Hideki Mori

Background: The Japanese Society for Helicobacter Research (JSHR) published the fifth edition of the guidelines for the management of Helicobacter pylori ( H. pylori ) infection in 2024 in Japanese language. Methods: This edition of JSHR guidelines was first developed in accordance with the Minds Clinical Practice Guideline and Grading of Recommendations Assessment, Development, and Evaluation system. This was published after inviting public comments and external evaluations. Consensus on clinical questions (CQs) was achieved using the modified Delphi method. Results: There was no change in the basic policy that all H. pylori infectious diseases are indications for eradication. Nucleic acid amplification was added to the diagnostic methods. Effects of proton-pump inhibitors (PPIs) on diagnostic tests were updated. The superiority of potassium-competitive acid blockers to PPIs in 1-week triple therapy with amoxicillin and clarithromycin has been shown. A flowchart for eradication therapy was provided for use in real-world settings. For gastric cancer prevention, eradication in earlier age is recommended. The most appropriate test and treatment strategies for adolescents are also described. Some CQs concerning gastric cancer prevention were identified, although evidence level was insufficient to make recommendations based on clinical importance. Conclusion: The revised guidelines facilitate the appropriate management of H. pylori infection and gastric cancer prevention.

Helicobacter pylori Management in Older Adults: Current Perspectives From Japan

Background/Objectives: Although vonoprazan-based triple therapy has improved the first- and second-line Helicobacter pylori eradication rates, a subset of patients still require third-line or later treatments. The present study aimed to evaluate the efficacy and safety of susceptibility-guided eradication strategies from third-line or later treatments in a multicenter setting. Methods: This retrospective multicenter study (2019–2024) enrolled 94 patients who had failed second-line eradication therapy and underwent H. pylori isolation and susceptibility testing. Based on sitafloxacin sensitivity, patients received vonoprazan, amoxicillin, and sitafloxacin (VAS) if sensitive, or vonoprazan, amoxicillin, and rifabutin (VAR) if resistant. Altogether, 75 patients received treatment according to this protocol. Results: Among the 75 patients, 61.3% were sitafloxacin-sensitive (VAS group), and 38.7% were resistant (VAR group). All strains were rifabutin-sensitive. The overall eradication rates were 92.0% and 95.8% in the intention-to-treat and per-protocol analyses, respectively. Adverse events occurred in 17.3% of cases. One patient in the VAR group discontinued therapy due to dizziness, whereas all other adverse events were mild and did not require treatment cessation. Subgroup analysis showed eradication rates of 93.5% (43/46) and 89.7% (26/29) for the VAS and VAR groups, respectively. The eradication rate for third-line therapy was 96.2% (50/52), whereas that for fourth-line therapy was 85.7% (18/21). Fifth-line therapy showed an eradication rate of 50.0% (1/2). Conclusions: Susceptibility-guided vonoprazan-based regimens from the third-line treatment onward achieved high eradication and tolerability in a multicenter cohort. This approach may offer a valuable treatment option for patients with refractory H. pylori infections.

A 60-year-old woman had persistent positive urea breath test (UBT) results despite three courses of Helicobacter pylori (H. pylori) eradication therapy. Endoscopy revealed extensive atrophic gastritis with a characteristic "reverse atrophic pattern" affecting the gastric corpus while sparing the antrum. Active H. pylori infection was excluded; however, positivity for anti-parietal cell and anti-intrinsic factor antibodies confirmed autoimmune gastritis (AIG). Further screening identified anti-glutamic acid decarboxylase antibodies and thyroid autoantibodies, leading to a diagnosis of autoimmune polyendocrine syndrome type III. This case highlights the potential for false-positive UBT results in AIG, emphasizing the importance of screening for associated autoimmune conditions.

We report a case of a 70‐year‐old woman with esophageal achalasia and concurrent superficial esophageal squamous cell carcinoma. Three adjacent superficial lesions were resected en bloc by endoscopic submucosal dissection (ESD), with no lymphovascular invasion. Given that the patient's dysphagia was effectively controlled with medication and dietary modifications, peroral endoscopic myotomy (POEM) was deferred following a careful assessment of the risk–benefit balance. As both ESD and POEM involve submucosal intervention, this case highlights the importance of individualized treatment based on symptom severity and lesion characteristics.

Background and Aim: Although standard triple therapy remains the first‐line eradication treatment for H. pylori worldwide, it is unclear whether metronidazole should be included empirically in second‐line eradication treatments. The aim of this study was to compare the efficacy of metronidazole‐containing regimens with that of metronidazole‐free regimens after failure of first‐line eradication using standard triple therapy.Methods: PubMed, the Cochrane Library, and the Igaku‐Chuo‐Zasshi database were searched to identify RCTs eligible for inclusion in this systematic review and meta‐analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated.Results: Thirteen eligible RCTs were included, with a total of 2039 patients assigned to metronidazole‐containing (975 patients) or metronidazole‐free (1064 patients) regimens. Metronidazole‐containing regimens had significantly lower eradication failure rates than regimens without metronidazole (OR 0.55; 95% CI, 0.39–0.78). Subgroup analysis based on the regional risk of metronidazole resistance demonstrated that metronidazole‐containing regimens had lower eradication failure rates not only in low‐risk regions but also in high‐risk regions (OR, 0.29; 95% CI, 0.11–0.74 and OR, 0.66; 95% CI, 0.49–0.91, respectively).Conclusion: After failure of standard triple therapy, secondary eradication treatment regimens containing metronidazole demonstrate higher eradication rates than those without metronidazole.

Liver impairment can alter the metabolic capacity of the organ significantly, potentially affecting the efficacy and safety of Helicobacter pylori (H. pylori) eradication regimens. Although this issue is highly significant, no standardized guidelines currently exist for H. pylori eradication therapy in patients with liver dysfunction. To bridge this gap, we systematically reviewed studies on the efficacy and safety of H. pylori eradication therapy in individuals with liver impairment. The systematic review included a search of PubMed, the Igaku Chuo Zasshi, and the Cochrane Library database to identify eligible randomized controlled trials (RCTs) and/or non-randomized controlled trials (NRCTs). Three RCTs and five NRCTs were included. Research on the effectiveness of H. pylori eradication treatment in patients with and without liver disease has produced inconsistent findings, with a study reporting higher eradication rates in the liver disease group, and others finding no significant difference, leaving no definitive consensus. Two studies reported eradication rates 80% in groups with liver impairment. Furthermore, even in cases of advanced liver impairment such as non-alcoholic steatohepatitis (NASH) or liver cirrhosis, eradication rates did not decline, and adverse events were either minimal or comparable with those observed in groups without liver impairment. H. pylori eradication therapy is appli­cable and safe for patients with liver disease; however, treatment indications should be determined carefully by considering reduced hepatic metabolic capacity and specific indications for eradication, while remaining vigilant for potential adverse effects.

Upper gastrointestinal stenosis, which can be congenital or acquired, can lead to dysphagia. The association between trisomy 17p syndrome, a rare chromosomal abnormality, and upper gastrointestinal stenosis is unclear. A 20‐year‐old man diagnosed with trisomy 17p syndrome was referred to our department due to recurrent vomiting. Esophagogastroduodenoscopy revealed stenotic areas in the esophagus, stomach, and duodenum. The congenital gastrointestinal stenosis present in both the duodenum and esophagus suggested that the stasis and reflux of digestive fluids exacerbated stenosis in the stomach and esophagus. Gastric acid suppression therapy and endoscopic dilation of the esophagus and duodenum effectively resolved the patient's vomiting symptoms.

Diabetic gastrointestinal neuropathy is a diabetes-related complication, associated with a complex interplay of hyperglycemic damage, autoimmune responses, oxidative stress, gastrointestinal hormones, and vascular insufficiency. Patients with diabetes should be monitored and therapeutic intervention introduced to prevent neuropathy due to diabetes prior to “the point of no return”. Determining gastric bioelectrical activity by body surface gastric mapping may be a promising option to monitor diabetic gastrointestinal neuropathy.

Obesity, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD) are characterized by the concepts of lipo- and glucotoxicity. NAFLD is characterized by the accumulation of different lipidic species within the hepatocytes. Bile acids (BA), derived from cholesterol, and conjugated and stored in the gallbladder, help the absorption/processing of lipids, and modulate host inflammatory responses and gut microbiota (GM) composition. The latter is the new “actor” that links the GI tract and liver in NAFLD pathogenesis. In fact, the discovery and mechanistic characterization of hepatic and intestinal farnesoid X receptor (FXR) shed new light on the gut–liver axis. We conducted a search on the main medical databases for original articles, reviews, meta-analyses of randomized clinical trials, and case series using the following keywords, their acronyms, and their associations: farnesoid X receptor, bile acids metabolism, gut microbiota, dysbiosis, and liver steatosis. Findings on the synthesis, metabolism, and conjugation processes of BAs, and their action on FXR, change the understanding of NAFLD physiopathology. In detail, BAs act as ligands to several FXRs with GM modulation. On the other hand, the BAs pool is modulated by GM, thus, regulating FXRs functioning in the frame of liver fat deposition and fibrosis development. In conclusion, BAs passed from their role of simple lipid absorption and metabolism agents to messengers between the gut and liver, modulated by GM.