Journal of Gastroenterology and Hepatology最新文献

Background and aim: The triglyceride-glucose (TyG) index and alanine aminotransferase (ALT) are emerging biomarkers linked to metabolic disturbances and liver health. Nonetheless, the combined impact of these markers on predicting new-onset steatotic liver disease (SLD) and its metabolic and alcohol-associated subtypes remains unclear. This study aimed to investigate the association of TyG and ALT, individually and combined, in incident SLD in the Korean Genome and Epidemiology Study (KoGES) and UK Biobank cohorts.

Methods: This study utilized data from two large population-based cohorts: KoGES (adults aged 40-69 years from South Korea [2001-2002]) and UK Biobank (participants aged 37-73 years from the United Kingdom [2006-2010]). Participants without baseline SLD were classified into four groups based on TyG index and ALT levels, and the incidence of SLD was compared among these groups to assess risk.

Results: Elevated baseline TyG index and ALT levels were significantly associated with a higher risk of new-onset SLD and its subtypes in both cohorts. The highest HRs and ORs were observed in individuals with both markers elevated (2.39 in KoGES; 3.89 in UK Biobank). Survival analyses confirmed significantly lower survival probabilities in high-risk groups (p < 0.001). Predictive accuracy was highest with the combined TyG index + ALT model, outperforming either marker alone (p < 0.001).

Conclusions: Elevated combined baseline TyG index and ALT levels were significantly associated with increased risk of SLD and its subtypes. Combined use of these markers may be valuable for early identification and risk stratification of individuals at risk for SLD.

Gastric cancer (GC) has become a serious threat to global health with escalating incidence and mortality. There is a lack of effective approach to evaluate prognostic survival and stratify high-risk patients due to the highly heterogeneous characteristics of GC. In this study, we integrated N6-methyladenosine (m⁶A) RNA modification, ferroptosis gene sets, and lncRNA transcriptomic data together, established and validated a novel six-lncRNA profile associating with the survival of GC. The m⁶A-ferroptosis lncRNA signature could identify high-risk GC patients and characterize the immunosuppressive tumor microenvironment (TME). In our GC cohort, the 3- and 5-year survival rates of the high-risk compared with low-risk subgroup were 27.8% versus 54.8% and 22.2% versus 50.0%, respectively. Multiplex immunofluorescence assays indicated that high-risk GC samples frequently had less infiltration of CD8⁺ T cells but exhibited abundant immunosuppressive M2-polarized macrophages and Tregs. The differentially expressed genes were primarily enriched in oxidative stress response, reactive oxygen species, RNA metabolic processes, the PI3K-Akt signaling axis, and leukocyte transendothelial migration pathways. Accordingly, high-risk patients might be sensitive to inhibitors targeted at PDK1, tyrosine kinase, PI3K, and HIF-proly1 hydroxylase, whereas the low-risk subgroup might benefit from blockade of ErbB, TrkA, PARP, and Ribosomal S6 kinase. Moreover, we demonstrated that the high-risk factor AC129507.1 in the lncRNA signature was a novel target of the m⁶A regulatory axis WTAP/YTHDF3/ALKBH5, and depletion of AC129507.1 could markedly induce ferroptosis in GC. Collectively, these findings provide a candidate strategy for risk classification and better clinical management of GC and shed new insight into the underlying mechanism of AC129507.1 in GC development.

Background and aim: The effectiveness of standard endoscopic treatment (SET) for non-variceal upper gastrointestinal bleeding (NVUGIB) may vary, particularly depending on the bleeding site, lesion size, and etiology. Recent studies suggest that hemostatic powder (HP) may effectively control bleeding secondary to malignant upper gastrointestinal lesions, but its efficacy in benign etiology for NVUGIB remains uncertain. This systematic review and meta-analysis aimed to compare the effectiveness of HP versus SET as first-line therapy for patients with non-malignant causes of NVUGIB.

Methods: We systematically searched PubMed, Embase, and Cochrane Library databases for randomized controlled trials (RCTs) from inception to January 2025. We used risk ratios (RR) for binary outcomes and mean differences (MD) for continuous outcomes with their corresponding 95% confidence intervals (CIs).

Results: We included 5 RCTs (708 patients). Compared to SET, HP was associated with marginally lower risk of further bleeding during esophagogastroduodenoscopy (EGD) (RR 1.04; 95% CI [1.001, 1.084]; p = 0.04) and similar rebleeding rate within 1, 3, 7, 15, and 30 days. The need for a second endoscopic treatment and the mean procedure time were similar between the groups. Subgroup analyses showed that HP has a lower risk of further bleeding during EGD only when analyzing Forrest IIa lesions, but not in active bleeding.

Conclusions: In patients with non-malignant NVUGIB, HP demonstrated lower risk of further bleeding during EGD in cases with non-bleeding visible vessels. There was no statistically significant difference in further bleeding during EGD for active bleeding, nor in rebleeding risk at 1, 3, 7, 15, or 30 days.

This case report describes a 73-year-old man with more than 1 year of intermittent dysphagia, initially suspected of having esophageal malignancy based on imaging and endoscopic findings. However, multiple mucosal biopsies revealed only mild dysplasia without eosinophilic infiltration. Endoscopic ultrasound performed at our hospital revealed a preserved four-layer esophageal wall structure with diffuse thickening of the muscularis propria at 30-40 cm from the incisors. Definitive diagnosis was ultimately achieved through peroral endoscopic myotomy (POEM) combined with biopsy, which revealed marked eosinophilic infiltration confined to the muscularis propria, consistent with eosinophilic esophageal myositis. POEM provided both diagnostic and therapeutic benefits, leading to substantial clinical improvement and weight gain over 1 year of follow-up without the use of corticosteroids.

Background: Barrett's esophagus is the known precursor to esophageal adenocarcinoma (EAC), a cancer with poor prognosis. While endoscopic surveillance detects early dysplasia and prevents progression, most Barrett's esophagus patients do not progress to EAC, leading to invasive and costly surveillance. This study aimed to identify cost-effective endoscopic surveillance strategies by risk stratifying patients based on Barrett's esophagus segment length and sex.

Methods: A Markov cohort model was developed to simulate the natural history of Barrett's esophagus to EAC. The model assessed 85 surveillance strategies and varied endoscopy intervals from 2 to 10 years for nondysplastic Barrett's esophagus and 6-12 months for dysplasia. Risk stratification was based on segment length (≤ 2 and ≤ 3 cm) and sex. Costs, utilities and transition probabilities were derived from published literature and clinical databases. Deterministic and probabilistic sensitivity analyses were performed, and cost-effectiveness was evaluated from a third-party payer perspective using a threshold of AU$50 000/QALY (2023 US dollars 35 945/QALY).

Results: The most cost-effective strategy was biennial surveillance for long-segment BE (> 2 cm) and 12-month surveillance for LGD, excluding surveillance in low-risk patients (ICER US$23 737/QALY). Risk-based surveillance consistently outperformed nonstratified strategies. Sensitivity analyses confirmed the robustness of the model, with key drivers being transition rates and endoscopy costs.

Conclusion: We identified cost-effective risk-stratified endoscopic surveillance strategies for Barrett's esophagus, particularly when excluding low-risk patients. Tailored risk-guided surveillance strategies could improve resource allocation and clinical outcomes in managing Barrett's esophagus. The conserved resources can then be utilized to identify high-risk individuals in the community.