Table 1.

Potential factors contributing to changes in exocrine function after acute pancreatitis.

Functional Compartment Contribution to Exocrine Pancreatic Dysfunction After Acute Pancreatitis
Acinar Cell
Acinar cell injury	Apoptosis and necrosis of acinar cells reduces functioning acinar cell mass, resulting in diminished pro-enzyme production. Pathogenic variants in PRSS1 and SPINK lead to changes in pro-enzyme production and function predisposing to premature autoactivation and increased injury to acinar cells. Alcohol exposure predisposes to more extensive acinar cell loss during AP.
Disruption of islet-acinar axis	Decreased secretory signaling from damaged islet cells impairs prandial and interdigestive pro-enzyme production.
Ductal Cell
Ductal cell injury	Necrosis of ductal cells may result in disruption or stenosis of the pancreatic duct, leading to impaired flow of enzymes from the acinus to the duodenum. Ongoing inflammation can lead to fibrosis and compression of the pancreatic ducts. Pathogenic variants in CFTR cause reduced duct cell function predisposing to onset of AP. Alcohol and smoking may contribute to reduced ductal cell function before and after AP.
Reduced bicarbonate secretion	Reduction in secretin production and/or response to signaling decreases bicarbonate secretion, which impairs neutralization of chyme and diminishes the efficacy of enzymes (e.g., patients with small bowel dysfunction during/following AP).
Islet Cell
Islet cell injury	Damage to islet cells reduces secretion of stimulatory hormones, including insulin. Loss of insulin production impairs acinar cell function and may lead to diabetes and subsequently diabetic neuropathy, which further impairs the islet-acinar axis
Stellate Cell
Stellate cell activation	Limits cholecystokinin-induced acinar cell secretion. Engulf damaged acinar cells, potentially contributing to long term EPI by reducing functional acinar cell mass. Expands extracellular matrix initially, and eventually leads to ductal fibrosis potentially causing ductal strictures and reduced delivery of enzymes to the duodenum.
Other
Systemic inflammation	Release of pro-inflammatory cytokines and chemokines into pancreatic capillaries results in immune cell recruitment to the pancreas which contributes to injury in all compartments.