In patients with acute pancreatitis, reparative changes of frank parenchymal necrosis, divided into granulation tissue, fibro-granulation tissue and fibrosis, occur depending on the duration and severity of the illness. Fibrosis in the apparently uninvolved areas in patients with acute pancreatitis develops in relation to frank parenchymal necrosis, and may consist of type I collagen in patients surviving longer. The role of fat necrosis in acute pancreatitis could be explained as follows: when extensive fibrin thrombi in the fat necrosis are resolved before the reparative change is accomplished, hemorrhage may extend into the surrounding tissue.

Copyright © 2007 S. Karger AG, Basel

Acute hemorrhagic pancreatitis or acute pancreatic necrosis is a fatal disease and is caused by the destructive effects of pancreatic enzymes. The dominant characteristics of acute pancreatic necrosis are parenchymal necrosis, hemorrhage and fat necrosis. If patients survive, a variety of sequelae, including reparative changes, follow.

Most patients with acute pancreatitis have considerable areas of intact parenchyma, even at death after an illness of only a few days [1]. Necrotizing pancreatitis is often accompanied by interstitial pancreatitis some distance from areas of necrosis. When these cases consequently become chronic or heal, interlobular fibrosis is prominent.

Fat necrosis is thought to be the initial event of acute pancreatitis. However, causal relationships between fat necrosis and advancement to fatal pancreatitis have not yet been fully explained.

Fig. 1. Reparative changes in frank parenchymal necrosis. Parenchymal necrosis is adjacent to the exocrine tissue via granulation in a patient with an illness of 10 days. HE. X100.

In this article, we describe in patients with acute pancreatitis both reparative changes in frank necrosis and the occurrence of fibrosis in apparently uninvolved areas away from the areas of necrosis, and discuss the role of fat necrosis in acute pancreatitis.

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