Comparison the cost-efficacy of furazolidone-based versus clarithromycin-based quadruple therapy in initial treatment of Helicobacter pylori infection in a variable clarithromycin drug-resistant region, a single-center, prospective, randomized, open-label study.

Helicobacter pylori (Hp) drug resistant rate to clarithromycin (CLA) has increased to 20% to 50%, which cause concerns regarding its effectiveness in eradicating Hp, we aim to evaluate the cost-effectiveness of CLA-based versus furazolidone (FZD)-based quadruple therapy, and assess factors that affect anti-Hp efficacy.One hundred eighty-five patients were enrolled in this single-center, prospective, randomized, open-label study. In FZD group, 92 patients were treated with FZD plus esomeprazole, bismuth potassium citrate, and amoxicillin for 14 days. In CLA group, 93 patients were treated with the same regimen except FZD was replaced by CLA. Patients were tested 4 weeks post-treatment to confirm eradication.Of the 185 enrolled patients, 180 completed the study. On intention-to-treat analysis, Hp eradication rates in FZD and CLA groups were 90.22% and 86.02% (P = .378); in per-protocol analysis, their eradication rates were 93.26% and 87.91%, respectively (P = .220). Overall incidence of total side effects in FZD and CLA groups was 19.57% and 13.98%, and their severe side effects were 3.26% and 2.15%, respectively (P > .05). Cost-effectiveness ratios of FZD and CLA groups were 0.75 and 1.02, and incremental cost-effectiveness ratio of FZD group over CLA group was -3.62. Eradication failures were not associated with factors including gender, age, body mass index, smoking, alcohol consumption, educational level, and urban-rural distribution in this observation (P > .05).Despite increasing drug resistance to CLA, Hp eradication rates in FZD and CLA groups have no significant difference at present; as FZD-based quadruple therapy is more cost-effective, we recommend this regimen be a first-line choice for Hp eradication.

Helicobacter pylori infection-induced H3Ser10 phosphorylation in stepwise gastric carcinogenesis and its clinical implications.

BACKGROUND: Our previous works have demonstrated that Helicobacter pylori (Hp) infection can alter histone H3 serine 10 phosphorylation status in gastric epithelial cells. However, whether Helicobacter pylori-induced histone H3 serine 10 phosphorylation participates in gastric carcinogenesis is unknown. We investigate the expression of histone H3 serine 10 phosphorylation in various stages of gastric disease and explore its clinical implication. MATERIALS AND METHODS: Stomach biopsy samples from 129 patients were collected and stained with histone H3 serine 10 phosphorylation, Ki67, and Helicobacter pylori by immunohistochemistry staining, expressed as labeling index. They were categorized into nonatrophic gastritis, chronic atrophic gastritis, intestinal metaplasia, low-grade intraepithelial neoplasia, high-grade intraepithelial neoplasia, and intestinal-type gastric cancer groups. Helicobacter pylori infection was determined by either 13 C-urea breath test or immunohistochemistry staining. RESULTS: In Helicobacter pylori-negative patients, labeling index of histone H3 serine 10 phosphorylation was gradually increased in nonatrophic gastritis, chronic atrophic gastritis, intestinal metaplasia groups, peaked at low-grade intraepithelial neoplasia, and declined in high-grade intraepithelial neoplasia and gastric cancer groups. In Helicobacter pylori-infected patients, labeling index of histone H3 serine 10 phosphorylation followed the similar pattern as above, with increased expression over the corresponding Helicobacter pylori-negative controls except in nonatrophic gastritis patient whose labeling index was decreased when compared with Helicobacter pylori-negative control. Labeling index of Ki67 in Helicobacter pylori-negative groups was higher in gastric cancer than chronic atrophic gastritis and low-grade intraepithelial neoplasia groups, and higher in intestinal metaplasia group compared with chronic atrophic gastritis group. In Helicobacter pylori-positive groups, Ki67 labeling index was increased stepwise from nonatrophic gastritis to gastric cancer except slightly decrease in chronic atrophic gastritis group. In addition, we noted that histone H3 serine 10 phosphorylation staining is accompanied with its location changes from gastric gland bottom expanded to whole gland as disease stage progress. CONCLUSIONS: These results indicate that stepwise gastric carcinogenesis is associated with altered histone H3 serine 10 phosphorylation, Helicobacter pylori infection enhances histone H3 serine 10 phosphorylation expression in these processes; it is also accompanied with histone H3 serine 10 phosphorylation location change from gland bottom staining expand to whole gland expression. The results suggest that epigenetic dysregulation may play important roles in Helicobacter pylori-induced gastric cancer.