Characteristic histopathological features are summarized as follows: (a) dense circumferential lymphoplasmacytic infiltration within and around the pancreatic ducts, especially the medium-sized, interlobular and main pancreatic ducts, and (b) prominent sclerotic collagen bundles with lymphoplasmacytic infiltration.
Although neutrophilic infiltration in a Japanese AIP patient has not previously been reported in the literature, one of our cases showed LPSP with eosinophilic infiltration (unpublished observation). The ductal lumen was narrowed by the infolding wall, typically a star-like or slit-like appearance (fig. 2). Even when lymphoplasmacytic infiltration is seen in the ductal epithelium, it is not desquamated. Neither protein plugs nor pancreatic stones were identified histologically. However, such a clinical case was reported as showing pancreatic stone in long-term follow-up in an AIP patient.
Injury to the lobuli (parenchyma) shows a basically obstructive pattern. Lymphoplasmacytic infiltration and inter- and intralobular fibrosis are the main histological findings, usually accompanied by lobular atrophy, acinar atrophy or loss, lymphoid aggregates or hyperplasia to various degrees. Prominent sclerotic collagen bundles with lymphoplasmacytic infiltration are characteristically found (figs. 3, 4). On immunohistochemistry, plasmacytes show various degrees of positivity for IgG4.
This inflammatory process always involves the intralobular small venules and usually the interlobular veins, which is called obstructive phlebitis. In some cases the splenic vein shows phlebosclerosis, but there is no thrombus formation. The arteries and arterioles accompanying the veins and venules are usually intact. The intrapancreatic bile duct is often involved when the pancreas head is
affected. In some cases, the extrapancreatic bile duct shows the same changes as the pancreas does (mentioned below). The pancreatic islets usually do not show cell infiltrates except in extremely advanced cases. The inflammatory process also involves the peripancreatic fat tissue (fig. 5) and lymph nodes, but neither fat necrosis nor calcification is seen. Typically, enlarged lymph nodes are composed of lymphoplasmacytes in the peripheral sinus with the capsule becoming fibrously thickened. When the inflammatory tumorous lesion is localized, the pancreatic parenchyma distal to the lesion becomes markedly atrophic, and remarkable acinar atrophy, fibrosis, inflammatory cell infiltration and aggregated islets are seen in these regions. The background pancreatic tissue does not show any remarkable findings; there are no characteristic features of chronic alcoholic pancreatitis characterized by interlobular fibrosis.
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