BackgroundAntibiotic resistance of Helicobacter pylori (H. pylori) is increasing worldwide, with geographical variations, impacting the treatment outcomes. This study assessed the antibiotic resistance patterns of H. pylori in Vietnamese children.Materials and MethodsSymptomatic children undergoing gastroduodenoscopy at two tertiary Children's Hospitals in Ho Chi Minh City were recruited. Antral and corpus biopsies were obtained and cultured separately. Susceptibility to amoxicillin (AMO), clarithromycin (CLA), metronidazole (MET), levofloxacin (LEV), and tetracycline (TET) was determined using E‐test. Polymerase chain reaction was performed on another antral biopsy to detect the urease gene, cytotoxin‐associated gene A (cagA), vacuolating cytotoxin A (vacA) genotypes, and 23S rRNA mutations conferring CLA resistance.ResultsAmong 123 enrolled children, a high primary resistance rate was found for CLA (68.5%, 61/89), followed by LEV (55.1%), MET (31.5%), AMO (25.8%), and TET (1.1%). Secondary resistance rates were 82.1% (7/28), 71.4%, 53.6%, and 3.6% for CLA, LEV, MET, and TET, respectively. Multidrug resistance was frequent (67.7%), with common patterns including CLA + LEV (20.3%) and CLA + MTZ + LEV (15.2%). Heteroresistance was detected in eight children (6.5%). The A2143G mutation was detected in 97.5% (119/122) of children. 86.1% of children had positive cagA strains and 27.9% had multiple vacA genotypes. No factor was significantly associated with antibiotic resistance.ConclusionsThe alarming rate of antibiotic resistance for H. pylori, especially for CLA, with emerging multi‐ and hetero‐resistant strains, pose a major treatment challenge that precludes CLA use as empirical therapy. Biopsies from both antrum and corpus can improve H. pylori culture, allowing tailored treatment based on antimicrobial susceptibility.

Infection with Helicobacter pylori (H. pylori) is the strongest known risk factor for gastric cancer. The molecular mechanisms of H. pylori-associated gastric carcinogenesis remain not elucidated. Recent findings indicate that H. pylori infection may promote gastric carcinogenesis by inducing inflammation and genetic instability in gastric epithelial cells. In addition, it is shown that the impact of H. pylori on infected cells is associated with bacterial virulence that is diverse among geographical regions as well as populations. Therefore, we aimed to investigate the effect of H. pylori strain DN18 from Vietnamese subject on the in vitro activity of NF-κB transcription factor, a key regulator of inflammation, and expression of its target genes in this study. Moreover, host genomic instabilities were studied through examining the formation of DNA double-strand break (DSB) by using phosphorylated histone H2AX (γH2AX) as a DSB marker. Our results showed that H. pylori strain DN18 induced activation of NF-kB pathway and increased transcriptional expression of inflammatory mediators in human gastric mucosal cell AGS. We also provided evidence that the H. pylori infection triggered accumulation of  DSBs marker γH2AX. In summary, our study showed the potential ability to cause inflammation and DNA damage to infected cells of H. pylori strains isolated from Vietnamese patients.