Date: | 2017 Sep |
PMID: | |
Category: | 2 |
Authors: | Jorg Kleeff 1 2, David C Whitcomb 3, Tooru Shimosegawa 4, Irene Esposito 5, Markus M Lerch 6, Thomas Gress 7, Julia Mayerle 8, Asbjørn Mohr Drewes 9, Vinciane Rebours 10, Fatih Akisik 11, J Enrique Domínguez Muñoz 12, John P Neoptolemos 13 |
Abstract: |
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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.
Acknowledgements:
The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of the National Cancer Institute, the National Institute of Health, or the National Institute of Diabetes and Digestive and Kidney Diseases.
The Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer (CPDPC) Research Consortia is supported and funded by grants from the National Cancer Institute and the National Institute of Diabetes and Digestive and Kidney Diseases under the following award numbers:
Project Number: | Awardee Organization |
U01DK108326 | Baylor College of Medicine |
U01DK108314 | Cedars-Sinai Medical Center |
U01DK108332 | Indiana University |
U01DK108323 | Kaiser Foundation Research Institute |
U01DK108288 | Mayo Clinic |
U01DK108327 | Ohio State University |
U01DK108300 | Stanford University |
U01DK108320 | University of Florida |
U01DK108306 | University of Pittsburgh |
U01DK108328 | University of Texas MD Anderson Cancer Center |
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