Chronic pancreatitis

Abstract

Chronic pancreatitis is defined as a pathological fibro-inflammatory syndrome of the pancreas in individuals with genetic, environmental and/or other risk factors who develop persistent pathological responses to parenchymal injury or stress. Potential causes can include toxic factors (such as alcohol or smoking), metabolic abnormalities, idiopathic mechanisms, genetics, autoimmune responses and obstructive mechanisms. The pathophysiology of chronic pancreatitis is fairly complex and includes acinar cell injury, acinar stress responses, duct dysfunction, persistent or altered inflammation, and/or neuro-immune crosstalk, but these mechanisms are not completely understood. Chronic pancreatitis is characterized by ongoing inflammation of the pancreas that results in progressive loss of the endocrine and exocrine compartment owing to atrophy and/or replacement with fibrotic tissue. Functional consequences include recurrent or constant abdominal pain, diabetes mellitus (endocrine insufficiency) and maldigestion (exocrine insufficiency). Diagnosing early-stage chronic pancreatitis is challenging as changes are subtle, ill-defined and overlap those of other disorders. Later stages are characterized by variable fibrosis and calcification of the pancreatic parenchyma; dilatation, distortion and stricturing of the pancreatic ducts; pseudocysts; intrapancreatic bile duct stricturing; narrowing of the duodenum; and superior mesenteric, portal and/or splenic vein thrombosis. Treatment options comprise medical, radiological, endoscopic and surgical interventions, but evidence-based approaches are limited. This Primer highlights the major progress that has been made in understanding the pathophysiology, presentation, prevalence and management of chronic pancreatitis and its complications.

Diabetes of the exocrine pancreas

“…Variants of these genes increase not only the risk of an individual developing pancreatitis but also the risk of DEP. Individuals with CP may carry more than one mutation in these disease‐associated genes, and new polymorphisms, complex gene–gene interactions, and gene–environmental interactions continue to be discovered . The interaction of environmental and metabolic risk factors with these susceptibility genes is apparent from the wide individual risk of developing CP from ethanol consumption; idiosyncratic drug reactions; and hypercalcemia and hypertriglyceridemia …”

Practical guide to the management of chronic pancreatitis

“…The risk of CP increases with the amount of alcohol consumed (OR:1.33 for 25 g/day and OR:3.19 for 100 g/day) compared with non-alcohol drinkers 9. Cessation of alcohol following acute alcoholic pancreatitis decreases the risk of developing CP 10. Smoking is a independent, dose-related risk factor for CP,5 11 significantly increasing the risk of developing CP compared with non-smokers (OR:7.8) 9…”

Risk factors and nomogram for diabetes mellitus in idiopathic chronic pancreatitis

“…1,2 Over time, chronic inflammation cause the parenchymal fibrosis, which leads to deterioration of pancreatic endocrine and exocrine function. 1,2 Over time, chronic inflammation cause the parenchymal fibrosis, which leads to deterioration of pancreatic endocrine and exocrine function.…”

“…Once patients are diagnosed with DM, antidiabetic drugs or insulin can be applied to regulate blood glucose and prevent further complications secondary to DM. 1 What is more, ICP is the predominant form of CP in India and China occurring in more than 70% CP patients and the second most frequent entity after alcoholic CP in Western countries. [12][13][14] However, for CP without a recognized cause, which is idiopathic chronic pancreatitis (ICP), no appropriate method can be applied to delay the occurrence of pancreatic endocrine disfunction.…”