Chronic pancreatitis

被引:0
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作者
Jorg Kleeff
David C. Whitcomb
Tooru Shimosegawa
Irene Esposito
Markus M. Lerch
Thomas Gress
Julia Mayerle
Asbjørn Mohr Drewes
Vinciane Rebours
Fatih Akisik
J. Enrique Domínguez Muñoz
John P. Neoptolemos
机构
[1] Vascular and Endocrine Surgery,Department of Visceral
[2] University Hospital Halle (Saale),Department of Molecular and Clinical Cancer Medicine
[3] Martin-Luther-University Halle-Wittenberg,Department of Medicine
[4] Institute of Translational Medicine,Division of Gastroenterology
[5] University of Liverpool,Department of Medicine A
[6] Cell Biology & Physiology,Department of Gastroenterology and Endocrinology
[7] and Human Genetics,Department of Medicine II
[8] University of Pittsburgh & UPMC,Department of Gastroenterology & Hepatology
[9] Tohoku University Graduate School of Medicine,Department of Radiology and Imaging Sciences
[10] Institute of Pathology,Department of Gastroenterology and Hepatology
[11] Heinrich-Heine University and University Hospital,Department of General Surgery
[12] University Medicine Greifswald,undefined
[13] Philipps-University Marburg,undefined
[14] University Hospital Grosshadern,undefined
[15] Ludwig-Maximillian University Munich,undefined
[16] Mech-Sense & Centre for Pancreatic Diseases,undefined
[17] Clinical Institute,undefined
[18] Aalborg University Hospital,undefined
[19] Pancreatology Unit,undefined
[20] DHU UNITY,undefined
[21] INSERM UMR1149,undefined
[22] Beaujon Hospital,undefined
[23] Indiana University School of Medicine,undefined
[24] Health Research Institute (IDIS),undefined
[25] University Hospital of Santiago de Compostela,undefined
[26] University of Heidelberg,undefined
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摘要
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.
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