United European Gastroenterology Journal最新文献

Background and aims: The incidence of acute pancreatitis is increasing in the Western world. About 10% of cases are caused by hypertriglyceridemia. Plasmapheresis was shown to reduce serum triglyceride (TG) levels, and current apheresis guidelines recommend its use in severe acute hypertriglyceridemia-induced pancreatitis (HIP). However, data on safety and efficacy are lacking. This study aimed to evaluate the clinical efficacy of plasmapheresis in hypertriglyceridemia-induced pancreatitis.

Methods: This is a retrospective multicenter cohort study of patients hospitalized for an episode of hypertriglyceridemia-induced pancreatitis from January 1, 2012 to December 31, 2022. The predefined composite primary endpoint was in-hospital mortality and organ failure. To reduce allocation bias, we performed propensity score matching.

Results: 245 episodes of hypertriglyceridemia-induced pancreatitis from 13 German centers were included. Of those, 95 episodes were treated with plasmapheresis. After propensity score matching, the final cohort consisted of 60 well-balanced pairs. Plasmapheresis was not associated with a difference in the primary composite outcome, in-hospital mortality, and organ failure (8/60 vs. 5/60; χ²(1) = 0.776; p = 0.378), nor was there any difference in the severity of pancreatitis episodes. It showed only a moderate reduction of serum triglyceride compared to the non-plasmapheresis group, but a significantly longer hospital stay in the plasmapheresis group (12 days; IQR 14 vs. 9 days; IQR 11; U = 1356; Z = -2.46; p = 0.014).

Conclusions: Plasmapheresis in patients with hypertriglyceridemia-induced pancreatitis was not associated with a better clinical outcome compared with conservative treatment in this propensity score-matched retrospective cohort study. Outside clinical studies, this costly and potentially complicative treatment should be considered with caution.

Introduction: Gastroenterology is a dynamic speciality that manages a wide range of gastrointestinal disorders. With the rising burden of gastrointestinal diseases, high-quality and standardised training is essential. United European Gastroenterology (UEG) aims to harmonise gastroenterology training across Europe.

Methods: This multicentre observational study analysed national gastroenterology training curricula from 51 UEG national member societies. Between February and December 2024, curricula were obtained via national societies and online resources. Analysis focussed on five domains: (1) clinical core knowledge, (2) technical and procedural skills, (3) research, (4) non-technical competencies and (5) mentoring and assessment structures.

Results: Median training duration was 60 months (IQR 48-72). Only 7.1% of curricula allowed part-time training; fewer than 17% permitted early sub-specialisation. Clinical core knowledge: All curricula defined core clinical competencies, including hepatology, upper gastrointestinal disorders, pancreatic and IBD care. Technical and procedural skills: Basic endoscopy was universally required, with a median of 300 gastroscopies and 200 colonoscopies. Advanced procedures featured in 70.0% of curricula, with substantial variation.

Research: Research training appeared in 76.2% of curricula, though structure and depth varied. Non-technical competencies: Non-technical competencies were covered in only 11.9%; communication (64.3%), leadership (26.2%), and professionalism (23.8%) were most common. Areas like shared decision-making, interprofessional collaboration, AI, and sustainability were rarely included. Training, mentoring and assessment frameworks: Training centre and trainer requirements were specified in 26.2% and 23.8% of curricula, respectively. One-third included formal mentoring. Competency-based objectives were present in 78.6% and logbooks in 42.9%. Few used structured tools: EPAs (7.1%), DOPS (9.5%) and Mini-CEX (2.4%). Exams were common; 9.5% used the ESEGH. The UEG Blue Book was cited in 24%.

Discussion: Competency-based training is widespread, but structured assessments and non-technical skills are inconsistently addressed. There is a need for minimum training standards and greater curricular alignment across UEG member societies to ensure consistent and high-quality gastroenterology training in Europe.

Introduction: Since the publication of the first European Society for the Study of Coeliac Disease (ESsCD) guidelines in 2019, significant advancements have emerged in the diagnosis of coeliac disease (CeD) in adults. These 2025 guidelines incorporate new evidence to refine diagnostic strategies, aiming for improved accuracy of testing, and enhance overall quality of clinical care.

Methods: A multidisciplinary panel of experts revised the ESsCD guidelines using the AGREE II instrument (Appraisal of Guidelines for Research and Evaluation II) and the GRADE methodology (The Grading of Recommendations Assessment, Development, and Evaluation). Clinical questions were structured using the PICO format, and statements and recommendations were finalised through a Delphi consensus process. Literature quality was assessed using AMSTAR-2 and QUADAS-2 tools.

Results: The updated guidelines are presented in two parts. Part 1 focuses on adult CeD diagnosis, introducing major changes such as a conditional no-biopsy approach for selected adults with high-titre IgA anti-TG2 serology (≥ 10 × ULN). Regarding serology, the use of validated high-performance ELISAs displaying a high diagnostic accuracy is emphasised, while routine use of IgA anti-Endomysium serology is no longer recommended for confirmation. Revised duodenal biopsy protocols now mandate at least four samples from the second part of the duodenum, with bulb biopsies conditionally included. The guidelines provide structured approaches for diagnosing potential CeD, seronegative villous atrophy, and CeD in individuals already on a gluten-free diet. HLA-DQ2/DQ8 typing is recommended for diagnostic clarification in select cases.

Conclusions: The updated 2025 ESsCD guidelines provide a comprehensive framework for the diagnosis of CeD in adults. By integrating evolving diagnostic strategies, minimising over-testing, and patient-centred care approaches, they aim to optimise patient outcomes, quality of life and use of diagnostic resources at the same time.

Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest cancers, with chemotherapy as the mainstay but highly variable efficacy and toxicity. Current regimens, such as FOLFIRINOX and gemcitabine-based combinations, are selected empirically without validated biomarkers to guide choice. Several strategies have been explored to personalize therapy. Patient-derived organoids and molecular classifiers such as PurIST have improved biological understanding but have limited clinical applicability. More recently, predictive transcriptomic signatures have emerged as practical tools. GemPred identifies patients likely to benefit from adjuvant gemcitabine; GemCore, validated in both resected and metastatic tumors, is compatible with small biopsies; and Pancreas-View integrates multiple drug-specific predictors, including for all FOLFIRINOX components and gemcitabine, enhanced by AI. These approaches, retrospectively validated in large cohorts and clinical trials, consistently link predicted sensitivity with improved survival. Beyond regimen selection, signatures enable treatment de-escalation, optimize first-line choices, and identify multidrug-resistant tumors. Ongoing prospective trials will establish their feasibility, supporting transcriptomic profiling as a step toward precision chemotherapy in PDAC.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is very common and associated with significant morbidity and mortality due to its potential progression to cirrhosis and liver cancer. Whereas hepatic fat accumulation is the key to MASLD progression, little is known regarding changes in liver fat content over time in the general population. We aimed to investigate changes in liver fat in a longitudinal study of the general population.

Methods: We conducted a longitudinal study involving 195 randomly selected individuals from the general population, evaluated at two time points, 5 years apart. Participants with hepatic steatosis at baseline did not receive any specific treatment. The primary objective was to assess changes in liver fat content, as estimated by controlled attenuation parameter (CAP) using transient elastography. We also examined the frequency of steatosis resolution and development. CAP variability was assessed in two measurements 7 days apart in a cross-sectional study of 101 volunteers, with a mean variability of 9.9%. Steatosis resolution was defined as reduction of CAP > 10% from baseline with a final value < 275 dB/m, while steatosis development was defined as increase in CAP > 10% with a final value ≥ 275 dB/m.

Results: Remarkable variations in liver fat content were observed. Among the 88 participants with steatosis at baseline, 34% had resolution of steatosis (CAP decreased from 300 to 237 dB/m; p < 0.001). Resolution was associated with weight loss and reductions in transaminases and gamma-glutamyl transferase levels. In contrast, 29% of the 107 participants without steatosis at baseline developed it during follow-up. Increase in liver stiffness measurement (≥ 8 kPa) was associated only with persistent hepatic steatosis but not with steatosis resolution.

Conclusions: There is marked variation in liver fat content among participants from the general population over a period of 5 years, indicating its dynamic nature. These variations should be considered in epidemiological studies of MASLD.

Background: Most T1 gastric cancer (GC) harbor lymph node metastasis (LNM) at a rate of < 20%; however, owing to the difficulty in accurately diagnosing LNM preoperatively, many patients with T1 GC undergo unnecessary invasive radical gastrectomy with lymphadenectomy. In the present study, we established an epigenetic liquid biopsy assay for the preoperative diagnosis of LNM in T1 GC.

Methods: A comprehensive biomarker discovery was performed by analyzing genome-wide DNA methylation profiling. We obtained 277 clinical specimens, including 177 surgical tissues and 100 pre-operative plasmas. DNA methylation biomarkers were trained and validated using quantitative methylation-specific polymerase chain reaction (qMSP) assays.

Results: We identified six novel differentially methylated regions, including at least two differentially methylated CpG probes (|Delta-beta| > 0.12 and p < 0.05) within 100 bp, through genome-wide biomarker discovery. A DNA methylation panel was generated using qMSP assays in clinical tissue specimens, with an area under the curve (AUC) of 0.80. This panel was validated in an independent clinical cohort, and a combined model, which integrated the DNA methylation model with preoperative computed tomography -based findings, was established through multivariate logistic regression analyses (AUC: 0.84). Finally, we translated this model into a liquid biopsy, and this cell-free DNA (cfDNA) methylation model exhibited robust performance for LNM identification in T1 GC (AUC: 0.86) and allowed 44% of patients to avoid unnecessary invasive operations, without missing any LNM-positive patients.

Conclusions: We have successfully developed a cfDNA methylation signature-based liquid biopsy diagnostic assay that allows for robust and less-invasive LNM detection in patients with T1 GC.