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Aim: To determine the efficacy of our therapeutic strategy for Helicobacter pylori (H. pylori) eradication and to identify predictive factors for successful eradication., Methods: From April 2006 to June 2010, we retrospectively assessed 2428 consecutive patients (1025 men, 1403 women; mean age 55 years, age range 18-92 years) with gastric histology positive for H. pylori infection referred to our unit for 13-C urea breath test (UBT), after first-line therapy with proton pump inhibitor (PPI) b.i.d. + amoxicillin 1 g b.i.d. + clarithromycin 500 mg b.i.d. for 7 d. Patients who were still positive to UBT were recommended a second-line therapy (PPI b.i.d. + amoxicillin 1 g b.i.d. + tinidazole 500 mg b.i.d. for 14 d). Third choice treatment was empirical with PPI b.i.d. + amoxicillin 1 g b.i.d. + levofloxacin 250 mg b.i.d. for 14 d., Results: Out of 614 patients, still H. pylori-positive after first-line therapy, only 326 and 19 patients respectively rechecked their H. pylori status by UBT after the suggested second and third-line regimens. "Per protocol" eradication rates for first, second and third-line therapy were 74.7% (95% CI: 72.7%-76.4%), 85.3% (95% CI: 81.1%-89.1%) and 89.5% (95% CI: 74.9%-103%) respectively. The overall percentage of patients with H. pylori eradicated after two treatments was 97.8% (95% CI: 97.1%-98.4%), vs 99.9% (95% CI: 99.8%-100%) after three treatments. The study found that eradication therapy was most effective in patients with ulcer disease (P < 0.05, P = 0.028), especially in those with duodenal ulcer. Smoking habits did not significantly affect the eradication rate., Conclusion: First-line therapy with amoxicillin and clarithromycin produces an H. pylori eradication rate comparable or superior to other studies and second-line treatment can still be triple therapy with amoxicillin and tinidazole.

Background/Aim: Helicobacter pylori (Hp) has been assigned as a class I carcinogen because of its relation to gastric carcinoma (GC). Infection with different genotypes of virulent Hp strain, CagA and/or VacA positive, play a role in the development of atrophic gastritis, duodenal ulcer (DU), and GC. Methods: This study was undertaken to investigate if patients with GC with Hp negative (Hp[sup -]) histological staining had a past infection by virulent strains of Hp CagA and/or VacA positive. 20 GC, 15 males and 5 females (mean age ± SD) 68.14 ± 9.8 y old Hp[sup -] to histological staining in antrum, corpus and in the lesion take part to the study. Two control group were included: 19 Hp infected patients with DU eradicated 10 years before, 14 males and 5 females, (mean age ± SD) 58 ± 18.2 y old. Hp[sup -] status was determined every year with histology Giemsa staining and follow-up after therapy was (average ± SD) 120 ± 32 months; range 96-44 months. 20 asymptomatic children, 10 males and 10 females, (mean age ± SD) 7 ± 4.47 years old, with Hp[sup -] faecal test (HPSA-Meridian). The immunoblot assay (Mikrogen-Germany) was used to detect serum antibodies against CagA and VacA of all patients. Results: The prevalence of CagA and VacA seropositivity was 90% and 95% in GC, 84% and 84% in DU Hp[sup -], 25% and 5% in children Hp[sup -] respectively. Serum CagA and VacA antibody positivity was not significantly different between GC and patients with DU eradicated 10 years before. In contrast a true significant positivity was found against children (t-student test; P<0.0001). Statistical difference was found in age between groups P<0.03. Conclusions: patients with GC, although Hp[sup -] at present, could be infected by Hp before the appearance of the disease as confirmed by CagA and VacA seropositivity. [ABSTRACT FROM AUTHOR]

Background/Aim: To evaluate the utility of 2 biopsies of antrum and gastric body on routinary endoscopy for the assessment of type III intestinal metaplasia (IM-3) and Helicobacter pylori (Hp) status, 1750 patients (pts) (895 males and 855 females, mean age 60.2) were considered from June'98 to June'00. Methods: Specimens were graded 0 to 3 for atrophy, IM-3 and Hp status. 620 pts treated previously with antibiotics or not eligible for biopsy were excluded from initial 2360 pts. Results: IM-3 (score >0), was found in 118 pts (6.7%), 86 pts (4.9%) only in the Antrum. 10 of 355 pts (2.8%) with normal endoscopy findings and 47 of 702 (6.6%) with non erosive endoscopic gastritis resulted IM-3 positive in the antrum. 709 pts (40.5%) were found positive for Hp in antrum or/and corpus. The presence of Hp and IM-3 in the antrum was not correlated (p=0.99; spearman test). A positive correlation (p=0.000) between duodenal ulcer and Hp was found when antral Hp posttivity was taken in account. Gastric carcinoma risk index (GCRI) (Meining et al, Virchows Arch 1998; 432: 311-314) was found in 358 pts (20.4%); in this group 131 pts (36.6%) were Hp positive, 82 pts (23%) have IM-3, 184 pts (51.4%) have atrophy. Conclusions: The incidence of IM-3 is low (6.7%) in routinary endoscopy. Normal endoscopy doesn't exclude the presence of IM-3. The biopsy is necessary to discover IM-3 in the antrum in 5.3% of pts with normal or aspecific endoscopic gastritis. Application of the GCRI might be useful to identifying a group of patients carrying a higher risk for gastric carcinoma. [ABSTRACT FROM AUTHOR]