Software Reference Architecture for Real-Time Mobile Digital Phenotyping: Evaluation of System Designs.

Pancreatitis comprises a group of inflammatory pancreatic disorders (; ). Acute pancreatitis is one of the most common gastrointestinal causes of hospital admission and ranges from mild self-limited inflammation to severe disease with persistent organ failure. Chronic pancreatitis is a progressive fibroinflammatory disease (; ; ). It is often associated with chronic abdominal pain, exocrine pancreatic insufficiency, diabetes, malnutrition, and reduced quality of life (; ; ). While acute and chronic pancreatitis differ in clinical presentation/onset and disease course, both conditions involve complex interactions between inflammation/immune response, metabolic disturbance and extra-pancreatic complications. For many years, pancreatitis was mainly studied from the perspective of pancreatic injury, enzyme activation, acinar cell damage, and systemic inflammation (; ; ; ). In recent years, the gut has become increasingly relevant to the study of pancreatitis. Gut microbiota is involved in mucosal barrier maintenance, immune regulation, microbial metabolite production, and host metabolic homeostasis (; ; ). These functions are directly relevant to several clinically important features of pancreatitis, including intestinal barrier dysfunction, bacterial translocation, infected necrosis, systemic inflammation, nutritional intolerance, and longer-term metabolic complications. For this reason, the relationship between pancreatitis and gut microbiota is not simply an extension of general microbiome research, but a disease-specific research area shaped by the pathophysiological links between intestinal ecology and pancreatic injury. The connection between gut microbiota and acute pancreatitis has been studied more extensively than that with chronic pancreatitis. Severe acute pancreatitis is often accompanied by intestinal barrier dysfunction and systemic inflammatory response. Enteric bacteria have long been considered a potential source of infectious complications (; ). Early studies therefore focused largely on probiotics, synbiotics, and bacterial translocation. However, the PROPATRIA trial showed that probiotic prophylaxis did not reduce infectious complications and was associated with increased mortality in patients with predicted severe acute pancreatitis (; ). This finding changed the way microbiota-based interventions were viewed in this field. Later studies began to focus more on microbial composition, dysbiosis, disease severity, host immune response, and metabolic changes. Recent studies have reported that gut microbiota dysbiosis may worsen the severity of acute pancreatitis in both patients and experimental models (; ). Compared with acute pancreatitis, the connection between chronic pancreatitis and gut microbiota has been less extensively studied, but it is becoming increasingly relevant. Chronic pancreatitis can alter digestion, nutrient absorption, bile acid metabolism, glucose homeostasis, and intestinal conditions through exocrine and endocrine pancreatic dysfunction (). These changes may reshape the intestinal microbial environment. Clinical studies have reported altered intestinal microbiota in patients with chronic pancreatitis, especially in those with diabetes and metabolic abnormalities ().