Pretreatment antibiotic-resistant H. pylori can, in part, explain the low cure rate of the infection and the variability in outcome in reported trials.

Background: The efficacy of omeprazole and amoxycillin dual therapy to treat Helicobacter pylori infection has been inconsistent, suggesting the presence of host or bacterial factors influencing treatment success. The aim of this study was to assess the role of pre‐treatment amoxycillin resistance in the efficacy of omeprazole and amoxycillin dual therapy. Methods: We studied 43 consecutive dyspeptic patients with H. pylori infection. Pre‐treatment H. pylori infection was established by the combination of positive rapid urease test, culture and histology. Amoxycillin susceptibility testing was performed by an Epsilometer test (E‐test) method and amoxycillin resistance was defined as minimum inhibitory concentration greater than 8 μg/mL. Patients received 20 mg omeprazole twice daily for 28 days and amoxycillin 1000 mg twice daily for 2 weeks. Adverse effects were documented using a questionnaire. H. pylori status was reassessed 6–8 weeks after the end of treatment by rapid urease testing and histological examination of gastric biopsies. Results: Forty‐two dyspeptic patients completed the study, and one patient dropped out. H. pylori infection was cured in 23 of 42 patients (55%). The cure rate was higher in patients harbouring amoxycillin‐sensitive organisms than in those with resistant strains: 66% (19/29) vs. 31% (4/13), respectively (P = 0.049). No significant differences in cure rates were evident in relation to age, sex, smoking habits or compliance. Conclusions: The effectiveness of amoxycillin–omeprazole dual therapy was greatly reduced in the presence of pre‐treatment amoxycillin‐resistant H. pylori. The success rate in patients with amoxycillin‐sensitive H. pylori was only 66%, suggesting the presence of additional factors affecting the efficacy of this therapy.

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Infection by Helicobacter pylori is the most important risk factor for gastric cancer. However, only a small fraction of colonized individuals, representing at least half of the world's population, develop this malignancy. In order to shed light on host-microbial interactions, gastric mucosa biopsies were collected from 119 patients suffering from dyspeptic symptoms. 8-Hydroxy-2'-deoxyguanosine (8-oxo-dG) levels in the gastric mucosa were increased in carriers of H.pylori, detected either by cultural method or by polymerase chain reaction, and were further increased in subjects infected with strains positive for the cagA gene, encoding the cytotoxin-associated protein, cagA. Oxidative DNA damage was more pronounced in males, in older subjects, and in H.pylori-positive subjects suffering from gastric dysplasia. Moreover, 8-oxo-dG levels were significantly higher in a small subset of subjects having a homozygous variant allele of the 8-oxoguanosine-glycosylase 1 (OGG1) gene, encoding the enzyme removing 8-oxo-dG from DNA. Conversely, they were not significantly elevated in glutathione S-transferase M1 (GSTM1)-null subjects. Thus, both bacterial and host gene polymorphisms affect oxidative stress and DNA damage, which is believed to represent a key mechanism in the pathogenesis of gastric cancer. The interplay between bacterial and host gene polymorphisms may explain why gastric cancer only occurs in a small fraction of H.pylori-infected individuals.

Background: In the last years, international traffic volume has significantly increased, raising the risk for acquisition of infectious diseases. Among travel-associated infections, increased incidence of legionellosis has been reported among travellers.