Foitzik T, Buhr H J
Chirurgische Klinik I, Klinikum Benjamin Franklin, Freie Universität Berlin.
Chirurg. 1997 Sep;68(9):855-64. doi: 10.1007/s001040050285.
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.
尽管进行了大量的实验和临床研究，但对于慢性胰腺炎（CP）的演变仍未达成共识。在20世纪70年代和80年代，萨勒斯一直强调CP因胰腺结石而从头演变。然而，近年来，临床和形态学研究为急性胰腺炎进展为慢性胰腺炎的最初提议提供了有力证据。所谓的坏死-纤维化序列理论得到了免疫组织化学研究的支持，该研究表明炎症介质主要导致组织破坏，免疫细胞浸润胰腺神经是CP疼痛产生的致病因素。虽然萨勒斯假设腺泡分泌亢进以及胰腺结石促进和抑制因子失衡引发了CP的演变，但坏死-纤维化序列理论还涉及其他病理机制（如导管通透性改变、缺血、氧化应激），这些机制已被证明会导致（急性）胰腺损伤。尽管有这个统一的模板，这也减少了为急性和慢性酒精性胰腺炎的发病机制确定独立机制的必要性，但仍存在一些悬而未决的问题，例如关于（如在遗传性CP中）可能解释胰腺对损伤的不同易感性和个体免疫反应的遗传因素。
