Current Opinion in Gastroenterology最新文献

Purpose of review: This review describes pathologic conditions of retrograde flow into the esophagus along with recent therapeutic advances and treatment options.

Recent findings: The esophagus facilitates anterograde and retrograde movement of contents, the latter of which is mediated by transient lower esophageal sphincter relaxations (TLESRs). Gastroesophageal reflux disease (GERD) often includes esophageal-specific symptoms such as heartburn or regurgitation. Volume regurgitation responds less frequently to acid suppression with proton pump inhibitors (PPIs) than heartburn, given its relationship with incompetence of the esophagogastric junction (EGJ) and increased frequency of TLESRs. Therefore, although the refluxate pH can be altered with PPIs, the frequency of reflux episodes is generally not reduced and surgical and endoscopic treatments may be favored. Other instances of abnormal retrograde esophageal flow respond better to medical therapy, or lifestyle interventions. Compared to gastric belching because of increased stomach distension, supragastric belching is caused by intake of air from pharynx into the esophagus followed by rapid expulsion of air. These conditions can be distinguished on esophageal tests such as high-resolution manometry and are likely to respond to behavioral modifications.

Summary: Retrograde flow into the esophagus can be a normal occurrence, but diagnostic testing to distinguish causes can guide appropriate intervention.

Purpose of review: The purpose of this review was to highlight most recent updates on nutritional aspects in gastroparesis (GP) focusing on dietary recommendations, utilization of enteral and parenteral nutrition, endoscopic and surgical interventions.

Recent findings: Recent data addressed eating patterns, nutritional interventions, and clarifications on the role of endoscopic and surgical interventions underlying an impact on nutritional management of GP patients. They support the importance of gastroparesis-specific diet in addition to drug therapy, and confirm the benefits of a modified low-fat, low-fiber diet. Current guidelines suggest a new approach to GP management based on predominant symptoms. Gastric peroral endoscopic pyloromyotomy (G-POEM) and surgical gastric electrical stimulator (GES) placement may be considered in individuals with nausea and vomiting before the need for jejunostomy tube placement for enteral feeding or parenteral nutrition.

Summary: Current literature supports the importance of dietary interventions, focusing on low-fat and low-fiber diets, in addition to drug therapies. Severely fiber-restrictive diets may not be necessary. There is enhanced understanding when jejunal feeding should be incorporated for refractory cases with consideration of G-POEM or/and GES even before jejunal tube placement. This approach will require patient evaluation in specialized motility centers.

Purpose of review: This review evaluates the current knowledge of gut microbiome alterations in acute pancreatitis, including those that can increase acute pancreatitis risk or worsen disease severity, and the mechanisms of gut microbiome driven injury in acute pancreatitis.

Recent findings: Recent observational studies in humans showed the association of gut microbiome changes (decreased gut microbiome diversity, alterations in relative abundances of certain species, and association of unique species with functional pathways) with acute pancreatitis risk and severity. Furthermore, in-vivo studies highlighted the role of gut microbiome in the development and severity of acute pancreatitis using FMT models. The gut barrier integrity, immune cell homeostasis, and microbial metabolites appear to play key roles in acute pancreatitis risk and severity.

Summary: Large human cohort studies that assess gut microbiome profile, its metabolites and impact on acute pancreatitis risk and severity will be crucial for development of innovative prediction, prevention and treatment strategies.

Purpose of review: Large nonpedunculated colorectal polyps ≥ 20 mm (LNPCPs) comprise 1% of all colorectal lesions. LNPCPs are more likely to contain advanced histology such as high-grade dysplasia and submucosal invasive cancer (SMIC). Endoscopic resection is the first-line approach for management of these lesions. Endoscopic resection options include endoscopic mucosal resection (EMR), cold-snare EMR (EMR), endoscopic submucosal dissection (ESD) and endoscopic full-thickness resection (EFTR). This review aimed to critically evaluate current endoscopic resection techniques.

Recent findings: Evidence-based selective resection algorithms should inform the most appropriate endoscopic resection technique. Most LNPCPs are removed by conventional EMR but there has been a trend toward C-EMR for endoscopic resection of LNPCPs. More high-quality trials are required to better define the limitations of C-EMR. Advances in our understanding of ESD technique, has clarified its role within the colorectum. More recently, the development of a full thickness resection device (FTRD) has allowed the curative endoscopic resection of select lesions.

Summary: Endoscopic resection should be regarded as the principle approach for all LNPCPs. Underpinned by high-quality research, endoscopic resection has become more nuanced, leading to improved patient outcomes.

Purpose of review: The incretin enhancers and mimetics, including dipeptidyl peptidase-4 (DPP-4) inhibitors, GLP-1 receptor agonists (GLP-1RA) and GLP-1/GIP co-agonists, have become mainstays in the treatment of type 2 diabetes (T2D). Recently, the approval of certain GLP-1RA and GLP-1/GIP co-agonists for the treatment of obesity has broadened their popularity and use. In this review, we summarize the evidence for an association of these drugs with acute pancreatitis and other adverse events of special interest to gastroenterologists.

Recent findings: In addition to pancreatic islets, GLP-1 receptors are expressed in the exocrine cells of the pancreas. There is inconsistent evidence for an association of DPP-4 inhibitors, GLP-1RA and co-agonists with risk for acute pancreatitis in individual trials. Meta-analyses of long-term randomized controlled trials indicate a small risk of acute pancreatitis associated with DPP-4 inhibitors but not GLP-1RA or co-agonists. Cholecystitis and cholelithiasis may be more common among those treated with GLP-1RA and GLP-1/GIP co-agonists. There is no evidence that any of these drugs are associated with an increased risk of pancreatic cancer.

Summary: While drugs that leverage the incretin system are increasingly being used for patients with T2D and obesity, caution in warranted in those with a history of pancreatitis and gallbladder disease.

Purpose of review: Acute pancreatitis is a common acute inflammatory disorder of the pancreas, and its incidence has been increasing worldwide. Approximately 10% of acute pancreatitis progresses to severe acute pancreatitis (SAP), which carries significant morbidity and mortality. Disordered immune response to pancreatic injury is regarded as a key event that mediates systemic injury in SAP. In this article, we review recent developments in immune biomarkers of SAP and future directions for research.

Recent findings: Given the importance of the NLRP3-inflammasome pathway in mediating systemic inflammatory response syndrome and systemic injury, recent studies have investigated associations of SAP with systemic levels of activators of NLRP3, such as the damage associated molecular patterns (DAMPs) for the first time in human SAP. For example, circulating levels of histones, mitochondrial DNAs, and cell free DNAs have been associated with SAP. A panel of mechanistically relevant immune markers (e.g., panel of Angiopoeitin-2, hepatocyte growth factor, interleukin-8 (IL-8), resistin and sTNF-α R1) carried higher predictive accuracies than existing clinical scores and individual immune markers. Of the cytokines with established relevance to SAP pathogenesis, phase 2 trials of immunotherapies, including tumor necrosis factor (TNF)-alpha inhibition and stimulation of IL-10 production, are underway to determine if altering the immunologic response can reduce the severity of acute pancreatitis (AP).

Summary: Circulating systemic levels of various DAMPs and a panel of immune markers that possibly reflect activities of different pathways that drive SAP appear promising as predictive biomarkers for SAP. But larger multicenter studies are needed for external validation. Studies investigating immune cellular pathways driving SAP using immunophenotyping techniques are scarce. Interdisciplinary efforts are also needed to bring some of the promising biomarkers to the bedside for validation and testing for clinical utility. Studies investigating the role of and characterization of altered gut-lymph and gut-microbiota in severe AP are needed.

Purpose of review: The burdens of pancreatic ductal adenocarcinoma (PDAC) and acute pancreatitis are increasing globally. We reviewed current literature on whether acute pancreatitis is a causal factor for PDAC and examined clinical manifestations of PDAC-associated acute pancreatitis.

Recent findings: Recent findings detail the timing of acute pancreatitis before and after PDAC occurrence, further solidifying the evidence for PDAC-associated acute pancreatitis and for acute pancreatitis as a causal risk factor for PDAC. The risk of PDAC remains elevated above the general population in patients with distant history of acute pancreatitis. PDAC risk also increases with recurrent acute pancreatitis episodes, independent of smoking and alcohol. Mechanisms linking acute pancreatitis to PDAC include inflammation and neutrophil infiltration, which can be attenuated by suppressing inflammation and/or epigenetic modulation, thus slowing the progression of acinar-to-ductal metaplasia. Clinical presentation and management of acute pancreatitis in the context of PDAC are discussed, including challenges acute pancreatitis poses in the diagnosis and treatment of PDAC, and novel interventions for PDAC-associated acute pancreatitis.

Summary: PDAC risk may be reduced with improved acute pancreatitis prevention and treatment, such as antiinflammatories or epigenetic modulators. Increased acute pancreatitis and PDAC burden warrant more research on better diagnosis and management of PDAC-associated acute pancreatitis.

Purpose of review: This review examines current research on healthcare disparities in pancreatitis, identifies knowledge gaps, and proposes strategies to develop targeted multilevel interventions to address inequities in pancreatitis care.

Recent findings: Current literature has identified patient, disease, and healthcare-level factors contributing to disparities in risk factors and health outcomes of pancreatitis. Moreover, social structures, economic systems, social vulnerability, and policy significantly influence the pancreatitis care continuum.

Summary: Understanding the root causes of health inequities is critical to developing effective approaches for the prevention, early detection, and management of pancreatitis.