We characterized the gastric microbiota for the first time in children with and without H. pylori and observed that when H. pylori is present, it tends to dominate the microbial community. In the H. pylori-negative patients, there was more relative abundance of gammaproteobacteria, betaproteobacteria, bacteroidia and clostridia classes and a higher bacterial richness and diversity.

Clarithromycin and metronidazole resistance was 29.1 and 23.9%, respectively, in 96 Helicobacter pylori strains obtained from pediatric patients. No resistance to amoxicillin was observed. Resistance according to patients' ages to clarithromycin and metronidazole was 45.4 and 18.2% in 22 patients from 4 to 8 years old, 30.2 and 20.7% in 53 patients from 9 to 13 years old, and 9.5 and 38.1% in 21 patients from 14 to 18 years old, respectively. The A2143G mutation was the most prevalent (82.1%) among clarithromycin-resistant strains.Helicobacter pylori is a gram-negative microaerophilic rod found in the human gastric mucosa associated with different digestive diseases, such as peptic ulcer, gastritis, and mucosaassociated lymphoid tissue lymphoma (7), and it is considered a risk factor in the development of gastric cancer (24). H. pylori infection is frequently acquired during childhood, and symptoms such as vomiting and epigastric or recurrent abdominal pain are associated with H. pylori infection (6).Amoxicillin, tetracycline, metronidazole, and clarithromycin are frequently used, combined with proton pump inhibitors or bismuth salts, for the treatment of H. pylori infections (22). However, side effects, poor compliance, and resistance to antibiotics are causes of treatment failure (4, 16). Resistance to metronidazole and clarithromycin is population dependent, and several studies suggest that clarithromycin resistance is higher in strains obtained from children than in those from adults (9).The aim of this study was to determine the rate of resistance to clarithromycin in H. pylori strains obtained from pediatric patients according to the age of the patients. Metronidazole and amoxicillin resistance was also studied. The mutation involved in clarithromycin resistance was detected by PCR-restriction fragment length polymorphism analysis.Ninety-six pediatric patients, aged from 4 to 18 years (mean age Ϯ standard deviation, 10.86 Ϯ 3.3 years), attending the Gastroenterology Unit at the Hospital del Niño Jesus during 1999 and 2000, were included in this study. Patients were referred for endoscopy due to different symptoms, with epigastric pain (74.2%), vomiting (33.3%), and recurrent abdominal pain (25.8%) being the most prevalent. Parents signed an informed consent form for the endoscopy, and the Ethical Committee supervised the study. Patients previously treated for H. pylori infections were not included. Strains were grouped according to the age of the patient at the time of endoscopy.Only culture-positive patients were included. H. pylori clinical isolates were obtained from gastric biopsy specimens according to standard procedures.Clarithromycin was obtained from Abbott Laboratories SA, Madrid, Spain, and metronidazole and amoxicillin were obtained from Sigma-Aldrich, Madrid, Spain. MICs were determined by an agar dilution technique with Mueller-Hinton agar plus 7% horse blood according to NCCLS recommendations (17). Plates with twofold dilutions of each antibiotic were inoculated with 1 to 2 l of 10 9 CFU/ml ...

The evolution of clarithromycin, metronidazole and amoxycillin resistance in 246 Spanish Helicobacter pylori clinical isolates, obtained from paediatric patients during a 9 year period, was determined by an agar dilution technique. Clarithromycin resistance (MIC 1 mg/L) was 2.27% (IC95 0.05-12.02) in 1991-1993, 20.98% (IC95 12.72-31.46) in 1994-1996 and 28.33% (IC95 20.48-37.28) in 1997-1999 (P < 0.01). Metronidazole resistance (MIC 8 mg/L) was 7.14% (IC95 1.49-19.48) in 1991-1993, 20.25% (IC95 12.04-30.79) in 1994-1996 and 43.90% (IC95 32.95-55.30) in 1997-1999 (P < 0.01). Amoxycillin resistance was not found (all strains showed MICs < 2 mg/L).

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VacA and CagA serological responses were detected in pediatric patients: 44 and 56%, respectively, in peptic ulcer (PU) patients, 33.3 and 44.4% in active chronic gastritis (ACG) patients, and 23.2 and 39.2% in non-ACG patients. Higher seroprevalence to CagA؉VacA and to CagA؉VacA؉35-kDa antigen was found among PU patients. However, a low level of sensitivity and specificity was found for indirect detection of PU patients.

The aim of this study was to determine the in vitro activity of ranitidine, ebrotidine, bismuth citrate, omeprazole, and lansoprazole against 113 clinical isolates of Helicobacter pylori cultured from gastric biopsies. An agar dilution method using Mueller-Hinton agar plus 7%, horse blood, an inoculum of 10(6) cfu/spot, and incubation in a CO2 incubator for 2 to 5 days was used. The minimum inhibitory concentrations for 50 and 90% of the isolates tested, respectively, were as follows: ranitidine, 1024 and 1024 mg/l; ebrotidine, 64 and 256 mg/l; bismuth citrate, 1 and 4 mg/l; omeprazole, 16 and 16 mg/l; and lansoprazole, 1 and 1 mg/l. Ebrotidine was more active than ranitidine, and lansoprazole was the most active compound against the Helicobacter pylori isolates tested.