| Research Abstract |
The incidence and histological features of pancreatic fibrosis, including chronic alcoholic pancreatitis, in patients with a history of chronic alcohol abuse were investigated histopathologically. Fibrosis was seen in 33 of 46 cases of alcoholic dependence syndrome, 20 of 53 cases of chronic alcoholism, and all 30 cases of chronic alcoholic pancreatitis. Fibrosis was categorized into two types : intralobular and perilobular sclerosis. In chronic alcoholic pancreatitis, fibrosis was found mainly in perilobular, or interlobular areas, and in some advanced cases extended into intralobular areas, so that the pancreatic tissue was completely replaced by fibrosis. Hence, interlobular fibrosis was found in all cases of chronic alcoholic pancreatitis. In contrast, in cases that had predominantly intralobular fibrosis, which were usually cases of alcoholic dependence syndrome, the pancreatic tissue had not completely disappeared, even at an advanced stage, and some parenchymal regeneration simi
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lar to that seen in hemochromatosis was observed.
Clinicopathological comparisons revealed the following results : accompanying liver cirrhosis was greater in the intralobular type than in the interlobular type of fibrosis. However, the greater frequency protein plugs, pancreatic stones, extensive fibrosis replacement, peripancreatic fibrosis, splenic vein involvement, choledochus involvement, pseudocyst and ductal hyperplasia in interlobular fibrosis compared to intralobular fibrosis were found.
In conclusion, the findings for the interlobular and intralobular distribution of fibrosis and differences in various components or accompanying diseases in pancreatic fibrosis suggets that this entity shows two distinct pathologic patterns with differing mechanisms.
Mechanism of periacinar, or intralobular fibrosis was electronmicroscopically investigated along comparison between alcoholics and non-alcoholics. In the stage of abundunt collagen fibers around the acini, many myofibroblasts and fibroblasts were present. There were microfibrils, 13-15nm in diameter, between myofibroblasts or fibroblasts and collagen fibers. Hence, periacinar collagenization might be caused by myofibroblasts as well as fibroblasts.
Prolyl hedroxylase distributed in the acinar cells immunohistochemically. Therefore, the acinar cells might play one of the components on pancreatic fibrosis. Less
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