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PubMed2001

Accuracy of the stool antigen test in the diagnosis of Helicobacter pylori infection before treatment and in patients on omeprazole therapy.

AIM: To evaluate the Helicobacter pylori stool antigen (HpSA) test in the assessment of H. pylori infection and the effect of omeprazole treatment on its accuracy. METHODS: Study 1: 140 dyspeptic patients were enrolled in the study and defined as H. pylori positive if histology and rapid urease test, or culture alone were positive. HpSA was performed on all patients and 13C-urea breath test (UBT) on 87. Study 2: 75 patients testing positive using both UBT and HpSA, were given omeprazole 20 mg for 2 weeks (Group A) or omeprazole 40 mg for 2 weeks (Group B), or OAC for 1 week (group C). A Helicobacter pylori stool antigen test was performed on all patients on days 3, 5, 7 and 14 during treatment, and also on days 7 and 14 post-treatment in groups A and B. UBT was performed in groups A and B on days 7 and 14 during treatment, and days 7 and 14 post-treatment. RESULTS: 80/140 patients were H. pylori positive. The sensitivity and specificity of HpSA were 93.8 and 90%, similar to UBT (93.9 and 92.1%). Omeprazole significantly reduced both HpSA and UBT values, resulting in a decreased accuracy. Of 25 patients receiving 20 mg omeprazole, HpSA gave 5 and 6 false negatives after 7 and 14 days treatment respectively, while UBT gave 4 and 7 false negatives after 7 and 14 days treatment. Of 25 patients receiving 40 mg omeprazole, HpSA gave 7 and 9 false negatives after 7 and 14 days of treatment, while UBT gave 8 and 9 false negatives after 7 and 14 days of treatment. Two weeks after stopping omeprazole treatment, the HpSA and UBT were positive in all cases. CONCLUSIONS: The Helicobacter pylori stool antigen test is valuable in the assessment of H. pylori infection. Short-term omeprazole treatment decreases the accuracy of both HpSA and UBT in a similar manner.

Adult↗
PubMed2001

Modified seven-day, quadruple therapy as a first line Helicobacter pylori treatment.

BACKGROUND: Cure rates of 7-day triple therapy seem to be decreasing. Quadruple therapies may be an alternative, although their complex administration makes patient acceptance difficult. OBJECTIVE: To test the usefulness of a thrice a day, quadruple therapy to cure Helicobacter pylori infection. PATIENTS AND METHODS: A total of 122 consecutive patients with peptic ulcer and Helicobacter pylori infection were treated with omeprazole 20 mg b.d., tetracycline chlorhydrate 500 mg t.d.s., metronidazole 500 mg t.d.s., and bismuth subcitrate 120 mg t.d.s. administered with meals for 7 days. Cure was tested by either endoscopy or breath test after 2 months, and by urea breath test 6 months after therapy. RESULTS: Seven patients were lost to follow-up. Of the remaining 115, 110 were cured at the first control, giving an intention-to-treat cure rate of 90.2% (95% CI: 83-95%) and a per protocol cure rate of 95.7% (95% CI: 90-98%). One hundred three patients returned for a 6-month breath test; all but one were cured. Side-effects were minimal or minor in 47 patients (40.8%) and moderate in four (3.4%). Compliance was good, 95% of patients taking more than 90% of the pills. Six (5%) patients stopped treatment after 1, 2, 4 (two patients) and 6 (two patients) days. CONCLUSION: Thrice a day quadruple therapy shows excellent cure rates, far above 90%, is well-tolerated and compliance is easy. Head-to-head comparison with triple therapies as first line Helicobacter pylori treatment seems warranted.

Administration, Oral↗
PubMed2001

Lack of symptom benefit following presumptive Helicobacter pylori eradication therapy in primary care.

BACKGROUND: Helicobacter pylori eradication regimens have failure rates under 10%, however little information is available on the effect of treatment success in reducing the subsequent prescription of anti-ulcer medications in primary care. AIMS: To determine, using a large prescription database in eastern Ireland, the success of presumptive eradication therapy in improving symptoms of dyspepsia in primary care, as judged by a reduction in the subsequent prescription of anti-ulcer medications. METHODS: In a cross-sectional study, we identified 3847 patients who received a prescription for eradication therapy for Helicobacter pylori, including 826 who were followed for 9-11 months. Those who subsequently received anti-ulcer medications were deemed failures to obtain symptom relief. RESULTS: For 3847 patients with a median follow-up of 8 months, the failure rate was 49%. Of 826 patients, followed for a longer period (9-11 months), the overall failure rate was 56% (range 44-62% depending on the eradication regimen used). Age over 65 years (hazard ratio=1.57, 95% confidence interval= 1.29-1.91, P < 0.001), prior use of anti-ulcer medications (hazard ratio=1.97, 95% confidence interval=1.63-2.37, P < 0.001) and prior use of aspirin/NSAIDs (hazard ratio=1.43, 95% confidence interval=1.18-1.73, P < 0.001) all predicted failure to obtain relief of symptoms of dyspepsia from eradication therapy. CONCLUSIONS: Such high failure rates of eradication therapy in reducing the subsequent consumption of anti-ulcer medications have both clinical and economic implications for the use of eradication therapy for Helicobacter pylori in primary care.

Adult↗
PubMed2002

Review article: Helicobacter species and hepatobiliary diseases.

Helicobacter species, which may colonize the biliary tract, have been implicated as a possible cause of hepatobiliary diseases ranging from chronic cholecystitis and primary sclerosing cholangitis to gall-bladder carcinoma and primary hepatic carcinomas. Research in this area has been limited by the lack of a gold standard in the diagnosis of these organisms in bile. Most published data to date have been based on molecular techniques that detect the DNA of Helicobacter species in bile, rather than evidence of viable organisms in bile. Helicobacter species have not been shown to induce histological injury to the biliary epithelium or liver parenchyma. The strongest association of the presence of these organisms in bile is with cholestatic conditions. This article reviews the literature on this newly developing field as it has evolved historically, taking pertinent methodological issues into account.

Bile↗
PubMed2003

Levofloxacin-based triple therapy vs. quadruple therapy in second-line Helicobacter pylori treatment: a randomized trial.

BACKGROUND: Levofloxacin has been shown to be effective in Helicobacter pylori eradication. Two 10-day levofloxacin-based triple therapies were compared with standard 7- and 14-day quadruple regimens in second-line treatment. METHODS: Two hundred and eighty consecutive patients who failed to respond to standard triple therapy (clarithromycin, amoxicillin, rabeprazole) were randomly assigned to four groups: (1) levofloxacin 500 mg o.d., amoxicillin 1 g b.d., rabeprazole 20 mg b.d. for 10 days (LAR, n = 70); (2) levofloxacin 500 mg o.d., tinidazole 500 mg b.d., rabeprazole 20 mg b.d. for 10 days (LTR, n = 70); (3) tetracycline 500 mg q.d.s., metronidazole 500 mg t.d.s., bismuth salt 120 mg q.d.s., rabeprazole 20 mg b.d. for 7 days (7TMBR, n = 70); and (4) for 14 days (14TMBR, n = 70). Helicobacter pylori status and side-effects were assessed 6 weeks after treatment. RESULTS: The eradication rate was 94% in the LAR group and 90% in the LTR group in both intention-to-treat and per protocol analyses. Helicobacter pylori eradication was achieved in 63 and 69% of the 7TMBR group and in 69 and 80% of the 14TMBR group in intention-to-treat and per protocol analysis, respectively. Side-effects were significantly lower in the LAR and LTR groups than in the 14TMBR group. CONCLUSION: Ten-day levofloxacin-based therapies are better than standard quadruple regimens as second-line option for H. pylori eradication.

Adolescent↗
PubMed1998

Screening for gastric cancer by Helicobacter pylori serology: a retrospective study.

BACKGROUND: Screening by serology for Helicobacter pylori in young dyspeptic patients has been shown to be effective in reducing demand for endoscopy. H. pylori has been implicated in the causation of gastric cancer and the reported seropositivity rate in patients with gastric cancer ranges from 69 to 94 per cent. The aim of this study was to assess the potential value of Helicobacter antibodies as a method of selecting dyspeptic patients over the age of 45 years for endoscopy. METHODS: A retrospective comparison of the antibody status to H. pylori was made between 154 patients with gastric cancer and a sex- and date of birth-matched dyspeptic control group. Results from the former group were correlated with demographic data and tumour characteristics. RESULTS: Significantly more patients with gastric cancer were seropositive than controls (77 versus 66 per cent). H. pylori was not related to the Laurén classification of the tumour. Tumour site was significant: body and antrum tumours were associated with Helicobacter whereas cardial tumours appeared to be unrelated. CONCLUSION: Screening by antibody assays to H. pylori would miss more than 30 per cent of current gastric cancers. The increasing incidence of cardial cancer would cause this percentage to rise in the future.

Adult↗
PubMed1996

Helicobacter pylori infections in IgA deficiency: lack of role for the secretory immune system.

During the last years considerable attention has been focused on the possibility of the development of an oral vaccine against Helicobacter pylori. However, Helicobacter infection is known to be life-long, despite a vigorous immune response, and the hypothesis that an increased local production of secretory IgA in the gastric mucosa, due to vaccination, should protect against the colonization of the bacterium may therefore be questioned. In this study, when comparing the seropositivity and titre against H. pylori in IgA-deficient patients and age-related normal blood donors, it appears that lack of secretory IgA does not seem to have any major influence on the prevalence of the infection, nor is it reflected in titres of specific IgG antibodies. These results many argue against a pivotal role for IgA in the defence against Helicobacter, and raise questions about current strategies for the development of an oral vaccine against H. pylori and may point to a need for alternative therapeutic strategies.

Adult↗
PubMed1999

The role of Helicobacter pylori in primary gastric MALT lymphoma.

AIMS: Helicobacter pylori has been claimed to be an important aetiological factor which raises the risk of mucosa-associated tissue lymphoid (MALT) lymphoma. However, some studies on gastric MALT lymphoma revealed a low rate of H. pylori infection suggesting that not all gastric lymphomas are related to H. pylori infection. The aim of this study was to verify the H. pylori infection frequency in a series of patients with primary gastric MALT lymphomas and to examine the relationship between H. pylori and the pathological features of those lymphomas. METHODS AND RESULTS: Thirty-one cases of resected gastric lymphoma were analysed: 10 cases (32%) were low-grade MALT lymphomas and 21 cases (68%) were high-grade MALT lymphomas. Helicobacter pylori was found in only 18 of 31 (58%) cases. Helicobacter pylori infection was significantly correlated with the grade and depth of invasion of MALT lymphoma since 63% of superficial low-grade MALT lymphomas were positive for H. pylori compared with 38% of advanced high-grade MALT lymphomas (P = 0.02). CONCLUSION: We confirmed the relationship between H. pylori infection and a subset of gastric MALT lymphoma. Our results also showed that not all low- and high-grade gastric MALT lymphomas are H. pylori-dependent. This suggests that H. pylori infection may play a promoter role in the development of MALT lymphoma, but its presence is not mandatory for the progression of the lymphoma in view of its low frequency in advanced high-grade MALT lymphoma.

Adult↗
PubMed1999

Evaluation of a molecular identification scheme based on 23S rRNA gene polymorphisms for differentiating canine and feline gastric Helicobacter spp.

A scheme for the rapid identification of Helicobacter spp. using restriction fragment length polymorphism digestion profiles of PCR amplified 23S rRNA genes is described. The efficacy of this scheme for speciation of the closely related gastric species H. felis, H. bizzozeronii and H. salomonis was evaluated. It was difficult to distinguish between some RFLP profiles obtained and often, more than one profile was seen with each species examined. Some evidence was found that the 23S rRNA gene copies of these species may not be identical. Moreover, the identification scheme was ineffective in discriminating these species from each other, although they could be differentiated, as a group, from other Helicobacter spp. The results indicate that this scheme should be carefully evaluated with a number of isolates if it is to be applied to additional, highly related Helicobacter spp.

Animals↗
PubMed1999

Helicobacter pylori and extra-digestive diseases.

Helicobacter pylori is a recently rediscovered gram-negative bacteria that causes peptic ulcer disease, gastric lymphoma and gastric carcinoma. Helicobacter pylori achieves its pathogenetic role by triggering an intense leucocyte infiltration of the gastric submucosa which is mediated by proinflammatory cytokines. This pathogenetic mechanism is common to many other diseases and, therefore, Helicobacter pylori seroprevalence has also been investigated in other diseases. It is now known that H. pylori seropositivity is associated with an increasing number of cardiovascular, respiratory, extra-gastroduodenal digestive, neurological, skin, autoimmune, growth and miscellaneous disorders. Although the precise role for H. pylori is unknown in these diseases, it is of tremendous interest to most clinicians and scientists as H. pylori is amenable to eradication therapy using simple and reliable drug regimens. The conditions associated with H. pylori seropositivity are highlighted in this concise article.

Apoptosis↗
PubMed1999

Ethanol intake preceding Helicobacter pylori inoculation promotes gastric mucosal inflammation in Mongolian gerbils.

BACKGROUND: Mongolian gerbils have been reported to be a suitable model for Helicobacter pylori-associated gastric mucosal injury, including gastric cancer. Although ethanol is known to be one of the harmful substances in the gastric mucosa, the relationship between ethanol and H. pylori infection remains unknown. The aim of the present study is to investigate the effect of ethanol treatment prior to H. pylori inoculation on associated gastric mucosal injury. METHODS: Male Mongolian gerbils were used for the study. Helicobacter pylori was orally inoculated after 15 h fasting (Hp group). Thirty minutes prior to H. pylori inoculation, a group of gerbils was orally treated with 40% ethanol (20 mL/kg; E + Hp group). Another group of animals was treated either with H. pylori culture media alone (controls) or with 40% ethanol plus culture media (E group). Gerbils were killed 2, 4 or 12 weeks after H. pylori inoculation. Helicobacter pylori infection was confirmed by both histological examination and serological tests. Mucosal damage was evaluated histologically according to the modified Sydney system. RESULTS: Although in the controls and E group no significant change to the gastric mucose was observed, persistent H. pylori infection was seen in the mucosa and mucosal leucocyte infiltration and severe epithelial damage was observed in the Hp and E + Hp groups after 4 weeks. The histological scores for polymorphonuclear cell infiltration and myeloperoxidase activity were higher in the E + Hp group at 4 weeks than in the Hp group (P < 0.05). CONCLUSIONS: Ethanol intake preceding H. pylori inoculation could promote the progression of gastric mucosal inflammation in Mongolian gerbils.

Alcohol Drinking↗
PubMed2000

Determination of the optimal cut-off value for the [13C]-urea breath test based on a Helicobacter pylori-specific polymerase chain reaction assay.

BACKGROUND: This study was conducted to determine the optimal cut-off value and breath sample collection time for the [13C]-urea breath test based on the assessment of Helicobacter pylori status with a gastric juice-based polymerase chain reaction (PCR) assay. METHODS AND RESULTS: A total of 104 patients took 100 mg [13C]-urea orally and breath samples were collected at 5, 10, 20, 30 and 60 min. The increment of 13CO2:12CO, ratio from the baseline (delta13C) was measured using a laser spectroanalyser. The PCR assay was positive in 63 and negative in 41 patients. The optimal cut-off value of delta13C was calculated for each sample collection time so that the distance from the geometric mean value among Helicobacter pylori-positive patients and that from the arithmetic mean value among negative patients were simultaneously maximized. The cut-off value of 2.7% at 20 min had the longest distance, being separated by 3.16 SD from the two mean values. Using this cut-off value, the urea breath test showed 100% specificity and 98% sensitivity for the diagnosis of Helicobacter pylori infection.

Breath Tests↗
PubMed2001

Prevalence of functional dyspepsia and its relationship with Helicobacter pylori infection in a Japanese population.

AIM: To investigate the prevalence of functional dyspepsia and Helicobacter pylori infection and their relationship in a Japanese population. METHODS: Two thousand five hundred people who visited Shimane Institute of Health Science for their annual medical check-up from September 1998 to August 1999 were prospectively enrolled in the study. After routine medical examination, including an upper gastrointestinal study and an ultrasonographic examination, all subjects were asked standard questions to check for the presence of any symptoms that suggested dyspepsia. Helicobacter pylori infection was determined by using a serum IgG antibody concentration with an ELISA. RESULTS: Of the 2,500 persons investigated, 2,263 showed no abnormal finding in any medical examination. The presence or absence of symptoms and H. pylori infection was investigated in these 2,263 cases. Of these, 201 people (8.9%) experienced nausea, fullness and/or early satiety and were diagnosed as having dysmotility-like dyspepsia, while 118 people (5.2%) experienced pain localized to the epigastrium and were diagnosed as having ulcer-like dyspepsia. The frequency of these symptoms had a tendency to decline with age, although this was not statistically significant. In contrast, the rate of H. pylori infection increased with age. There was no significant relationship between H. pylori infection and any type of functional dyspepsia. CONCLUSIONS: Helicobacter pylori infection does not influence the prevalence of the dysmotility-like and ulcer-like dyspeptic symptoms.

Adult↗
PubMed2001

Influence of Helicobacter pylori infection on the prevalence of reflux esophagitis in Japanese patients.

BACKGROUND AND AIM: Reflux esophagitis is caused by esophageal motor dysfunction in patients with sufficient gastric acid secretion. Helicobacter pylori causes atrophic gastritis and influences gastric acid secretion. Hiatus hernia (HH) of the esophagus causes motor dysfunction in the lower esophagus. Therefore, this study aimed to test whether H. pylori infection, gastric mucosal atrophy and HH are predictive factors for reflux esophagitis. METHODS: Helicobacter pylori infection was examined in 781 patients by the measurement of serum immunoglobulin (Ig)G antibody, bacteriological culture and histological examination of biopsy specimens. The prevalence of HH, endoscopically identified gastric mucosal atrophy (closed- or open-type) and reflux esophagitis were investigated by reviewing endoscopic films. Investigated patients were divided into three age groups, under 49, 50-69, and over 70 years. The prevalence of esophagitis, H. pylori infection, gastric mucosal atrophy, and HH were compared to identify the possible predictive factors for reflux esophagitis by using logistic regression analysis. RESULTS: Sixty-nine patients with reflux esophagitis were found among the 781 investigated cases. The odds ratios of negative H. pylori infection, endoscopically identified closed-type gastric mucosal atrophy, and HH for the prevalence of reflux esophagitis were 1.342, 1.751 and 5.527, respectively. These results indicated that the presence of H. pylori infection was only a weak negative risk factor, and that HH was the most reliable endoscopic predictive factor for reflux esophagitis. CONCLUSION: Helicobacter pylori infection is a weak negative risk factor for the prevalence of reflux esophagitis, while HH is the most reliable predictive factor.

Aged↗
PubMed2003

Anti-Helicobacter pylori therapy in India: differences in eradication efficiency associated with particular alleles of vacuolating cytotoxin (vacA) gene.

BACKGROUND AND AIMS: The efficiency of Helicobacter pylori eradication varies geographically, as do many parameters that might affect therapeutic efficiency, including bacterial genotype. The aim of the present study was to determine the efficiency of H. pylori eradication using a 10-day proton pump inhibitor-based triple-therapy regimen (omeprazole, clarithromycin and amoxycillin) in an eastern Indian patient population, and to find out the relationship, if any, of the success or failure of the therapy to known features of bacterial genotype. METHODS: Helicobacter pylori infections were analyzed in 66 duodenal ulcer patients by upper gastrointestinal endoscopy, rapid urease tests, histology and culture. The cytotoxin-associated gene (cagA) and vacuolating cytotoxin (vacA) gene status of cultured strains were studied by polymerase chain reaction. Treatment was given for 10 days and endoscopy was repeated at 4 and 12 weeks post therapy to monitor ulcer healing and H. pylori eradication. RESULTS: Ulcer healing was observed in 60 patients (96.77%). Helicobacter pylori was eradicated in 41 (62.12% intention to treat, 66.13% per protocol) of the 66 duodenal ulcer patients, but not in the other 25. The bacteria from 47 patients were genotyped. The only significant disease-associated difference in patterns observed was that the vacA m1 allele was represented more disproportionately among patients with eradication failures (68%) than in those with successful eradication (39%) (P < 0.05) No significant association of vacAs1 (signal sequence allele) or cag pathogenicity island status with persistence was detected. CONCLUSIONS: This study highlights the public health need for cheaper, more cost-effective anti-H. pylori therapies for developing countries, and suggests that subtle features of bacterial genotype can influence therapeutic efficiency. The possibility that particular vacA mid region alleles affect persistence, perhaps through toxin action on particular gastric cell types, merits further study.

Adult↗
PubMed1998

The role of gastric Helicobacter and N-methyl-N'-nitro- N-nitrosoguanidine in carcinogenesis of mice.

BACKGROUND: The aim of this study was to determine whether gastric epithelial proliferation due to gastric Helicobacter infection in mice represents a preneoplastic lesion. MATERIALS AND METHODS: Helicobacter heilmannii infected and uninfected mice were treated with 150 microg/ml N-methyl-N'-nitro-N-nitrosoguanidine in drinking water for either 20 or 38 weeks. Mice were killed 12 or 18 months after bacterial inoculation. RESULTS: All infected mice developed lymphoplasmocytic gastritis and epithelial hyperplasia. Proliferative gastric lesions were characterised by nodular hypertrophy of the glandular mucosa, multifocal epithelial hyperplasia, and elevated BrdU labeling index. Intestinal metaplasia and true atrophy were not present but proliferative glands were poorly differentiated, lined by mucus-type epithelial cells with no parietal, chief or other specialized cell types. Neoplasms developed only in MNNG-treated mice. of the 180 treated mice the following neoplasms developed: 14 squamous cell carcinomas of mouth and forestomach; 37 hemangiosarcomas of the intestinal serosa; and 15 splenic lymphomas. No tumors were present in the glandular gastric mucosa, and infection did not affect tumor incidence. p53 overexpression occurred in 79% of hemangiosarcomas and 71% of squamous cell carcinomas but not in normal or proliferative gastric glandular mucosa. CONCLUSIONS: Gastric proliferative lesions in Helicobacter-infected mice are not preneoplastic, and the combination of an alkylating agent and non-neoplastic proliferation does not result in gastric carcinogenesis in mice.

Animals↗
PubMed2001

Helicobacter pylori infection is associated with a decreased risk of developing oesophageal neoplasms.

BACKGROUND: The role of Helicobacter pylori infection in the development of oesophageal malignancies was investigated through a multivariate conditional logistic regression analysis in a nested case-control study. METHODS: Blood samples and a questionnaire on smoking and alcohol habits were collected from a cohort of 32,906 city residents during a health-screening programme between 1974 and 1992. Forty-four cases of oesophageal cancer and 149 matched controls were selected. The mean interval between screening and cancer diagnosis was 11.9 years. H. pylori seropositivity was determined by an enzyme-linked immunosorbant assay measuring IgG. Occupation was included in the statistical analysis as an indicator of socio-economic status. RESULTS: Helicobacter pylori seropositivity was present in 10 of the cases (22.7%) and 67 of the controls (45.0%). In a multivariate model, with adjustment for occupation, tobacco and alcohol consumption, the odds ratio for developing an oesophageal malignancy when infected with H. pylori was 0.29 (95% confidence interval (CI): 0.12-0.67). Current smokers had an odds ratio of 17.3 (95% CI: 3.0-99.4) and the odds ratio for ex-smokers was 5.9 (95% CI: 1.15-29.9). High alcohol consumption was no longer significantly associated with oesophageal neoplasms after tobacco smoking was included into the model, odds ratio 1.22 (95% CI: 0.46-3.2). The protective effect of H. pylori was more pronounced for oesophageal adenocarcinoma (seven cases, odds ratio 0.16, 95% CI: 0.00-1.06) than for squamous-cell carcinoma (29 cases, odds ratio 0.41, 95% CI: 0.14-1.2). CONCLUSIONS: Helicobacter pylori infection is associated with a decreased risk of developing an oesophageal malignancy. Current smokers and ex-smokers have instead a definite increased risk of oesophageal neoplasms.

Adenocarcinoma↗
PubMed1996

Hypertrophic gastropathy in Helicobacter felis-infected wild-type C57BL/6 mice and p53 hemizygous transgenic mice.

BACKGROUND & AIMS: Helicobacter pylori infection causes gastritis and peptic ulcers and is linked epidemiologically to gastric cancer. To analyze host genetic factors and the influence of Helicobacter on cell proliferation, we used an inbred and p53 hemizygous mouse model of Helicobacter felis-induced gastritis. METHODS: H. felis was inoculated by gastric intubation into SPF C57BL/6 wild-type and p53 hemizygous mice that were followed up for 1 year and compared with uninfected controls of the same genotype using histology, proliferating cell nuclear antigen (PCNA) staining, and 5-bromo-2'-deoxyuridine (BrdU) analysis. RESULTS: Infected animalls developed sustained anti-H. felis serum immunoglobulin G antibody responses. Six months after infection, both wild-type and p53 hemizygous mice showed active chronic inflammation and marked mucosal hyperplasia compared with uninfected controls. One year after infection with H. felis, the wild-type and p53 hemizygous mice showed severe adenomatous and cystic hyperplasia of the surface foveolar epithelium. BrdU uptake and PCNA staining were markedly increased in both sets of infected mice compared with controls. Infected p53 hemizygous mice had a higher proliferative index than the infected wild-type mice. CONCLUSIONS: H. felis can induce a hypertrophic gastropathy in the C57BL/6 genotype; loss of one p53 allele, although insufficient to initiate carcinogenesis at 1 year, enhances the proliferative index, which may lead to an increased risk of cancer induction.

Alleles↗