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Paediatric and hereditary aspects of chronic pancreatitis
1Department of Child Health, Singleton Hospital, Swansea, UK. J.A.Dodge@btinternet.com
Insights
Cystic fibrosis (CF) is a leading cause of chronic pancreatitis in children. This study proposes that impaired protease activation in CF leads to pancreatic damage via chronic overstimulation and duct obstruction.
Area of Science:
- Pediatric Gastroenterology
- Pancreatology
- Genetics
Background:
- Cystic fibrosis (CF) is the most common cause of chronic pancreatitis in children.
- Pancreatitis is rarely the initial presenting symptom of CF.
Purpose of the Study:
- To propose a hypothesis for the development of pancreatic lesions in cystic fibrosis.
- To explore the underlying mechanisms of pancreatitis in CF and contrast them with hereditary pancreatitis.
Main Methods:
- Literature review and hypothesis formulation.
- Analysis of protease activation pathways and their role in pancreatic injury.
Main Results:
- Impaired pancreatic protease activation in the small intestine is hypothesized to cause chronic hyperstimulation pancreatitis in CF.
- This leads to intra-acinar zymogen activation and protein precipitation in ducts when bicarbonate secretion decreases.
- Oxidant stress is suggested as a contributing factor in CF-related and other forms of childhood pancreatitis.
Conclusions:
- The proposed mechanism highlights impaired protease regulation as central to CF-associated pancreatitis.
- Understanding these pathways may inform future therapeutic strategies for pediatric pancreatitis.
- Oxidant stress is a potential common pathway in various forms of childhood pancreatitis.
Abstract:
Cystic fibrosis is by far the commonest cause of chronic pancreatitis in children, but pancreatitis itself is only rarely its presenting feature. In this paper an hypothesis for the development of the pancreatic lesions is presented. Impaired activation of pancreatic proteases in the small intestine is perceived as the pivotal problem that leads to continual feedback release of cholecystokinin, thus, in effect, causing a chronic hyperstimulation pancreatitis with intra-acinar activation of zymogens and, when bicarbonate secretion falls, precipitation of 'Reg' and other proteins in the duct system. This position contrasts with that in hereditary pancreatitis in which a mutation in the cationic trypsinogen gene leads to a form of trypsin that resists degradation by mesotrypsin and enzyme Y. A survey of the literature suggests that oxidant stress is a plausible contributor to pancreatic injury in both these diseases and in several other conditions linked with childhood pancreatitis.
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