Pancreatic pain.
Abdominal pain is an important clinical symptom in pancreatic diseases. There is increasing evidence that pain in chronic pancreatitis and pancreatic cancer is triggered by pancreatic neuropathy. Damage to intrapancreatic nerves seems to support the maintenance and exacerbation of neuropathic pain. In chronic pancreatitis, intrapancreatic nerves are invaded by immune cells. This observation led to the hypothesis that neuro-immune interactions play a role in the pathogenesis of chronic pancreatitis and the accompanying abdominal pain syndrome. Similarly, pancreatic cancer cells infiltrate the perineurium of local nerves, which may in part explain the severe pain experienced by the patients. Furthermore, perineural invasion extending into extrapancreatic nerves may preclude curative resection and thus often leads to local recurrence. In recent years, the involvement of a variety of neurotrophins and neuropeptides in the pathogenesis of pancreatic pain was discovered. This review summarises recent data on the mechanisms of neuropathy and pain generation in pancreatic disorders.
Ceyhan
Güralp O
GO
Department of Surgery, Klinikum Rechts der Isar, Technische Universität München, Ismaningerstrasse 22, D-81675 Munich, Germany.
Michalski
Christoph W
CW
Demir
Ihsan E
IE
Müller
Michael W
MW
Friess
Helmut
H
D015746:Abdominal Pain / Q000209:etiology* / Q000503:physiopathology*; D000818:Animals; D006801:Humans; D009414:Nerve Growth Factors / Q000378:metabolism; D009443:Neuritis / Q000276:immunology / Q000503:physiopathology; D010179:Pancreas / Q000276:immunology / Q000294:innervation / Q000473:pathology; D010190:Pancreatic Neoplasms / Q000150:complications* / Q000276:immunology / Q000503:physiopathology*; D050500:Pancreatitis, Chronic / Q000150:complications* / Q000276:immunology / Q000503:physiopathology*; D050916:TRPV Cation Channels / Q000378:metabolism
D009414:Nerve Growth Factors; D050916:TRPV Cation Channels; C494484:TRPV1 receptor