Bockman D E, Boydston W R, Anderson M C
Am J Surg. 1982 Aug;144(2):243-9. doi: 10.1016/0002-9610(82)90518-9.
Tissue samples from seven patients with chronic pancreatitis were studied by light and electron microscopy, using samples from the pancreas of seven organ donors as a reference group. Tubular complexes were observed in four of the patients with chronic pancreatitis. Tubular complexes, which have been interpreted as resulting from "ductular reduplication" in other studies of chronic pancreatitis, and "ductular proliferation" in studies of pancreatic adenocarcinoma, were studied carefully to determine their origin. Extensive retrogressive changes in acinar cells leading to diminished zymogen granules, decreased cell height, and concomitant increase in luminal diameter were consistent with the interpretation that phenotypic modulation of acinar cells to take on the characteristics of ductular cells produced the tubules. This it is concluded that in chronic pancreatitis, as has been shown for pancreatic adenocarcinoma, the tubular complexes originate from acinar cells rather than from proliferation of preexisting ductules. Fibrosis and thickening of the basal lamina of exocrine pancreatic cells and capillaries were consistent with an altered capability for transmission of material between blood vessels and exocrine cells.
对7例慢性胰腺炎患者的组织样本进行了光镜和电镜研究,并以7例器官捐献者的胰腺样本作为参照组。在4例慢性胰腺炎患者中观察到了管状复合体。管状复合体在其他慢性胰腺炎研究中被解释为“小导管重复”,在胰腺癌研究中被解释为“小导管增生”,对其起源进行了仔细研究。腺泡细胞广泛的退行性变化导致酶原颗粒减少、细胞高度降低以及管腔直径相应增加,这与腺泡细胞表型调节以具备小导管细胞特征从而产生小管的解释一致。由此得出结论,在慢性胰腺炎中,如同在胰腺癌中所显示的那样,管状复合体起源于腺泡细胞而非既存小导管的增殖。胰腺外分泌细胞和毛细血管基底膜增厚及纤维化,与血管和外分泌细胞之间物质传输能力改变一致。