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World J Gastroenterol. Nov 14, 2013; 19(42): 7231-7240
Published online Nov 14, 2013. doi: 10.3748/wjg.v19.i42.7231
Pathophysiology of chronic pancreatitis
Christina Brock, Lecia Møller Nielsen, Dina Lelic, Asbjørn Mohr Drewes
Christina Brock, Lecia Møller Nielsen, Dina Lelic, Asbjørn Mohr Drewes, Mech-Sense, Department of Gastroenterology and Hepatology, Aalborg University Hospital, DK-9000 Aalborg, Denmark
Asbjørn Mohr Drewes, Center for Sensory-Motor Interactions (SMI), Department of Health Science and Technology, Aalborg University, DK-9220 Aalborg, Denmark
Author contributions: All authors contributed to the manuscript.
Supported by The Danish Council for Strategic Research
Correspondence to: Christina Brock, DVM, PhD, Mech-Sense, Department of Gastroenterology and Hepatology, Aalborg University Hospital, Mølleparkvej 4, DK-9000 Aalborg, Denmark. cb@mech-sense.com
Telephone: +45-99-326246 Fax: +45-99-326507
Received: June 6, 2013
Revised: August 19, 2013
Accepted: August 28, 2013
Published online: November 14, 2013
Core Tip

Core tip: The reported prevalence of chronic pancreatitis (CP) is approximately 0.5%. Etiological risk-factors associated with CP are multiple and throughout the review the M-ANNHEIM classification is used comprising environmental factors (alcohol consumption, nicotine habits and nutrition), hereditary, well characterized mutations, ductal obstruction and autoimmune factors. CP is characterized by progressive fibrotic destruction of glandular tissue, inflammation or duct obstruction, leading to irreversible functional impairment of both exocrine and endocrine functions. In view of the multi-factorial disease and the complex clinical picture, it is not surprising that treatment of patients with CP is challenging and often unsuccessful.