Progression of Pancreatic Fibrosis

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There are no precise morphological tools or studies of fibrosis patterns to distinguish between more progressive and steady states in chronic pancreatitis cases. In the end stage, chronic pancreatitis is represented by massive or extensive interlobular fibrosis and total permanent loss of the exocrine pancreatic

Fig. 8. Collagen fibrils between a myofibroblast and an acinar cell in a 73-year-old male with chronic alcoholism. Note the presence of many fine filaments (arrows), 8-15 nm in diameter, between the myofibroblast (M) and collagen fibrils (C), and many micropinocytic vesicles (arrowheads) in the cytoplasmic surface of the myofibroblast. A = Acinar cell. Uranyl acetate, lead citrate and tannic acid stain.

Fig. 8. Collagen fibrils between a myofibroblast and an acinar cell in a 73-year-old male with chronic alcoholism. Note the presence of many fine filaments (arrows), 8-15 nm in diameter, between the myofibroblast (M) and collagen fibrils (C), and many micropinocytic vesicles (arrowheads) in the cytoplasmic surface of the myofibroblast. A = Acinar cell. Uranyl acetate, lead citrate and tannic acid stain.

Fig. 9. Immunoreactivity against anti-prolyl hydroxylase was localized mainly in the acinar cells of the pancreas. X200.
Fig. 10. Leakage of filamentous material (asterisk) via the disrupted limiting membrane of zymogen granules (Z) in a 53-year-old male with chronic alcoholism. Uranyl acetate, lead citrate and tannic acid stain.

tissue, which are frequently found in chronic alcoholic pancreatitis and chronic obstructive pancreatitis. On the other hand, mild cases show both periductal and mild interlobular fibrosis in patients with congenital biliary dilatation, which causes biliary or bile pancreatitis. According to Klöppel et al. [38], biliary pancreatitis is not likely to evolve into chronic pancreatitis. We investigated the difference between progressive pancreatitis and non-progressive, or steady, pancreatitis, and found that the pathologic states and findings common to chronic alcoholic pancreatitis and chronic obstructive pancreatitis are duct obstruction, as mentioned above, and interlobular or perilobular fibrosis, although in chronic obstructive pancreatitis cases fibrosis was also distributed in the intralobular areas. In the latter, interlobular fibrosis was also found in patients with congenital biliary dilatation. In our previous study [9], interlobular fibrosis in patients with congenital biliary dilatation was mostly immunonegative for a-SMA in pancreatoduodenectomized (PD) materials (patients' mean age 35.7 years) (fig. 11). In biopsied cases (patients' mean age 5.0 years), however, a-SMA immunoreactivity was observed in the interlobular fibrotic area in two of three cases, and was also found in the periductal area in all PD materials. Hence, such a-SMA immunoreactivity has occurred at least once in the interlobular area in patients with congenital biliary dilatation and may have subsequently changed in nature. The transient nature of a-SMA

Fig. 11. Interlobular fibrosis was immunonegative for a-SMA, while periductal fibrosis was positive for a-SMA, in a patient with congenital biliary dilatation. X50.

immunoreactivity may be related not only to the healing of inflammatory injuries, but also to apoptosis [15]. On the other hand, periductal, but not interlobular, a-SMA immunoreactivity which is accompanied by bcl-2 immunoreactivity is considered to be due to reflux of the bile duct contents, resulting in a continuously progressive state of fibrosis. According to Burton et al. [39], the ductal expression of a-SMA decreases in chronic pancreatitis, whereas septal and lobular expression dramatically increases. Hence, a-SMA-negative interlobular fibrosis in patients with congenital biliary dilatation may not show any apparent progression.

Therefore, duct obstruction and interlobular fibrosis admixed with myofi-broblast proliferation, as seen in chronic alcoholic pancreatitis and chronic obstructive pancreatitis, are identified as markers or hallmarks of progression in chronic pancreatitis.

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