Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic pancreatitis and pancreatic adenocarcinoma represent two pathologic phenomena with marked production of connective tissue stroma containing numerous small blood vessels. The aim of this study was to characterise quantitatively the vascular supply of pancreatic adenocarcinoma and fragments of the periductal tissue collected from patients with chronic pancreatitis. The study material included 18 cases of pancreatitis and 22 cases of pancreatic ductal adenocarcinoma. Microvessels were marked using monoclonal anti-CD34 antibodies. The number of blood vessels in the fibrous stroma was significantly higher in the chronic pancreatitis samples compared to the pancreatic carcinoma group (mean vessel count 298 and 194 vessel/mm2; median 251 and 187 vessel/mm2 respectively; p<0.01). Distributions of the vascular diameter in both studied groups were very similar. The obtained results suggest that the development of vascular network accompanying chronic pancreatitis is more effective in some parts of pancreas compared to angiogenic intensity in pancreatic adenocarcinoma.
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PMID:Microvascular density in chronic pancreatitis and pancreatic ductal adenocarcinoma. 1467 65

To elucidate the distribution and role of myofibroblasts and CD34-positive stromal cells in various pancreatic lesions, we performed an immunohistochemical study using a streptoavidin-biotin immunoperoxidase technique. We selected 43 pancreatic lesions from 1 biopsied, 22 surgically resected and 12 autopsied specimens: acute pancreatitis (n=3), chronic non-obstructive pancreatitis (n=4), obstructive pancreatitis (n=7), islet cell tumor (n=4), serous cystadenoma (n=7), mucinous cystadenoma (n=6), and invasive ductal carcinoma (n=12). In normal pancreas, myofibroblasts and CD34-positive stromal cells were predominantly present in the peridcutal and periacinar areas, respectively. Both myofibroblasts and CD34-positive cells were observed in the stroma of chronic pancreatitis. In four islet cell tumors, myofibroblasts were present in the stroma of the tumor center, but no CD34-positive stromal cells were identified. Additionally, myofibroblasts and CD34-positive stromal cells were located in the inner layer and the outer layer of the capsule of three islet cell tumors, respectively. In nine of the thirteen cystadenomas, only myofibroblasts were recognized in the cyst wall. In the remaining four cystadenomas, a small number of CD34-positive cells were observed in the cyst wall. In 12 invasive ductal carcinomas, the stroma possessed a lot of myofibroblasts, but there were no or few CD34-positive stromal cells. In conclusion, it seems that the abundant amount of CD34-stromal cells in the main lesions is characteristic of chronic inflammatory lesions. Myofibroblasts and CD34-positive stromal cells may play a role in regulating the tumor growth in the capsule of islet cell tumors of the pancreas.
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PMID:The distribution and role of myofibroblasts and CD34-positive stromal cells in normal pancreas and various pancreatic lesions. 1470 72

Pancreatic fibrosis in patients with congenital biliary dilatation (CBD) or choledochal cyst was studied to determine why biliary pancreatitis seldom progresses to chronic pancreatitis/more progressive state. Pancreatic collagenization in eight patients (three adults with pancreatoduodenectomy and five children with biopsy of the pancreas performed when excising the cyst) with CBD was evaluated histopathologically and immunohistochemically. Interlobular and periductal fibrosis with both collagen Type I and Type III immunoreactivities was found in six out of eight cases and in all four cases in which the pancreatic duct was included, respectively. The interlobular area was seldom immunoreactive for alpha-smooth muscle actin (alpha-SMA), a marker for myofibroblasts, but was usually positive for CD34, a human progenitor cell antigen. In contrast, the periductal area was usually immunoreactive for alpha-SMA, but usually negative for CD34 and immunopositive for bcl-2, indicating a continuously progressive state of fibrosis, in which 'pre-existing'alpha-SMA immunoreactivity in the interlobular area may change in nature and lead to CD34-positive fibrosis or apoptosis. In conclusion, biliary pancreatitis is not likely to evolve into chronic pancreatitis/more progressive state because 'pre-existing'alpha-SMA immunoreactivity in the interlobular area may change in nature.
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PMID:alpha-Smooth muscle actin immunoreactivity may change in nature in interlobular fibrosis of the pancreas in patients with congenital biliary dilatation. 1518 3

A case of solid pancreatic hamartoma in a 58-year-old Japanese woman is presented. She had no symptoms, and a pancreatic mass was incidentally found on screening ultrasonography 4 months before admission. The patient was not alcoholic and had no history of pancreatitis. Physical examination and laboratory data were unremarkable. Preoperative imaging demonstrated a nodule in the body of the pancreas, measuring 2.0 cm in maximum diameter, which showed marked delayed enhancement during dynamic CT. The patient underwent a distal pancreatectomy under the preoperative diagnosis of pancreatic endocrine tumor and had an uneventful postoperative course. A well-demarcated solid nodule, 1.9 cm in diameter, was evident in the body of the pancreas. Microscopically, the lesion was composed of non-neoplastic, disarranged acinar cells and ducts embedded in a sclerotic stroma with elongated spindle cells, lacking discrete islets. The stromal spindle cells were immunoreactive for CD34 and CD117. The histological diagnosis was solid hamartoma of the pancreas. There was no recurrence 5 months after surgery. Herein is reported a case of solid hamartoma of the pancreas and review of the literature. A search through the literature found only two cases of solid hamartoma of the pancreas, among the 14 cases previously reported as pancreatic hamartoma.
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PMID:Solid pancreatic hamartoma. 1749 75

In autoimmune pancreatitis (AIP), mechanism(s) of paradoxical glycemic control improvement (GCI) often occurring after pancreatic resection and steroid therapy are not fully elucidated. Using image quantitation, AIP cases (n = 10) with pre- and post-surgical glucose values were compared with chronic pancreatitis (CP) and normal pancreas (NP) regarding percent chromogranin immunohistochemistry (IHC) positivity as a surrogate marker of endocrine endowment; intra-islet T and B lymphocyte and plasma cell enumeration with CD3, CD20, and IgG4 IHC; and CD34 IHC islet vascularity quantitation. Postsurgical GCI, noted in 8/10 (80%) AIP cases, approached statistical significance (P = 0.07) compared to CP. Endocrine endowment reduction, noted by a lower percent of chromogranin + pancreatic parenchyma, was seen in AIP (4.54%) and CP (3.20%) compared to NP (7.95%); only the CP decrease was statistically significant (P = 0.02) since AIP often had ductular endocrine neogenesis. Regression suggested an inverse correlation between endocrine endowment and GCI in AIP (R = 0.62, P = 0.06). AIP islets were smaller and disrupted by inflammatory cell infiltration. Compared to CP, AIP islets had higher CD3 + and CD20 + cell densities. IgG4 + plasma cells were often present at a high density in AIP but typically preserved the islets. Intra-islet CD34 staining showed a lower average vascularity in AIP compared to NP (P = 0.05). This study reaffirms postsurgical GCI in AIP. Prominent intra-islet inflammation and decreased vascularity in AIP may contribute to diabetogenic effects. Endocrine cell neogenesis and relative islet preservation despite islet inflammatory infiltration may explain the paradoxical GCI in AIP.
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PMID:Autoimmune pancreatitis-related diabetes: quantitative analysis of endocrine islet cells and inflammatory infiltrate. 2063 32

Non-neoplastic tumor-like lesions in the pancreas are uncommon. Here, we present a case of multiple solid pancreatic hamartomas in a 78-year-old Japanese woman. Her computed tomography revealed a pancreatic mass, measuring 1.8 cm in maximum diameter. However, no symptoms were found. She was not an alcoholic and had no history of pancreatitis. The patient underwent a pancreatoduodenectomy, and three well-demarcated solid nodules measuring 1.7 cm, 0.4 cm, and 0.3 cm in diameter were found in the pancreatic head. Microscopically, the lesions were composed of non-neoplastic, disarranged acinar cells and ducts embedded in a sclerotic stroma with elongated spindle cells that lacked discrete islets. The stromal spindle cells were immunoreactive for CD34 and CD117. The histological diagnosis was multiple solid hamartomas of the pancreas. There has been no recurrence 30 mo after surgery. So far, 18 cases of pancreatic hamartoma have been reported in the English literature, including our case. Six out of these 18 cases seemed to fit the criteria of solid pancreatic hamartoma. Although the number of cases was limited, solid pancreatic hamartomas seem to be benign tumor-like lesions, which are found incidentally in healthy middle-aged adults, but occasionally involve the whole pancreas, resulting in a poor prognosis. Solid pancreatic hamartoma was sometimes associated with minor pancreatic abnormality, and multiple small lesions other than the main tumors were detected in a small number of cases. From these findings, one may speculate that solid pancreatic hamartoma could be the result of a malformation during the development of the pancreas.
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PMID:Multiple solid pancreatic hamartomas: A case report and review of the literature. 2329 30

Pancreatic hamartoma is a rare tumor, and its characteristic histopathologic features have not yet been fully evaluated. In this study, we collected 9 cases of pancreatic hamartoma to elucidate distinctive histopathologic features that can serve to establish this tumor as a clear disease entity and thus formulate useful histopathologic criteria for this tumor. The cases comprised 4 men and 5 women with a mean age of 62.7 years. The average tumor diameter was 3.3 cm. All patients underwent surgical treatment, and none showed any recurrence postoperatively. Macroscopically, pancreatic hamartomas were well-demarcated tumors with a solid or solid and cystic appearance. Microscopically, these tumors comprised mature acini and small-sized to medium-sized ducts showing a distorted architecture with various amounts of fibrous stroma. Strikingly, the tumors consistently lacked concentric elastic fibers in their duct walls, peripheral nerves, and well-formed islets of Langerhans, all of which exist in both the normal and atrophic pancreas. Immunohistochemically, scattered chromogranin A-positive neuroendocrine cells were observed in the acinar and ductal components. Ductal components were positive for S-100 protein. Spindle-shaped stromal cells expressed CD34 and/or c-kit. These histopathologic features were distinct from those of 5 cases of pancreatic ductal adenocarcinoma, 3 cases of type 1 autoimmune pancreatitis (lymphoplasmacytic sclerosing pancreatitis), 3 cases of alcoholic chronic pancreatitis, and 5 cases of normal pancreas. In conclusion, pancreatic hamartomas share some distinctive histopathologic features and clinical outcomes (neither recurrence nor metastasis) that allow them to be interpreted as malformative lesions. The term "hamartoma" is appropriate for these unique lesions.
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PMID:Distinctive histopathologic findings of pancreatic hamartomas suggesting their "hamartomatous" nature: a study of 9 cases. 2371 57