Probiotic Supplementation for Treatment of Helicobacter pylori Infection: A Double-Blind Randomized Clinical Trial

Background/Aims@#The effects of probiotic supplementation on Helicobacter pylori (H. pylori) eradication therapy are not completely understood. In this study, we investigated the effects of continuous probiotic administration on eradication rates, recrudescence, and symptom response following completion of a course of H. pylori therapy. @*Methods@#This prospective, randomized, double-blind placebo-controlled trial was performed between June 2018 and 2020. Twohundred seventy patients who received a standard triple regimen for H. pylori eradication, were included in the study. Participants were randomized to receive a probiotic as adjunctive therapy (Enterococcus faecium 4.5×108 and Bacillus subtilis 5.0×107; Medilac-S®, Hanmi Pharmaceuticals, Seoul, Korea) or a placebo (one tablet thrice daily) for 28 days, following H. pylori eradication. Participants who showed successful eradication underwent a repeat 13C-urea breath test after 6 months. @*Results@#Eradication rates in the probiotic and placebo groups were 77.1% and 72.4%, respectively (P=0.48) using per-protocol analysis. Using intention-to-treat analysis, eradication rates were 67.4% and 65.9%, respectively (P=0.43). Of 149 patients who were followed-up after 6 months, four patients had recrudescence (2.7%). Recrudescence rates did not differ between the probiotic and placebo groups. Of the 76 patients who had non-ulcer dyspepsia, 60 (78.9%) showed symptom resolution after 6 months. This beneficial effect was most pronounced in patients with postprandial distress syndrome (P=0.02). @*Conclusions@#Consecutive probiotic supplementation following H. pylori eradication therapy did not increase eradication rates or decrease recrudescence rates.

Tailored Therapy Using Bismuth Add-on Standard Triple Therapy vs. Concomitant Therapy: A First-line Regimen for Helicobacter pylori Infection

Background/Aims@#Compared with other regimens, concomitant therapy (CT) used as a first-line regimen for Helicobacter pylori (H. pylori) infection is associated with higher eradication rates. We compared the efficacy of tailored therapy (TT) using bismuth added to standard triple therapy (STT) with CT. @*Methods@#This consecutive study performed between September 2020 and 2021 included 210 patients with H. pylori infection. Two participating gastroenterologists prescribed TT and CT. Multiplex PCR assays were performed before eradication therapy to identify the relevant point mutations and confirm clarithromycin resistance in the TT group (n=105). Patients who showed negative PCR results received 14-day STT and those with positive PCR results received a 14-day regimen of bismuth added to STT. The other group (n=105) received 10-day CT. @*Results@#Based on per-protocol analysis, eradication rates in the TT and CT groups were 89.2% (91/102) and 81.6% (84/103), respectively. We observed no statistically significant intergroup differences in eradication rates (P=0.12). The frequency of estimated clarithromycin resistance confirmed using multiplex PCR assays was 32.4% (34/105), and the eradication rate associated with bismuth add-on STT was 76.5% (26/34) in patients with clarithromycin resistance. @*Conclusions@#Considering the current and emerging trends in antibiotic resistance, a therapeutic strategy using TT (bismuth add-on STT) is recommended to minimize unnecessary administration of antibiotics.

Helicobacter pylori-associated Chronic Atrophic Gastritis and Progression of Gastric Carcinogenesis / 대한소화기학회지

Chronic inflammation due to a Helicobacter pylori (H. pylori) infection is a representative cause of gastric cancer that can promote gastric carcinogenesis by abnormally activating immune cells and increasing the inflammatory cytokines levels. H. pylori infections directly cause DNA double-strand breaks in gastric epithelial cells and genetic damage by increasing the enzymatic activity of cytidine deaminase. Eventually, gastric cancer is induced through dysplasia. Hypermethylation of tumor suppressor genes is an important cause of gastric cancer because of a H. pylori infection. In addition, the changes in gastric microbiota and the mucosal inflammatory changes associated with a co-infection with the Epstein-Barr virus are associated with gastric cancer development. DNA damage induced by H. pylori and the subsequent responses of gastric stem cells have implications for gastric carcinogenesis. Although the pathogenesis of H. pylori has been established, many uncertainties remain, requiring more study.