The majority of patients with acute pancreatitis in Western Sydney present with mild disease and have a low risk of morbidity or mortality. The ratio of gallstone to alcohol aetiology was 2:1. Idiopathic pancreatitis is responsible for more cases than expected.

Acute pancreatitis is a common acute surgical condition associated with high morbidity and mortality in severe cases. New guidelines for management have recently been published by the American College of Gastroenterology and by the International Association of Pancreatology in collaboration with the American Pancreatic Association. The main differences between the new and previous versions of the guidelines relate to the use of endoscopic retrograde cholangiopancreatography (ERCP) and the addition of the new severity category of 'moderately severe acute pancreatitis' All patients with pancreatitis should have its cause determined by features of the history, results of laboratory tests (liver function tests, serum calcium triglyceride levels) and findings on transabdominal ultrasound. Those with idiopathic pancreatitis should have endoscopic ultrasound as a first-line investigation. Acute pancreatitis should be managed with aggressive hydration with intravenous fluids and fasting. Oral feeding can be recommenced in mild pancreatitis once pain and nausea and vomiting have resolved. Patients with mild biliary pancreatitis should have a laparoscopic cholecystectomy during their index admission. In addition to aggressive intravenous fluid resuscitation and fasting, patients with severe pancreatitis should have enteral feeding (nasoenteric or nasogastric feeds) commenced 48 hours after presentation. Total parenteral nutrition should be avoided where possible. All patients with organ failure or severe pancreatitis as defined by the revised version of the Atlanta classification should be managed in an intensive care setting. Patients with biliary pancreatitis and concurrent cholangitis should have endoscopic retrograde cholangiopancreatography within 24 hours of presentation.

Based on the aberrant protein expression profiles, the anterior hippocampus appears to be more involved in schizophrenia pathogenesis than the posterior hippocampus. Furthermore, consistent with previous findings, we found molecular evidence to support abnormal neuronal cytoarchitecture and function, neurotransmission and mitochondrial function in the schizophrenia hippocampus.

BACKGROUND: Determining the risk of developing severe acute pancreatitis (AP) on presentation to hospital is difficult but vital to enable early management decisions that reduce morbidity and mortality. The objective of this study was to determine global gene expression profiles of patients with different acute pancreatitis severity to identify genes and molecular mechanisms involved in the pathogenesis of severe AP. STUDY DESIGN: AP patients (n = 87) were recruited within 24 hours of admission to the Emergency Department and were confirmed to exhibit at least 2 of the following features: (1) abdominal pain characteristic of AP, (2) serum amylase and/or lipase more than 3-fold the upper laboratory limit considered normal, and/or (3) radiographically demonstrated AP on CT scan. Severity was defined according to the Revised Atlanta classification. Thirty-two healthy volunteers were also recruited and peripheral venous blood was collected for performing RNA-Seq. RESULTS: In severe AP, 422 genes (185 upregulated, 237 downregulated) were significantly differentially expressed when compared with moderately severe and mild cases. Pathway analysis revealed changes in specific innate and adaptive immune, sepsis-related, and surface modification pathways in severe AP. Data-driven approaches revealed distinct gene expression groups (endotypes), which were not entirely overlapping with the clinical Atlanta classification. Importantly, severe and moderately severe AP patients clustered away from healthy controls, whereas mild AP patients did not exhibit any clear separation, suggesting distinct underlying mechanisms that may influence severity of AP. CONCLUSION: There were significant differences in gene expression affecting the severity of AP, revealing a central role of specific immunological pathways. Despite the existence of patient endotypes, a 4-gene transcriptomic signature (S100A8, S100A9, MMP25, and MT-ND4L) was determined that can predict severe AP with an accuracy of 64%.