Complications Caused by Progression of Pancreatitis Itself

Protein Plugs and Stones (Pancreatolithiasis)

Protein plugs consist of condensed pancreatic juice (or secretion) composed of protein suspected to be of zymogenic origin, and composed of erythrocytes, desquamated epithelium of the small duct and mucoproteins originating from the epithelium. As it becomes more condensed, collagen is produced as one of the components. Histologically, pancreatic stones show a

Fig. 1. Chronic alcoholic pancreatitis characterized by interlobular (perilobular) fibrosis. HE. X40.

lamellar structure with calcification. There are two types: true stone, located in the pancreatic duct, and false stone, seen in necrotic parenchymal areas with calcification.

Klöppel et al. state in their hypothesis that the necrosis-fibrosis sequence is the basic pathogenetic event in the evolution of chronic pancreatitis [2], and that protein plugs and pancreatic stones are formed as the result of progression of chronic pancreatitis and then become causes of duct obstruction as well as further progression of the disease.

Tumor-Forming Pancreatitis

Tumor-forming pancreatitis (TFP) (fig. 2) [3] is a clinical term that our study showed is divided into two subtypes. One shows tissue repair with a background of chronic alcoholic pancreatitis, and the other consists of lymphoplas-macytic infiltration and fibrosis without a background of chronic alcoholic pancreatitis. The former, with a background of chronic alcoholic pancreatitis, is described in this section.

Tumorous lesions can be seen as a pathological repair process after ductal and parenchymal injury and consist of three layers, observed from the center of the lesion to the periphery (fig. 3).

Fig. 2. Tumor-forming pancreatitis. Pancreatoduodenectomy specimen. The tumorous lesion (white arrows) showed an abscess-necrotic layer at the center and transition to surrounding fibrosis at the periphery. Black arrows indicate protein plugs. The background pancreas is very firm and shows chronic pancreatitis.

Fig. 2. Tumor-forming pancreatitis. Pancreatoduodenectomy specimen. The tumorous lesion (white arrows) showed an abscess-necrotic layer at the center and transition to surrounding fibrosis at the periphery. Black arrows indicate protein plugs. The background pancreas is very firm and shows chronic pancreatitis.

Fig. 3. Tumorous lesion in tumor-forming pancreatitis. The lesion consisted of an abscess-necrotic area with fibrogranulation and fibrous layers, from the center (lower right) to periphery (upper left). HE. X40.

The first is an abscess-necrosis layer, consisting of condensed pancreatic juice, protein plugs, stones, neutrophils and small pieces of desquamated ductal epithelium. This core layer is hence considered to originate from the pancreatic duct.

The second is a fibrogranulation layer, and includes capillaries with swollen endothelium, lymphocytes, plasmacytes, and hemosiderin deposition. These tissues are inter-mixed with fibrosis.

The third is a fibrous layer, with successive transition to the surrounding fibrosis in the non-swollen pancreatic tissue. The thickness of each layer differs in each case. Some tumorous swelling involves several pancreatic ducts, which means that swelling lesions might conglomerate to form a larger one. A background of tumorous swelling shows a chronic pancreatitis pattern in which exocrine pancreatic tissue is rather well-preserved irrespective of pancreatitis.

To conclude: TFP is a 'stage' of tumor-forming in the natural course of 'chronic pancreatitis' with rather well-preserved exocrine tissue. Tumorous swelling presents histological findings of the tissue repair process for cen-triductal acute inflammation, caused by protein plugs and pancreatic stones.

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