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Chronic pancreatitis (CP) is a common GI disorder with an incidence of 4/100 000 and a prevalence of 41/100 000.1 Owing to the chronic nature of the disease, patients with CP are often admitted to hospital and represent a serious socioeconomic burden across continents. Patients with CP have an increased mortality by more than threefold compared with the normal population, and the 20-year survival rate is reduced to 45% compared with 65% of the normal population.1 The disease mostly occurs in repeated episodes of acute inflammatory bouts of the pancreas parenchyma that progressively leads to exocrine and endocrine insufficiency, chronic pain and cachexia. Besides known lifestyle risk factors such as alcohol and nicotine, predisposing genetic mutations have been identified with cystic fibrosis transmembrane conductance regulator (CFTR), carboxypeptidase-A, cationic trypsinogen and serine protease inhibitor Kazal-type 1 being the most prominent candidates. Histologically, CP is characterised by a progressive loss of acinar cells that are replaced by activated pancreatic stellate cells (PSCs), and accumulation of extracellular matrix components such as collagen, vimentin and fibronectin. Furthermore, infiltrating immune and inflammatory cells are frequently detected in CP specimen, which has led to the notion of a ‘never healing wound’. The molecular mechanisms by which acinar damage either results in complete regeneration of the pancreas or eventually progresses to fibrosis and functional …
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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