropositivity was significantly higher in patients with gastric cancer compared to control patients (p=0.04). This study revealed a higher seroprevalence of Helicobacter pylori in gastric cancer patients and IgA was a better predictor of Helicobacter pylori seropositivity in gastric cancer patients.

Adolescent↗