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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CT has become an important tool in the diagnosis and management of diseases that affect the stomach and duodenum. By depicting the bowel lumen, wall, and extramural structures, CT can provide unique information that complements standard air contrast radiography and endoscopy. Proper scanning methods and knowledge of normal anatomy are necessary for optimal results. We utilize the gas contrast technique for organ-specific examination in patients with known or suspected gastroduodenal disease. Gastric adenocarcinoma is an important indication for CT evaluation. Unfortunately, early hopes that CT could accurately stage gastric cancer have not been realized. CT is not as accurate as laparotomy in staging early gastric cancer, primarily owing to its inability to detect small peritoneal implants, diagnose metastases in normal-sized lymph perigastric nodes, and predict pancreatic invasion. Nevertheless, CT retains an important role in depicting gross metastatic disease and guiding percutaneous biopsy, particularly in patients who are deemed poor surgical candidates or have undergone prior gastric resection. A variety of conditions other than primary gastric adenocarcinoma produce recognizable abnormalities on CT. Gastric lipoma, leiomyosarcoma, and varices have a distinctive appearance. Others, including gastritis and uncomplicated peptic ulcer, produce nonspecific gastric wall thickening. Endoscopic correlation and biopsy are required for specific diagnosis in these cases. The duodenum, by virtue of its location in the anterior pararenal compartment of the retroperitoneum, may be involved by numerous benign and malignant conditions. In blunt trauma, complicated pancreatitis, and peptic ulcer disease, as well as primary and metastatic malignancy, CT can provide data that may alter patient management.
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PMID:CT of the stomach and duodenum. 265 48

Ninety-two children with pancreatic disorders were treated over a 10-year period. Thirty-three had blunt trauma, while 69 had medical, metabolic, or neoplastic diseases. Children with trauma had either duct disruption (3), gland fracture (4), or pseudocysts formation (26). Operation was required in 30. Pseudocysts were treated with observation alone in three cases, ultrasound-guided percutaneous aspiration in three, surgical external drainage in two, distal pancreatectomy in four, cyst gastrostomy in ten, and cyst-Roux-en-Y jejunostomy in six. Other disorders included pancreatitis (44), neoplasms (10), nesidioblastosis (4), and pancreaticosplenic abscess (2). Treatment for neoplasms included surgical excision in nine and biopsy in one (adenocarcinoma). Patients with nesidioblastosis underwent 95% (near total) pancreatic resection (two after previous unsuccessful 80% resection). Pancreatitis was familial in two cases, necrotizing in two, idiopathic in 11, and secondary to medications in six cases (steroids, 2; L-asparaginase, 4), gallstones in 17, and choledochal cysts in 6. Pancreatitis resolved after observation and conservative therapy in ten idiopathic cases, 4/6 medication-related cases, and following correction of biliary tract disease (15/17) or choledochal cysts (6). Pancreatic resection or drainage was required in the remaining cases. Pancreatic disorders can be accurately detected with computed tomography (CT) scan in most cases (excluding insulinoma). Ultrasound (US) is useful in cases of biliary tract disease and pseudocyst formation. Traumatic pseudocysts can resolve spontaneously or with US-guided percutaneous drainage (in the presence of normal ducts). Children with neoplasms, abnormal pancreatic ducts, or recurrent pancreatitis require resection or appropriate drainage procedures. Overall survival was 95%.
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PMID:Pancreatic disorders in infancy and childhood: experience with 92 cases. 276 44

Immunohistochemical studies of neuron-specific enolase were performed on pancreatic tissues from patients with insulinoma, nonfunctioning islet cell tumor, chronic pancreatitis, and pancreatic adenocarcinoma, and from 5 normal patients. The concentration of neuron-specific enolase was also measured in the sera of patients and in the pancreatic tissue, and the tissues were stained for carbohydrate antigen 19-9 by immunohistochemical techniques. Neuron-specific enolase was localized in nerve fibers, normal islet cells, and islet cell tumors; its concentration was elevated only in the tissue of islet cell tumors and in serum from patients with insulinoma. In the pancreatic tissue of pancreatitis or pancreatic adenocarcinoma, various changes in acini and islets were present. The altered islets stained clearly for neuron-specific enolase and could easily be distinguished from altered, unstained acini in cases of pancreatitis or pancreatic adenocarcinoma. Islets in the pancreatic tissue remained intact with various morphologic changes, although acini had degenerated severely. Carbohydrate antigen 19-9 was localized in all the carcinoma cells in the pancreatic tissue and in some of the normal pancreatic ducts. No cells were simultaneously immunostained by anti-neuron-specific enolase and anti-carbohydrate antigen 19-9 antibodies. Thus, neuron-specific enolase is a good marker for islet cell tumor, and is valuable for examining islets in pancreas with various disorders both alone and in combination with other tumor markers.
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PMID:Immunohistochemical study of neuron-specific enolase and CA 19-9 in pancreatic disorders. The value of neuron-specific enolase as a marker for islet cell and nerve tissue. 301 9

Paraganglioma is a neoplasm of neuroectodermal origin that occurs rarely in the bowel. This case report illustrates the previously undescribed CT appearance of a duodenal paraganglioma. An intensely enhancing mass in the region of the pancreatic head was found. The intense enhancement ruled out adenocarcinoma and focal pancreatitis. An islet cell tumor of the pancreas was the major differential diagnostic consideration.
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PMID:Case report: CT of a duodenal paraganglioma. 317 86

A 62-year-old Chinese woman suffering from pancreatic carcinoma coexisting with chronic calcifying pancreatitis is reported. Ultrasonography and computed tomography disclosed multiple intraductal calcifications in the pancreatic head and body and a tumor at the tail. Laparotomy revealed cancerous peritonitis in addition to verifying the presence of calcifications at the head and body and a cancer at the tail. Histology confirmed adenocarcinoma. The incidence of pancreatic carcinoma in chronic calcifying pancreatitis varied from 0.8 to 25% in a thorough review of the literature. It is emphasized that patients with chronic calcifying pancreatitis should be closely followed for detection of possible coexisting pancreatic malignancies.
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PMID:Pancreatic carcinoma associated with chronic calcifying pancreatitis in Taiwan: a case report and review of the literature. 328 30

A primate lymphotropic lentivirus was isolated on the human T-cell line HuT 78 after cocultivation of a lymph node from a pig-tailed macaque (Macaca nemestrina) that had died with malignant lymphoma. This isolate, originally designated M. nemestrina immunodeficiency virus (MnIV) and now classified as simian immunodeficiency virus (SIV/Mne), was inoculated intravenously into three juvenile rhesus monkeys (Macaca mulatta), three juvenile pig-tailed macaques (M. nemestrina), and two juvenile baboons (Papio cynocephalus). All six macaques became viremic by 3 weeks after inoculation, whereas neither of the baboons developed viremia. One pig-tailed macaque died at 15 weeks with suppurative peritonitis secondary to ulcerative, necrotizing colitis. Immunologic abnormalities included a marked decrease in CD4+ peripheral blood lymphocytes. Although five macaques mounted an antibody response to SIV/Mne, the animal that died at 15 weeks remained antibody negative. Three other macaques (two rhesus and one pig-tailed) died 66 to 87 weeks after inoculation after exhibiting progressive weight loss, anemia, and diarrhea. Histopathologic findings at necropsy included various manifestations of immune deficiency, nephropathy, subacute encephalitis, pancreatitis, adenocarcinoma, and lymphoid atrophy. SIV/Mne could be readily isolated from the spleens and lymph nodes of all necropsied macaques, and from the cerebrospinal fluid, brains, bone marrow, livers, and pancreas of some of the animals. SIV antigens were localized by avidin-biotin immunohistochemistry to pancreatic islet cells and to bone marrow endothelial cells. The data suggest that African baboons may be resistant to infection by SIV/Mne, whereas Asian macaques are susceptible to infection with this pathogenic primate lentivirus.
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PMID:Inoculation of baboons and macaques with simian immunodeficiency virus/Mne, a primate lentivirus closely related to human immunodeficiency virus type 2. 328 32

This report describes a rapid, easy, and safe means of saving the spleen while resecting or fully mobilizing the pancreatic tail. The pancreas is separated from the spleen by dividing the splenic artery and vein distal to the tip of the pancreas. The spleen survives on the short gastric vessels, which are carefully preserved. The technique has been applied successfully in 22 of 25 consecutive patients with chronic pancreatitis (n = 13), acute pancreatitis and pancreatic necrosis (n = 3), cystic neoplasm of the pancreas (n = 4), islet cell tumor (n = 2), and ductal adenocarcinoma (n = 3). The spleen could not be saved in three patients because of splenic hilar involvement by tumor or scar. Normal postoperative blood cell counts and spleen scans proved splenic viability and function. There was only one complication, a late splenic abscess that developed in a spleen of twice-normal size. It is concluded that in most instances the distal pancreas can be mobilized for resection or inspection without the need for splenectomy. Splenomegaly may be a contraindication because the short-vessel gastric blood supply may be inadequate to nourish the increased tissue mass. The technique is applicable to the treatment of pancreatic tumors, trauma, and pancreatitis.
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PMID:Conservation of the spleen with distal pancreatectomy. 335 79

The presentation of pancreatic adenocarcinoma as acute or chronic pancreatitis has been well documented; however, there has been only one previous report of either functioning or nonfunctioning pancreatic neuroendocrine tumors associated with pancreatitis. At the Medical University of South Carolina in Charleston, from March 1982 through September 1987, we have managed four patients with nonfunctioning pancreatic islet cell tumors or carcinoids, which presented with attacks of pancreatitis. Three of the patients had recurrent bouts of upper abdominal and lower dorsal back pain with elevation of the serum amylase. One patient presented initially with acute upper abdominal pain and elevation of the serum amylase. Each patient had an endoscopic retrograde cholangeography pancreatography (ERCP) pattern involving the pancreatic duct which was characterized by diffuse dilatation proximal to the site of obstruction. One of the four had a tumor blush on splanchnic angiography. Each patient had CT evidence of a mass in the head of the pancreas; however, one of the four was found to have diffuse involvement of the entire gland at operation. Surgical therapy varied: (a) local excision of the ampullary area with re-anastomosis of the pancreatic duct to the duodenum and choledochoduodenostomy; (b) bypass with cholecystoduodenostomy and caudal pancreaticojejunostomy; (e) total pancreatectomy; or (d) bypass with a Roux-en-Y cholecystojejunostomy and gastrojejunostomy. The choice of the procedure was based on the patient's condition and operative findings.
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PMID:Nonfunctioning pancreatic neuroendocrine tumors presenting as pancreatitis: report of four cases. 337 32

This study describes the immunohistologic distribution of carcinoembryonic antigen (CEA) in 30 fetal pancreata, 5 normal adult pancreata, 11 cases of chronic pancreatitis without carcinoma, 16 cases of chronic pancreatitis with carcinoma, and 20 cases of primary pancreatic adenocarcinoma. The position of CEA-cross-reacting antigen, especially of nonspecific cross-reacting antigen (NCA), was also studied in the case of chronic pancreatitis and pancreatic adenocarcinoma. For this purpose, both monospecific antibodies to CEA and NCA, as well as cross-reacting antibodies, were used in an indirect immunoperoxidase technique. CEA reactivity could not be detected, neither during pancreatic development nor in chronic pancreatitis with or without associated adenocarcinoma. In 15 of 20 pancreatic adenocarcinomas, CEA positivity was found both with membranous and cytoplasmic localization. With the use of the cross-reacting antibodies, all cases of chronic pancreatitis and pancreatic adenocarcinomas showed positive staining of both ductal and tubular structures. Antibodies to NCA closely mimicked the results obtained with the cross-reacting antibodies both in pancreatitis and adenocarcinoma. From the authors' results it can be concluded that CEA is not a developmental antigen of the pancreas. Furthermore, NCA cross-activity of anti-CEA antibodies is an important reason of false positive reaction in chronic pancreatitis. Moreover, true CEA positivity in the pancreas appears to be restricted to adenocarcinoma of the exocrine pancreas.
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PMID:Immunohistochemistry of CEA in the human pancreas during development, in the adult, chronic pancreatitis, and pancreatic adenocarcinoma. 338 42

Levels of CA 19-9 in the serum and duodenal juice of nine patients with pancreatic adenocarcinoma (PC), ten patients with chronic calcifying pancreatitis (CCP) and ten healthy volunteers (C) were determined by immunoassay. Duodenal juice was obtained by duodenal intubation during the secretin caerulein test. Elevated CA 19-9 levels in the serum were significantly more frequent in PC than in CCP patients, but two PC patients gave levels only slightly above the cut-off value of 37 U/ml. CA 19-9 levels in duodenal juice were significantly higher in PC than in CCP patient, but there was some overlap between them; no overlapping was seen between PC or CCP group and controls. Two PC patients with duodenal juice CA 19-9 levels overlapping those of CCP were the same who showed only a slight rise in serum CA 19-9 levels. The CA 19-9 to total protein ratio in duodenal juice did not permit better discrimination between PC and CCP. We conclude that CA 19-9 assay in duodenal juice can differentiate healthy subjects from patients with pancreatic diseases, but it cannot improve the differential diagnosis between CCP and PC patients with a slight rise of CA 19-9 levels in serum.
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PMID:Value of CA 19-9 assay in serum and duodenal juice in the differential diagnosis of pancreatic disease. 348 62


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