Hye-Kyung Jung, Seung Joo Kang, Yong Chan Lee, Hyo-Joon Yang, Seon-Young Park, Cheol Min Shin, Sung Eun Kim, Hyun Chul Lim, Jie-Hyun Kim, Su Youn Nam, Woon Geon Shin, Jae Myung Park, Il Ju Choi, Jae Gyu Kim, and Miyoung Choi, Korean College of Helicobacter and Upper Gastrointesinal Research. Gut and Liver -0001;0:. https://doi.org/10.5009/gnl20288

Moon Kyung Joo, Chan Hyuk Park, Joon Sung Kim, Jae Myung Park, Ji Yong Ahn, Bong Eun Lee, Jeong Hoon Lee, Hyo-Joon Yang, Yu Kyung Cho, Chang Seok Bang, Beom Jin Kim, Hye-Kyung Jung, Byung-Wook Kim, and Yong Chan Lee, Korean College of Helicobacter and Upper Gastrointestinal Research. Gut and Liver 2020;14:707-26. https://doi.org/10.5009/gnl20246

Helicobacter pylori (H. pylori) infection is one of the most common infectious diseases worldwide. Although its incidence is gradually decreasing, about half of the world's population still get infected. H. pylori infection is responsible for substantial gastrointestinal morbidity worldwide. It is the most common cause of gastric and duodenal ulcers as well as gastric cancer. Since the revision of the H. pylori Clinical Practice Guidelines in 2013, the eradication rate of H. pylori has gradually decreased with the use of classical triple therapy, wherein amoxicillin, clarithromycin, and proton pump inhibitors are administered, for 7 days. According to a nationwide randomized controlled study conducted by the Korean College of Helicobacter and Upper Gastrointestinal Research released in 2018, the intention-to-treat eradication rate was only 63.9%, which was due to increased antimicrobial resistance induced by the use of antibiotics, especially clarithromycin. The update of clinical practice guideline for treatment of H. pylori was developed based on evidence-based medicine by conducting a meta-analysis. The draft recommendations were finalized after expert consensus on three recommendations regarding the indication for treatment and eight recommendations on the treatment itself. These guidelines are designed to provide patients, nurses, medical school students, policymakers, and clinicians with clinical evidence to guide primary care and treatment of H. pylori infection. These may differ from current medical insurance standards and will be revised further, if necessary, based on research-based evidence.

The role of the gastric mucosal microbiome in Helicobacter pylori-negative gastric cancer (GC) remains unclear. Therefore, we aimed to characterize the microbial alterations and host inflammatory cytokine responses in H. pylori-negative GC. Gastric mucosal samples were obtained from 137 H. pylori-negative patients with GC (n = 45) and controls (chronic gastritis or intestinal metaplasia, n = 92). We performed 16S rRNA gene sequencing (n = 67), a quantitative reverse transcription-polymerase chain reaction to determine the relative mRNA expression levels of TNF (tumor necrosis factor), IL1B (interleukin 1 beta), IL6 (interleukin 6), CXCL8 (C-X-C motif chemokine ligand 8), IL10 (interleukin 10), IL17A (interleukin 17A), TGFB1 (transforming growth factor beta 1) (n = 113), and the correlation analysis between sequencing and expression data (n = 47). Gastric mucosal microbiota in patients with GC showed reduced diversity and a significantly different composition compared to that of the controls. Lacticaseibacillus was significantly enriched, while Haemophilus and Campylobacter were depleted in the cancer group compared to the control group. These taxa could distinguish the two groups in a random forest algorithm. Moreover, the combined relative abundance of these taxa, a GC microbiome index, significantly correlated with gastric mucosal IL1B expression, which was elevated in the cancer group. Overall, altered gastric mucosal microbiota was found to be associated with increased mucosal IL1B expression in H. pylori-negative GC.

Background: We examined the association between body mass index (BMI) and development of endoscopic intestinal metaplasia. Methods: This retrospective cohort study included 142,832 Korean adults free of endoscopic intestinal metaplasia and atrophic gastritis who underwent upper endoscopy at baseline and subsequent visits and were followed for up to 5 years. A parametric proportional hazards model was used to estimate the adjusted HR with 95% confidence interval (CI) for incident intestinal metaplasia. Results: In more than 444,719.1 person-years of follow-up, 2,281 participants developed endoscopic intestinal metaplasia (incidence rate, 5.1 per 1,000 person-years). Increased BMI categories were associated with increased risk of new-onset intestinal metaplasia in a dose-response manner. After adjustment for age, sex, center, year of screening exam, smoking status, alcohol intake, exercise, total calorie intake, history of diabetes and hypertension, and history of Helicobacter pylori infection, the multivariable adjusted HRs (95% CIs) for incident intestinal metaplasia comparing BMIs of 30 kg/m2 with a BMI of 18.5–22.9 kg/m2 were 0.84 (0.64–1.09), 1.03 (0.93–1.16), 1.07 (0.96–1.20), and 1.48 (1.20–1.83), respectively. These associations did not differ by clinically relevant subgroups. Risk of endoscopic atrophic gastritis also increased as the baseline BMI category increased. Conclusions: In a large cohort of Korean men and women, obesity was independently associated with increased incidence of endoscopic atrophic gastritis and intestinal metaplasia. Impact: Excessive adiposity appears to play a role in development of stomach precursor lesions of stomach cancer, requiring further studies to determine whether strategies to reduce obesity will also help reduce precancerous lesions and, in turn, gastric cancer.