Abstract.
Pancreatitis is usually inflammation of the pancreas without infection. Our understanding of pancreatitis has been built on autopsy studies, surgical biopsies and surrogate markers of inflammation and fibroses, including abdominal imaging techniques and pancreatic functional studies. However, the discovery that a number of different environmental factors and various genetic abnormalities are seen in patients with similar appearing pancreatitis phenotypes teaches us that end-stage pathology is not the disorder. Understanding complex associations and interactions requires that the components and their interactions be organized, stratified and functionally defined. Systems biology, in the broad sense, provides the approach and tools to define the complex mechanisms driving pathology. As the mathematics behind these pathways and mechanisms are defined and calibrated, the potential pathology of patients with early signs of disease can be predicted, and a number of patient-specific targets for intervention can be defined.
Keywords. Pancreas, pancreatitis, acute pancreatitis, chronic pancreatitis, fibrosis, stellate cell, inflammation, systems biology, genetics, genetic testing, meta-analysis, cystic fibrosis transmembrane conductance regulation, trypsin, trypsinogen, pancreatic secretory trypsin inhibitor, CFTR, PRSS1, SPINK1, SAPE, alcohol, tobacco, smoking