Mechanism of Interlobular Fibrosis of the Pancreas

The most commonly cited theory for the cause of chronic alcoholic pancreatitis is the deposition of protein plugs which later calcify, leading to duct obstruction with subsequent fibrotic replacement of the acinar tissue upstream from the occlusion [12]. However, duct obstruction is considered to be an essential mechanism for fibrosis in chronic obstructive pancreatitis distal to a stricture of the pancreatic duct. Chronic obstructive pancreatitis is observed secondary to slow-growing pancreatic carcinomas, ampullary carcinomas, odd-itis, and pancreatic duct scars [13]. According to our previous study [2], in chronic alcoholic pancreatitis cases fibrosis is mainly distributed in the interlobular or perilobular areas with a nodular pancreatitis pattern (fig. 4), whereas

Fig. 5. Chronic obstructive pancreatitis in a patient with pancreas head carcinoma showed inter- and intralobular fibrosis with acinar atrophy. HE. X50.

in pancreatic head carcinomas, which cause complete obstruction of the main pancreatic duct, fibrosis is found in the inter- and intralobular areas with the lobular/acinar atrophy mentioned above (fig. 5).

Recently, we investigated the mechanism of interlobular fibrosis of the pancreas based on histological changes in the pancreatic tissue in ampullary carcinoma patients with various degrees of stricture in the main pancreatic duct [14]. The results were as follows: incomplete obstruction of the main pancreatic duct caused diffuse mild interlobular fibrosis and an expansive lobular appearance (fig. 6), which may ultimately lead to a nodular lobular pattern. These findings are similar to those of chronic alcoholic pancreatitis, except for excessive fibrosis with patchy distribution. In addition, such fibrosis is accompanied by the appearance of cells with anti-a-smooth muscle actin (a-SMA) immunoreactivity (fig. 7), which is a marker for myofibroblasts [15, 16]. It is well known that myofibroblasts play an important role not only in wound healing, but also in collagenization, which is followed by fibrosis in many organs [17-20]. Moreover, Tanaka et al. [21] demonstrated an experimental canine model of chronic pancreatitis which showed histological changes similar to those of human chronic alcoholic pancreatitis by combining alcohol administration with incomplete pancreatic duct obstruction. Therefore, such incomplete obstruction of the pancreatic duct plays an important role at the onset of interlobular fibrosis, which is categorized as chronic alcoholic pancreatitis [14].

Fig. 6. Mild fibrosis distributed in the interlobular area, with a rather expansive lobular appearance, in a patient with an ampullary carcinoma. HE. X50. Reproduced with permission [40].

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