Abstract
Chronic pancreatitis is best described as a relentless, continuous inflammatory destruction of the pancreas parenchyma, characterized by irreversible destruction of the exocrine tissues, fibrosis, and at the late stage, the destruction of endocrine cells. Current therapies for chronic pancreatitis patients focus on pain relief by medical and minimally invasive endoscopic treatment as well as surgical management with resection of diseased parenchyma and drainage of obstructed ducts. Radical treatment of chronic pancreatitis has been successful with total pancreatictomy and islet autotransplantation (TP-IAT) that may prevent maladaptive intractable pain pathways and also avoid pancreatogenic diabetes in the well-selected patient. Distinct loss of pancreatic islet cells occurs in about 30%-50% of patients during the progression of chronic pancreatitis when severe fibrosis develops at the late stage of the disease. Profound β cell apoptosis induced by stresses encountered during islet isolation and transplantation further compromises β cell survival and function after TP-IAT. The molecular mechanisms that lead to β cell dysfunction in chronic pancreatitis remain largely undelineated. In this review, we summarize factors that may contribute β cell apoptosis during the disease progress and after TP-IAT and discuss potential interventional approaches that may prevent islet cell death during these processes. Such information is critical to the development of therapeutic protocols that can preserve the viability and function of β cell in patients with chronic pancreatitis.
Highlights
Chronic pancreatitis (CP) is characterized by longstanding inflammation of the pancreas that is notable for the development of progressive pain, fibrosis and loss of exocrine and endocrine function [1]
Distinct loss of pancreatic islet cells occurs in about 30% - 50% of patients during the progression of chronic pancreatitis when severe fibrosis develops at the late stage of the disease
We summarize factors that may contribute to β cell apoptosis during the disease progress and after total pancreatictomy and islet autotransplantation (TP-IAT) and discuss potential interventional approaches that may prevent islet cell death during these processes
Summary
Chronic pancreatitis (CP) is characterized by longstanding inflammation of the pancreas that is notable for. The pathophysiology of chronic pancreatictis is dominated by acinar cell death and loss of exocrine function of the pancreas. We summarize molecular mechanisms that lead to cell dysfunction during the progress of chronic pancreatitis and after TP-IAT and discuss interventional therapies that might improve the viability and function of cells. Dong et al / Advances in Bioscience and Biotechnology 3 (2012) 782-787 lead us to a better understanding of the pathogenetic mechanisms leading to cell death in chronic pancreatitis, and help develop efficient therapeutic treatment protocols for this disease
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