Background: Colorectal cancer (CRC) is a significant global health issue, ranking as the third most commonly diagnosed cancer and the second leading cause of cancer-related deaths. Countries with a high Human Development Index (HDI) report the highest incidence rates, driven by dietary and lifestyle factors. In contrast, low-to-middle HDI countries are experiencing rising CRC rates due to urbanization and westernization. Japan exemplifies this shift, with increasing CRC incidence linked to the adoption of westernized diets. Despite advances in screening and treatment, CRC-related mortality remains substantial, with 53,088 deaths reported in Japan.
Summary: This review examines global and regional CRC trends, focusing on incidence, mortality, and risk factors such as genetic predispositions, diet, and lifestyle influences. The review highlights the growing burden of CRC in Japan and other regions where dietary changes and urbanization are prevalent. Key findings include the significant impact of processed foods, sugary beverages, obesity, alcohol, and smoking on CRC risk, as well as the protective effects of vitamin D, calcium, and fermented foods. The role of inflammatory bowel disease and diabetes in CRC risk is also discussed. Furthermore, the review emphasizes the importance of public health initiatives, including organized screening programs, in mitigating the CRC burden.
Key messages: Understanding the interplay between genetic, lifestyle, and environmental factors is crucial for developing effective prevention strategies. Enhancing CRC screening, early detection, and public health interventions can significantly reduce CRC-related mortality. Continued research and collaboration are essential for advancing CRC prevention and improving global health outcomes.
Introduction: Contrast-enhanced computed tomography (CE-CT) has been gaining attention as an initial investigation in the management of colonic diverticular bleeding (CDB), yet the role of CE-CT other than its diagnostic yield has not been adequately clarified. We aimed to determine whether the use of urgent CE-CT improves identification of stigmata of recent hemorrhage (SRH) in subsequently performed early colonoscopy (≤24 h of arrival) or other clinical outcomes of CDB.
Methods: We conducted a randomized, open-label, controlled trial at 23 institutions in Japan. Outpatients with suspected CDB were randomly assigned to undergo either urgent CE-CT followed by early colonoscopy (urgent-CE-CT + early-colonoscopy group) or early colonoscopy alone (early-colonoscopy group). The primary outcome was SRH identification. Secondary outcomes included successful endoscopic hemostasis, early (<30 days) and late (<1 year) rebleeding, length of hospital stay, and transfusion requirements.
Results: In total, 240 patients, mostly in a hemodynamically stable condition, were randomized. A contrast extravasation on CE-CT was observed in 20 of 115 patients (17.4%) in the urgent-CE-CT + early-colonoscopy group. SRH was identified in 23 of 115 patients (20.0%) in the urgent-CE-CT + early-colonoscopy group and 21 of 118 patients (17.8%) in the early-colonoscopy group (difference, 2.2; 95% confidence interval [CI], -7.9 to 12.3; p = 0.739). Successful endoscopic hemostasis was achieved in 21 patients in each group (18.3% and 17.8%, respectively) (difference, 0.5; 95% CI, -9.4 to 10.4; p = 1.000). There were also no significant differences between groups in early and late rebleeding, length of hospital stay, and transfusion requirements.
Conclusion: The use of urgent CE-CT before early colonoscopy did not improve SRH identification or other clinical outcomes in patients with suspected CDB in a hemodynamically stable condition. The routine use of urgent CE-CT as an initial investigation is not recommended in this population, also considering the low rate of extravasation-positive cases (UMIN registry number, UMIN000026865).
Introduction: Potassium-competitive acid blockers are effective against proton pump inhibitor-refractory gastroesophageal reflux disease; however, their long-term use is associated with economic disadvantages. Endoscopic procedures may reduce potassium-competitive acid blocker use. This study aimed to determine the optimal treatment strategy for patients with proton pump inhibitor-refractory gastroesophageal reflux disease from a cost-effectiveness perspective.
Methods: Using a Markov state transition model to simulate symptom changes in patients with proton pump inhibitor-refractory gastroesophageal reflux disease, the cost-effectiveness of two strategies was compared: endoscopic treatment (anti-reflux mucosectomy or endoscopic submucosal dissection for gastroesophageal reflux disease) followed by potassium-competitive acid blocker versus medication with high-dose potassium-competitive acid blocker. In both strategies, potassium-competitive acid blocker maintained symptoms at the lowest controllable dose. The time horizon varied from 10 to 50 years. The quality-adjusted life year and incremental cost-effectiveness ratio were calculated. Willingness to pay was set at 5,000,000 Japanese yen.
Results: The quality-adjusted life years gained were 0.90 and 0.95 for the endoscopic treatment and medication strategies, respectively. The incremental cost-effectiveness ratio varied with the follow-up period after the initial treatment, with the endoscopic treatment strategy being more cost-effective than the medication strategy at ≥50 years of follow-up. A dose reduction success rate of <84.1% for high-dose potassium-competitive acid blocker and an endoscopic treatment success rate of >66.8% were required to determine the superiority of the endoscopic treatment strategy at the 50-year follow-up after treatment.
Conclusions: The endoscopic treatment strategy is not cost-effective unless the patient is followed up for >50 years after the initial treatment.
Introduction: Autism is a neurological disability that often appears after the age of three in children, also known as an autism spectrum disorder (ASD). Several studies have examined the influence of some environmental factors, and many parameters related to the behavior of autistic patients have been measured in order to find ways to reduce ASD. This study investigates the relationship between ASD and serum levels of vitamin D3, B12, folic acid, and the gut microbiome.
Methods: The serum levels of vitamin D3, B12, and folic acid in ASD patients were measured by the ELISA method and compared to healthy groups. DNA was extracted from stool samples of ASD patients and the control group, and then the gut microbiome was investigated via a metagenomics approach. Metagenomics sequencing was performed to analyze the 16S rRNA gene sequencing for phylum and sub phylum level microbiome.
Result: The result showed no significant change in the VitD3 and folate levels of ASD patients compared to the control group (p = 0.157 and p = 0.0505, respectively). There was a significant difference in the VitB12 level between control healthy individuals and ASD patients, in which the serum VitB12 concentration was significantly lower than the control group (p = 0.0001). Our results regarding gut metagenomics showed that the abundance of the Actinobacteria by the phylum level was significantly higher in the ASD patients compared to the control group (p = 0.0013). The abundance of the Firmicutes by the phylum level was significantly lower in the ASD patients compared to the control group (p = 0.0016). The abundance of Bifidobacteriaceae, and Ruminococcaceae by the family level was significantly higher in the ASD patients compared to the control group (p = 0.0004 and p = 0.0489, respectively). Our results indicated less species richness in the ASD patients compared to the control group.
Conclusion: Patients with ASD have lower serum levels of vitamin B12 and different gut microbiome compared to healthy controls. Low vitamin B12 levels and altered gut microbiome are significantly associated with ASD in this study. However, further research is needed to determine whether these factors could serve as predictors of severe outcomes in ASD.
Introduction: Eosinophilic gastrointestinal disease (EGID) is divided into eosinophilic esophagitis (EoE) and non-eosinophilic esophagitis eosinophilic gastrointestinal disease (non-EoE-EGID), based on the involved gastrointestinal organs. The present survey was performed to provide an overview of the current status of the epidemiology, diagnosis, and treatment of EGID in Asia.
Methods: Responses to the questionnaire were obtained from 228 doctors at various institutions in eight Asian countries. The questionnaire consisted of 52 questions on EoE and non-EoE EGID.
Results: Responses to questionnaire were obtained from 228 doctors from eight countries. The most common participation facilities were university hospitals, followed by public hospitals, private hospitals, and private clinics. 1-10 were the most frequent patients per year in each institution for both EoE and non-EoE-EGID. The 30s and 40s are common age groups for both EoE and non-EoE-EGID. Although endoscopic findings vary among countries, 15 or more eosinophil infiltrations in high-power fields as a diagnostic criterion are used in all countries for EoE. As treatments, the prescription rates of Proton pump inhibitor, diet, topical and systemic steroids, and biologics were similar among the eight countries in EoE. Non-EoE-EGID showed a similar trend to EoE in epidemiology, symptoms, diagnosis, and treatment.
Conclusion: The questionnaire survey partially revealed the current status of the epidemiology, symptoms, diagnosis, and treatment of EGID in Asian countries.
Introduction: Helicobacter pylori is a highly prevalent pathogen affecting approximately 50% of the world population, causing chronic gastritis and subsequently adenocarcinoma. Antibiotic resistance rates in H. pylori are increasing, thus demanding alternative treatment options. Some beneficial bacteria, including probiotics and gastrointestinal commensals, were shown to inhibit H. pylori growth, viability, and initial attachment to the gastric epithelium.
Methods: In this review, we systematically summarized the currently available literature for in vitro inhibition of H. pylori through beneficial bacteria from the Lactobacillales order. We performed research on PubMed and Google Scholar in accordance with the PRISMA guidelines.
Results: A multitude of species were shown to possess anti-H. pylori activity, although the majority of investigated bacteria belonged to only one bacterial genus: Lactobacillus. Anti-H. pylori activity was mediated through transcriptional modulation of virulence factors, competition for binding sites, the induction of a dormancy state of H. pylori, and the secretion of anti-H. pylori compounds.
Conclusion: Many bacterial compounds that show probiotic properties are capable of inhibiting H. pylori in in vitro experiments. However, a huge variety of test methods to detect anti-H. pylori effects demands standardization.
Introduction: The activity of the mitogen insulin-like growth factor (IGF) is controlled by IGF-binding protein (IGFBP). Colorectal cancers (CRCs) are heterogeneous, with left- and right-sided CRCs, showing different clinical and molecular characteristics. This case-control study, nested in the Japan Collaborative Cohort study, assessed associations between serum levels of IGF-related molecules and incidences of CRC by location.
Methods: A baseline survey obtained serum samples from 39,242 participants. Subjects diagnosed with CRC during follow-up were regarded as cases. Conditional logistic regression modeling was used to calculate odds ratios (ORs) for cancer incidence associated with IGF-related molecules.
Results: This analysis included 176 cases and 524 controls. No IGF-related molecules appeared associated with risks of overall or left-sided CRC. Both total IGFBP3 and free IGFBP3 (estimated as IGFBP3 - [IGF1 + IGF2]) were associated with incidence of right-sided CRC (p for trends = 0.027 and 0.003, respectively), with the third tertile of total and free IGFBP3 showing the highest risk (OR = 6.25 and 7.96, respectively). Free IGF, estimated as (IGF1 + IGF2)/IGFBP3, was inversely associated with incidence of right-sided CRC (p for trends = 0.014), with the third tertile showing the lowest risk (OR = 0.18). Among subjects followed for over 3 years, the association of IGF-related molecules with overall CRC was similar. Free IGFBP3 was associated with the incidence of right-sided CRC (p for trends = 0.004). Free IGF was inversely associated with the incidence of right-sided CRC (p for trends = 0.002). However, free IGFs were associated with a risk of left-sided CRC (p for trends = 0.041), with the third tertile showing the highest risk (OR = 3.10).
Conclusions: Serum IGF-related molecules are associated with the risk of CRC. These associations might differ by tumor location.
Introduction: Ulcerative colitis (UC) represents an inflammatory bowel disease characterized with a multifaceted pathogenesis, which may be attributed to influence by genetic factors. This study aimed to identify and validate novel markers associated with UC, with a specific focus on their regulation through DNA methylation.
Methods: Gene expression and DNA methylation profiling of intestinal mucosal tissues from UC and healthy controls was retrieved from the GEO repository. Differentially expressed and methylated genes were examined in UC. Subsequently, overlapped analyses were performed to identify highly expressed and hypomethylated genes, as well as lowly expressed and hypermethylated genes. Functional annotation, transcription factor-mRNA network analysis, and protein-protein interaction (PPI) network analysis were conducted for above genes. Dextran sodium sulfate (DSS)-induced LOVO and Caco-2 cells were established to stimulate UC injury. The expression and methylation of B4GALNT2 was verified by real-time quantitative polymerase chain reaction and methylation-specific PCR. Cell Counting Kit-8, flow cytometry, Western blot, and enzyme-linked immunosorbent assay were used to measure cell survival, apoptosis, and cytokine levels after B4GALNT2 overexpression.
Results: Our study screened 1 downregulated and hypermethylated gene (B4GALNT2) and 114 upregulated and hypomethylated genes in UC. They were markedly associated with immune response. Totally, 10 potential transcription factors were predicted. The PPI network revealed their complex interactions. B4GALNT2 was confirmed to be downregulated and hypermethylated in DSS-induced intestinal epithelial cells and in DSS-induced UC mouse model. B4GALNT2 overexpression enhanced cell viability and weakened apoptosis and cytokine production and release of DSS-induced intestinal epithelial cells.
Conclusion: Collectively, this study integrally analyzed DNA methylation and gene expression in UC as well as identified and verified B4GALNT2 as a key epigenetic marker.
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