Pancreatitis

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Acute pancreatitis

Acute pancreatitis results from the enzymatic autodestruction of the parenchyma and the accompanying acute inflammatory response. It is most commonly associated with biliary tract disease or alcoholism. The diagnosis rests on clinical findings and laboratory evidence, and the radiologic appearance is usually not suggestive of a mass lesion. For this reason, it is seldom aspirated. Aspirates are composed of a background of necrotic debris with degenerating cells, foamy histiocytes, fat necrosis, calcifications and acute inflammation.

Chronic pancreatitis

Chronic pancreatitis may be difficult to distinguish radiologically from a neoplastic process. The cytologic appearance varies depending on the stage of the disease. Earlier stages are more cellular and contain a mixed lymphohistiocytic infiltrate. Later stages are sparsely cellular with less chronic inflammation and may show a relative predominance of islet cells due to atrophy of the acinar epithelium and the extensive fibrosis of the pancreatic parenchyma.

Early stages of chronic active pancreatitis

Both ductal and acinar cells
Background inflammation
Granulation tissue
Fat necrosis

Late chronic pancreatitis

Mostly ductal cells
Few to no acinar cells
Some islet cells
Monolayered sheets
Cohesive, few single cells
Maintained polarity
Minimal nuclear overlapping
Mild anisonucleosis
Smooth nuclear membranes
Rare/normal mitoses
No coagulative necrosis

In both acute and chronic pancreatitis, the ductal epithelium may show marked reactive atypia which can be very hard to distinguish from an adenocarcinoma. Mitoses, prominent nucleoli, hypercromasia and nuclear enlargement are present both in reactive conditions and ductal adenocarcinoma.