Structures by Inflammation

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Involvement of Inflammation of the Splenic Vein

Involvement of the splenic vein [4] often occurs. The clinical manifestation of splenic vein obstruction is splenomegaly and varicose veins in the stomach (many in the gastric fundus) and esophagus, generally called localized (or left-sided) portal hypertension.

In our histopathological study of surgical and autopsy specimens from 12 patients with chronic alcoholic pancreatitis, fibrosis in the pancreatic parenchyma continuously extended to the wall of the splenic vein in 11 specimens; 5 patients showed organized thrombus formation with recanalization, 4 presented with phlebosclerosis and in 2 there were no apparent changes. In 2 of the 5 patients with organized thrombus formation in the splenic vein, localized portal hypertension had been clinically diagnosed: these patients had shown splenomegaly and varicose veins in the fundus of the stomach, but not liver cirrhosis.

Two mechanisms can lead to thrombus formation within the splenic vein. One is an extrinsic factor, a direct mass effect or cellular infiltration into the venous wall. The other is an intrinsic factor, an inflammatory process involving the vein. In the peripancreatic area, once fibrosis persistently compresses the splenic vein wall over a prolonged period (which might be considered a mild w

Fig. 4. Phlebosclerosis in chronic pancreatitis. Interlobular fibrosis was continuous to the peripancreatic lesion and involved the splenic vein (arrow). EVG. X 12.5.

mechanical trauma), endothelial cells become injured, finally leading to phlebosclerosis and thrombus formation. This fibrotic extension involving the splenic vein is important for the mechanism of thrombus formation.

Involvement of Inflammation to the Duodenum

Diffuse involvement in the duodenum (fig. 5) is rare and its clinical manifestation is characterized by duodenal stenosis. Our single case presented so-called groove pancreatitis in a broad sense, which is a rare form of segmental chronic pancreatitis involving a so-called 'groove' area between the head of the pancreas, the duodenum, and the common bile duct [5].

In chronic pancreatitis with duodenal stenosis, the following histopatho-logical findings can be found in the duodenum and adjacent pancreatic head tissue: cyst formation, myoid stromal proliferation, spindle cell and smooth muscle fiber proliferation, and Brunner's gland hyperplasia.

Cysts can be observed in the muscularis propria, submucosa, and mucosa of the duodenum, with or without extraduodenal-peripancreatic extensions, and show various shapes and sizes: oval, slit-like, irregular, and collapsed. We have managed three surgically-resected cases showing duodenal stenosis in patients

Varicose Veins Splenic Hilum
Fig. 5. Chronic pancreatitis involving the duodenum. Chronic pancreatitis in the head showed groove pancreatitis in the broad sense, also spreading to the duodenal wall. The duodenal wall was markedly thickened.

with chronic alcoholic pancreatitis [6]. The cysts were 15, 17 and 23 mm in diameter. In general, the majority are pseudocysts, the wall of which consists of granulation tissue surrounding the cyst and including slight hemosiderin deposition, spindle cells positive for a-SMA (smooth muscle actin), a marker of myofibroblasts, and smooth muscle proliferation. Cysts are thought to be derived from a ductal component of the ectopic pancreatic tissue, because some are occasionally accompanied by an epithelial lining with or without ductal structures.

Dense myoid stromal proliferation, spindle cell and smooth muscle fiber proliferation and pancreatic acinar tissue shows the characteristic histological pattern described as myoadenomatosis or pancreatic hamartoma.

Brunner's gland hyperplasia is typically seen coexisting with proliferation of smooth muscle fibers of the muscularis mucosae. Each gland is surrounded by these muscle fibers.

In the case of duodenal stenosis, cysts are seen especially in association with granulation tissue, including marked proliferation of a-SMA-positive spindle cells and smooth muscle fibers. Proliferation of myofibroblasts and smooth muscle fibers are observed not only in the tissue surrounding the cyst, but also in the submucosal layer of the duodenum.

Generally, myofibroblasts are known to play an important role in wound healing and subsequent contraction of the tissue. Therefore, proliferation of myofibroblasts and smooth muscle fibers around the cysts, especially the former, may indicate the healing process of localized inflammation of duodenal wall cysts. This proliferation may also play a role in duodenal stenosis.

Recently, such pancreatitis has been referred to under the unifying name of paraduodenal pancreatitis [7] that shows the characteristic histopathological and clinical findings described in this small chapter.

Involvement of Inflammation of the Intrapancreatic Bile Duct

In TFP, the intrapancreatic bile duct shows luminal stenosis and fibrous thickening of the wall, caused by either circumferential or nodular protruding fibrosis.

Involvement of Inflammation of the Colon

Though cases with chronic pancreatitis involving the colon are very rare (fig. 5), the frequency of colonic 'stenosis' has been reported to range from 1.5% [8] to 2-3%. According to the literature [8], the most frequently involved site (52%) is the splenic (left colonic) flexure. Histopathological findings are rarely described. In our one case, a 65-year-old male patient underwent distal pancreatectomy due to suspicion of pancreatic cancer involving the transverse colon. Histologically, pericolonic and colonic inflammation and fibrosis were seen. Fibrosis was seen from the pericolonic area to the submucosal layer of the colon, accompanied by abscess in the subserosal layer.

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