[New aspects in the pathophysiology of chronic pancreatitis].
Despite numerous experimental and clinical investigations there is no consensus on the evolution of chronic pancreatitis (CP). In the 1970s and 1980s, Sarles persistently emphasised the de novo evolution of CP due to pancreatolithiasis. In recent years, however, clinical and morphological studies have provided strong evidence for the initial proposal of acute pancreatitis progressing to chronic pancreatitis. The so-called necrosis-fibrosis-sequence theory is supported by immunohistochemical work suggesting that inflammatory mediators primarily contribute to tissue destruction and that infiltration of pancreatic nerves by immune cells is a pathogenetic factor for the generation of pain in CP. While Sarles postulates that acinar hypersecretion and an imbalance of pancreatic stone promoting and inhibiting factors trigger the evaluation of CP, the necrosis-fibrosis-sequence theory also involves other pathomechanisms (e.g. changes in ductal permeability, ischemia, oxidative stress) which have been shown to cause (acute) pancreatic injury. Despite this unifying template, which also lessens the need to identify independent mechanisms for the pathogenesis of acute and chronic alcoholic pancreatitis, there are still open questions, e.g. on genetic factors that (like in hereditary CP) may explain the different susceptibility of the pancreas to injury and the individual immunological response.
Foitzik
T
T
Chirurgische Klinik I, Klinikum Benjamin Franklin, Freie Universität Berlin.
Buhr
H J
HJ
D002769:Cholelithiasis / Q000503:physiopathology; D002908:Chronic Disease; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D010179:Pancreas / Q000503:physiopathology; D010183:Pancreatic Ducts / Q000503:physiopathology; D010195:Pancreatitis / Q000503:physiopathology*; D019283:Pancreatitis, Acute Necrotizing / Q000503:physiopathology; D019512:Pancreatitis, Alcoholic / Q000503:physiopathology; D012307:Risk Factors
D018836:Inflammation Mediators