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Treatment of Helicobacter pylori infection: management of patients with ulcer disease by general practitioners and gastroenterologists.

ABSTRACT: Knowledge of the importance of Helicobacter pylori infection is still fragmentary. Currently only a minority of patients with ulcers receive adequate eradication therapy. Ideally there should be no difference in the level of knowledge between general practitioners and gastroenterologists. Yet in practice there is a substantial difference. The results obtained in highly selected clinical trials do not reflect results of practice in the real world. The gap can only be narrowed through careful mass education. The role of testing for H pylori infection in primary care practice needs to be clarified and the problem of erratic treatment by general practitioners and specialists needs to be resolved. Adequate response to these problems will require the creation of "regional platforms" where both primary care physicians and specialists decide on empirical therapy, eradication strategy and referral of dyspeptic patients.

SUBMITTER: Tytgat GN

PROVIDER: S-EPMC1766598 | biostudies-other | 1998 Jul

REPOSITORIES: biostudies-other

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microRNA profiling in duodenal ulcer disease caused by Helicobacter pylori infection in a Western population.

Project description:The aim of this study was to identify and assess the utility of miRNAs as diagnostic surrogate markers for H.pylori infection. For this purpose, we analyzed the miRNA expression profile by microarrays in the antral mucosa of well characterized dyspeptic patients and then applied the most significant set of miRNAs to an independent validation group. Our results shows that a set of miRNAs are deregulated during chronic gastric inflammation and that this set may be may be useful as a surrogate marker for determining the presence of H.pylori.

2012-09-01 | GSE32174 | GEO

GWAS of peptic ulcer disease implicates Helicobacter pylori infection, other gastrointestinal disorders and depression.

Project description:Genetic factors are recognized to contribute to peptic ulcer disease (PUD) and other gastrointestinal diseases, such as gastro-oesophageal reflux disease (GORD), irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). Here, genome-wide association study (GWAS) analyses based on 456,327 UK Biobank (UKB) individuals identify 8 independent and significant loci for PUD at, or near, genes MUC1, MUC6, FUT2, PSCA, ABO, CDX2, GAST and CCKBR. There are previously established roles in susceptibility to Helicobacter pylori infection, response to counteract infection-related damage, gastric acid secretion or gastrointestinal motility for these genes. Only two associations have been previously reported for duodenal ulcer, here replicated trans-ancestrally. The results highlight the role of host genetic susceptibility to infection. Post-GWAS analyses for PUD, GORD, IBS and IBD add insights into relationships between these gastrointestinal diseases and their relationships with depression, a commonly comorbid disorder.

| S-EPMC7895976 | biostudies-literature

microRNA profiling in duodenal ulcer disease caused by Helicobacter pylori infection in a Western population.

2012-09-01 | E-GEOD-32174 | biostudies-arrayexpress

Inflammatory bowel disease-specific pregnancy knowledge of gastroenterologists against general practitioners and obstetricians.

Project description:BackgroundPatients with inflammatory bowel disease (IBD) tend to have smaller family sizes. Health care professionals (HCPs) may inadvertently provide inaccurate advice to patients resulting in voluntary childlessness or unfavourable pregnancy outcomes.ObjectiveThe study aims to objectively measure IBD-specific pregnancy-related knowledge of general practitioners (GPs) and obstetricians/gynaecologists (OB/GYNs) in comparison with gastroenterologists (GEs) using the validated Crohn's and Colitis Pregnancy Knowledge (CCPKnow) questionnaire.MethodsGPs, OB/GYNs and GEs in two Australian states completed the CCPKnow (range 0-17) and demographic questionnaires. The CCPKnow addresses issues pertaining to conception, IBD inheritance, risk of congenital abnormalities, medication use in the peri-conceptual period, pregnancy and breastfeeding, and mode of delivery.ResultsIn total, 337 HCPs responded. GPs (n = 188/2086) and OB/GYNs (n = 94/228) had significantly lower knowledge than GEs (n = 55/165) for the composite CCPKnow (medians 11, 13 and 17, respectively, p < 0.001), and almost all domains. GEs were the only group to attain a median CCPKnow score in the top category (14-17). More than 70% of GPs and OB/GYNs expressed discomfort with initiation of IBD medications around conception/pregnancy. GPs (43.6%) and OB/GYNs (45.7%) perceived thiopurine use to be unsafe during pregnancy and to cause serious harm to the baby.ConclusionsOur study demonstrates that GPs and OB/GYNs have inadequate and variable IBD-specific pregnancy-related knowledge including use of IBD medications. These results support the need for GEs' prime role in a team-based management for IBD patients who are pregnant or planning pregnancy.

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Associations between cytokine gene polymorphisms and susceptibility to Helicobacter pylori infection and Helicobacter pylori related gastric cancer, peptic ulcer disease: A meta-analysis.

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| S-EPMC5409176 | biostudies-literature

Duodenal ulcer promoting gene of Helicobacter pylori.

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| S-EPMC3130061 | biostudies-literature

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Project description:BACKGROUND: Helicobacter pylori affects gastric epithelium integrity by acceleration of apoptosis. However, it remains unclear what product of the bacteria causes apoptosis, or whether or not the apoptosis is involved in the development of ulcers. AIMS: To elucidate the factor from H pylori that causes acceleration of apoptosis and the role of apoptosis in the development of duodenal ulcer in H pylori infection. PATIENTS: Five H pylori negative healthy volunteers, 47 H pylori positive patients with duodenal ulcer, and 35 H pylori positive patients with gastric ulcer. METHODS: An endoscopic examination was carried out to diagnose ulcers and determine their clinical stage. To analyse apoptosis, a cell cycle analysis was performed using biopsy specimens. RESULTS: There was a significant correlation between the urease activity of the H pylori strain and the level of apoptosis induced by this bacterial strain. Moreover, in duodenal ulcer patients infected with H pylori, the patients with an active ulcer exhibited a significantly higher level of apoptosis than those with ulcers at both the healing and scarring stages. CONCLUSION: These findings suggest that acceleration of apoptosis in the antral mucosa caused by the urease of H pylori plays a crucial role in the development of ulcers in the duodenum.

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Comparative genomics of Helicobacter pylori isolates recovered from ulcer disease patients in England.

Project description:BackgroundGenomic diversity of H. pylori from many different human populations is largely unknown. We compared genomes of 65 H. pylori strains from Nottingham, England. Molecular analysis was carried out to identify rearrangements within and outside the cag-pathogenicity-island (cag PAI) and DNA sequence divergence in candidate genes. Phylogenetic analysis was carried out based on various high-resolution genotyping techniques.ResultsAnalyses of virulence genes (cagT, cagE, cagA, vacA, iceA, oipA and babB) revealed that H. pylori strains from England are genetically distinct from strains obtained from other countries. The toxigenic vacA s1m1 genotype was found to be less common and the plasticity region cluster was found to be disrupted in all the isolates. English isolates showed a predominance of iceA1 alleles and a functional proinflammatory oipA gene. The English H. pylori gene pool revealed several Asian/oriental features. This included the predominance of cagA - glr (cagA right junction) motif types III and II (up to 42%), presence of vacA m1c alleles and phylogenetic affinity towards East Asian / Amerindian gene pools based on fluorescent amplified fragment length polymorphism (FAFLP) analysis and glmM sequence analysis.ConclusionOverall, our results demonstrated genetic affinities of H. pylori in England with both European and the Asian gene pools and some distinctive genetic features of virulence genes that may have evolved in this important European population.

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Association of CYP2C19, TNF-α, NOD1, NOD2, and PPARγ polymorphisms with peptic ulcer disease enhanced by Helicobacter pylori infection.

Project description:ObjectivesTo assess the correlation between a number of genetic variations of CYP2C19, TNF-α, NOD1, NOD2, and PPARγ genes with the severity of Helicobacter pylori (H. pylori) infections and peptic ulcers (PU).MethodsA retrospective cross-sectional design was used in this study. Formalin-fixed paraffin-embedded (FFPE) tissue was used to extract genomic DNA that was collected from Jordanian patients who visited endoscopy clinics between 2014 to 2018 at the King Abdullah University Hospital (KAUH), Irbid, Jordan. Genotyping of the studied single nucleotide polymorphisms (SNPs) were applied using the sequencing protocol. Results: A total of 251 patients (mean age: 42.12 ± 16.09 years) and healthy controls (mean age: 52.76 ± 19.45 years) were enrolled in this study. This study showed no significant association between patients and the studied polymorphisms except for rs2075820 of the NOD1 (p=0.0046). It is hypothesized that the heterozygous genotype (TC); 44.8% in patients versus 61.3% in controls has a decreased risk of peptic ulcers (OR: 0.49). The alleles frequency association was insignificant in all studied SNPs with a p-value more than 0.05.ConclusionThis study provided evidence regarding the association of the rs2075820 with H. pylori infections. The other studied SNPs were not statistically significant.

| S-EPMC7989310 | biostudies-literature

Repurposing Dihydropyridines for Treatment of Helicobacter pylori Infection.

Project description:Antibiotic resistance is a major cause of the increasing failures in the current eradication therapies against Helicobacter pylori. In this scenario, repurposing drugs could be a valuable strategy to fast-track novel antimicrobial agents. In the present study, we analyzed the inhibitory capability of 1,4-dihydropyridine (DHP) antihypertensive drugs on the essential function of the H. pylori response regulator HsrA and investigated both the in vitro antimicrobial activities and the in vivo efficacy of DHP treatments against H. pylori. Six different commercially available and highly prescribed DHP drugs-namely, Nifedipine, Nicardipine, Nisoldipine, Nimodipine, Nitrendipine, and Lercanidipine-noticeably inhibited the DNA binding activity of HsrA and exhibited potent bactericidal activities against both metronidazole- and clarithromycin-resistant strains of H. pylori, with minimal inhibitory concentration (MIC) values in the range of 4 to 32 mg/L. The dynamics of the decline in the bacterial counts at 2 × MIC appeared to be correlated with the lipophilicity of the drugs, suggesting different translocation efficiencies of DHPs across the bacterial membrane. Oral treatments with 100 mg/kg/day of marketed formulations of Nimodipine or Nitrendipine in combination with omeprazole significantly reduced the H. pylori gastric colonization in mice. The results presented here support a novel therapeutic solution for treatment of antibiotic-resistant H. pylori infections.

| S-EPMC6969910 | biostudies-literature

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