BACKGROUND AND AIMS:Autoimmune gastritis (AIG) is characterized by chronic hypergastrinemia and is associated with an increased risk of gastric neuroendocrine neoplasms (gNENs). Because proton pump inhibitors (PPIs) further increase gastrin secretion, concerns have been raised regarding a potential additive effect on gastric neoplastic risk. This study aimed to evaluate the association between PPI exposure and gNEN occurrence in patients with AIG using a large real-world database. METHODS:We conducted a retrospective propensity score-matched cohort study using the TriNetX Global Collaborative Network. Patients with AIG were identified using diagnostic codes for chronic atrophic gastritis or pernicious anaemia, excluding Helicobacter pylori infection, gastric cancer, multiple endocrine neoplasia or other competing gastric conditions. Two cohorts were defined: patients with AIG receiving PPIs and patients without PPI exposure. The primary outcome was the overall occurrence of gNENs. A prespecified secondary analysis excluded patients with gNENs diagnosed before the index date to evaluate incident tumours. Secondary outcomes included hypergastrinemia, intestinal metaplasia and gastric polyps. RESULTS:A total of 153,687 patients with AIG were identified. After 1:1 propensity score matching, 40,489 patients were included in each cohort. After propensity score matching, gNENs were recorded in 241 patients (0.60%) without PPI exposure and 360 patients (0.89%) receiving PPIs. PPI exposure was associated with a significantly higher occurrence of gNENs (risk ratio [RR] 1.49, 95% CI 1.27-1.76), which was confirmed by time-to-event analysis (hazard ratio [HR] 1.44, 95% CI 1.22-1.70; log-rank p < 0.001). The association persisted after exclusion of patients with pre-existing gNENs (RR 1.61, 95% CI 1.26-2.06; HR 1.52, 95% CI 1.19-1.95). PPI exposure was also associated with higher occurrences of hypergastrinemia (HR 1.17, 95% CI 1.00-1.37), intestinal metaplasia (HR 1.53, 95% CI 1.36-1.71) and gastric polyps (HR 2.48, 95% CI 2.25-2.73). No gastric adenocarcinomas were identified during follow-up. CONCLUSIONS:In this large real-world propensity score-matched study, PPI exposure was associated with a greater occurrence of both overall and incident gNENs in patients with AIG. PPI use was also consistently associated with gastric mucosal alterations, including hypergastrinemia, intestinal metaplasia and gastric polyps. Although the absolute risk of gNENs remained low, these findings support judicious long-term PPI prescribing in patients with AIG and reinforce the importance of appropriate endoscopic surveillance in this high-risk population.
BACKGROUND:Intestinal ultrasound (IUS) is increasingly used to monitor activity and predict treatment outcomes in Crohn's disease (CD), but its role in predicting primary non-response (PNR) to Upadacitinib (UPA) and identifying maintenance relapse remains unclear. METHODS:In this multicenter prospective cohort study, 122 patients with active CD treated with UPA were followed through week 52. Demographic, clinical, biochemical, endoscopic and IUS data were collected longitudinally. Univariable logistic regression, ROC analysis and likelihood ratio test (LRT) identified the best PNR predictors. Survival analysis evaluated the association between post-induction ultrasound targets and the risk of relapse during 15-mg maintenance. RESULTS:Among baseline IUS parameters, IBUS-SAS > 60.20 demonstrated the highest odds ratio for predicting UPA PNR (OR 16.63, 95% CI 6.54-42.29, p < 0.001). Compared with clinical and endoscopic parameters, the inclusion of IBUS-SAS significantly improved PNR prediction (AUC 0.865 vs. 0.670, LRT p < 0.001, 95% CI 0.802-0.929, Sensitivity 82.98%, Specificity 77.33%, PPV 69.64% and NPV 87.88%). Early at week 4, worse IUS findings were significantly correlated with PNR, with IBUS-SAS > 47.80 showing the highest odds ratio (OR 26.25, 95% CI 2.46-280.20, p = 0.007). Among clinical and endoscopic responders, failure to achieve IUS response/remission was associated with an increased risk of relapse during 15-mg maintenance. (Log-rank p = 0.005, p < 0.001). CONCLUSION:Early IUS monitoring provides incremental value for predicting UPA PNR beyond clinical and endoscopic parameters. Failure to achieve IUS response/remission may identify patients at increased risk of relapse during 15-mg maintenance.
Optimal bowel cleansing of stool makes it easier to achieve quality indicators for colonoscopy, including identification of sessile serrated lesions and adenomas, cecal intubation and decreases the risk for post-colonoscopy CRC. Recommendations from the US Multi-Society Task Force on Bowel Preparation facilitates this process.
Adequate bowel preparation is critical to the effectiveness of colonoscopy. Bowel preparations have evolved over the years and now there are many options available to patients. These options fall into three categories of regular volume, low-volume and ultra-low volume preparations. It is important to select a preparation that maximises patient adherence and improves patient experience.
BACKGROUND:Adequate bowel preparation (BP) is the foundation to successful colonoscopy. Inadequate bowel preparation (IBP) leads to numerous consequences beyond just procedural inconvenience. IBP can obscure polyps, lesions or early signs of colorectal cancer (CRC) while increasing procedure length, shortening surveillance intervals and increasing health care costs. Efforts to improve BP quality, therefore, are critical for high-quality endoscopic examinations, which optimise the success of CRC screening programmes. Achieving adequate BP begins with clearly understanding and grading BP quality on every examination, aiming for a minimum threshold of adequate BP in > 90% of colonoscopies. Additionally, recognition of patient-specific risk factors for IBP allows for tailored instructions and utilisation of navigational and outreach tools along with enhanced educational materials towards optimising BP. Finally, understanding patient preferences and improving the patient experience can increase the chances of succeeding with not only completion of the index examination but also optimising compliance for any repeat examinations across screening, surveillance and diagnostic indications. METHODS:This manuscript will review the current evidence regarding the consequences of IBP, while discussing patient-specific risk factors and barriers to adequate BP, concluding with methods to improve BP adequacy and practical tips for clinicians.
BACKGROUND:Chimeric antigen receptor T-cell (CAR-T) therapy has revolutionised the treatment of hematologic malignancies, and its use is expanding rapidly into numerous other disease states including autoimmune diseases. However, CAR-T therapy is associated with a spectrum of immune-related toxicities. In addition to the already well characterized cytokine release syndrome and immune effector cell-associated neurotoxicity syndrome, it has become apparent that rarely, CAR-T can cause gastrointestinal mucosal inflammation, termed immune effector cell-mediated enterocolitis (IEC-EC). AIMS:This state-of-the-art review highlights the CAR-T mechanism and details the epidemiology, pathophysiology, clinical manifestations, endoscopic and histopathologic features, and management of IEC-EC. METHODS:This review presents the current state of knowledge through a comperhensive and detailed synthesis of all case series reported in the literature to date. RESULTS:Occurring in up to approximately 6% of patients typically following B cell maturation antigen-targeted CAR-T therapy, IEC-EC presents with severe diarrhoea and malabsorption, responds poorly to treatment, and portends a dire prognosis. Multi-disciplinary management should centre on early diagnosis, supportive cares, assessment and treatment of infections, and step-up pharmacotherapy, often featuring biologics and small molecules drawn from the inflammatory bowel disease pharmacologic armamentarium. CONCLUSIONS:Clinicians should maintain a high degree of vigilance for IEC-EC in patients presenting with gastrointestinal symptoms following CAR-T treatment. Early recognition and multi-disciplinary treatment may improve patient outcomes.
