Currently, those recommended to undergo pancreatic cancer (PC) surveillance include appropriately aged individuals at high risk of PC due to an identifiable genetic susceptibility or those without identifiable genetic susceptibility who nonetheless have a strong family history of PC. With increases in identification of individuals at high risk for PC and increased use of PC surveillance in clinical practice, there has been increasing debate about who should undergo surveillance as well as how surveillance should be performed including use of imaging and blood-based testing. Furthermore, there is increasing interest in the outcomes of PC surveillance in high-risk individuals with some studies demonstrating that surveillance leads to downstaging of PC and improvements in survival. In this review, we summarize the current state of PC surveillance in high-risk individuals, providing an overview of the risk factors associated with PC, selection of high-risk individuals for PC surveillance, and the current, but non-uniform, recommendations for performing PC surveillance. Additionally, we review approaches to apply various imaging and blood-based tests to surveillance and the outcomes of PC surveillance.

Acute pancreatitis is a common inflammatory gastrointestinal disease without any successful treatment. Pancreatic exocrine acinar cells have high rates of protein synthesis to produce and secrete large amounts of digestive enzymes. When the regulation of organelle and protein homeostasis is disrupted, it can lead to endoplasmic reticulum (ER) stress, damage to the mitochondria and improper intracellular trypsinogen activation, ultimately resulting in acinar cell damage and the onset of pancreatitis. To balance the homeostasis of organelles and adapt to protect themselves from organelle stress, cells use protective mechanisms such as autophagy. In the mouse pancreas, defective basal autophagy disrupts ER homoeostasis, leading to ER stress and trypsinogen activation, resulting in spontaneous pancreatitis. In this review, we discuss the regulation of autophagy and its physiological role in maintaining acinar cell homeostasis and function. We also summarise the current understanding of the mechanisms and the role of defective autophagy at multiple stages in experimental pancreatitis induced by cerulein or alcohol.

Acute pancreatitis (AP) is a disease spectrum ranging from mild to severe with an unpredictable natural course. Majority of cases (80%) are mild and self-limiting. However, severe AP (SAP) has a mortality risk of up to 30%. Establishing aetiology and risk stratification are essential pillars of clinical care. Idiopathic AP is a diagnosis of exclusion which should only be used after extended investigations fail to identify a cause. Tenets of management of mild AP include pain control and management of aetiology to prevent recurrence. In SAP, patients should be resuscitated with goal-directed fluid therapy using crystalloids and admitted to critical care unit. Routine prophylactic antibiotics have limited clinical benefit and should not be given in SAP. Patients able to tolerate oral intake should be given early enteral nutrition rather than nil by mouth or parenteral nutrition. If unable to tolerate per-orally, nasogastric feeding may be attempted and routine post-pyloric feeding has limited evidence of clinical benefit. Endoscopic retrograde cholangiopancreatogram should be selectively performed in patients with biliary obstruction or suspicion of acute cholangitis. Delayed step-up strategy including percutaneous retroperitoneal drainage, endoscopic debridement, or minimal-access necrosectomy are sufficient in most SAP patients. Patients should be monitored for diabetes mellitus and pseudocyst.