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)

CEA is a beta1-glycoprotein (mol. w. approx. 200 000) which in embryonic life is usually found as a cell membrane associated antigen in the gastrointestinal (GI) tract and pancreas. Furthermore, it is secreted into body fluids. In healthy adults a very low serum concentration may be found. The clinical significance of CEA lies in its increased formation in primary and secondary adenocarcinomas of colon and rectum and pancreatic carcinoma, where values of 20 ng/ml and more are observed. However, other gastrointestinal (e.g. oesophagus, stomach, gall-bladder) and extragastrointestinal tumors (e.g. lung, breast, urogenital, prostatic, ovarial carcinomas) as well as non-malignant diseases mainly of the GI tract (e.g. hepatitis, cirrhosis, pancreatitis, colitis, diverticulitis) may provoke less frequent and lower increases in the CEA level. Healthy smokers also tend to show a slight increase in CEA concentration. A certain relationship exists between the CEA level and the size and extent of the tumor so that a decrease following operation may account for complete tumor removal, whereas a persistent or recurring increase in the CEA level is highly suspicious of metastases and/or recurrent tumor. Difficulties in proving and purifying CEA are mainly caused by multiple cross-reactions of CEA with other substances, e.g. blood group substances (A, B, Lea, Leb) and normal or other antigens (NGP, NCA, CEX, CCEA 2, NCA 2, CCA-III, FSA, BCGP). The radioimmunoassay is the most suitable method to determine CEA levels in body fluids. The 3 procedures used differ in the precipitation of the specific immune complex by ammonium sulphate (AS), Z-gel (ZG) or a second antibody (SA). Depending on the method, the upper normal limit in serum or plasma corresponds to approximately 2.5 (AS, ZG) or 12.5 (SA) nanogramme/milliliter. CEA determination in the urine is of interest in patients suffering from bladder carcinoma.
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PMID:[Carcinofetal antigens. II. Carcinoembryonic antigen (CEA). (author's transl)]. 108 Feb 18

A retrospective study of 76 children with hemolytic uremic syndrome (HUS) who were admitted to the Alberta Children's Hospital in Calgary. Alberta between January 1982 and December 1988 was undertaken to explore the gastrointestinal manifestations of the syndrome. The children (mean age of 4.0 +/- 3.1 years) presented primarily during the summer months with a microangiopathic hemolytic anemia (Hgb 94 +/- 26 g/L), thrombocytopenia (platelets 87 +/- 83 X 10(9)/L), and acute renal failure (oligoanuria with a BUN of 26 +/- 15 mmol/L, and a creatinine of 294 +/- 90 mumol/L). Forty-three children required dialysis for 10 +/- 17 days. The duration of hospitalization was 17 +/- 17 days. Four children died of complications attributable to HUS. The following symptoms and gastrointestinal manifestations of HUS were noted: fever (33%), vomiting (80%), abdominal discomfort/tenderness (59%), diarrhea (100%), hemorrhagic colitis (79%), rectal prolapse (13%), colonic stricture (3%), colonic perforation (1%), intussusception (1%), indirect hyperbilirubinemia (49%), and elevated hepatocellular enzymes (58%). Of the last 29 children studied, 19 (66%) had elevated levels of amylase and lipase in the presence of acute renal failure, and six (21%) had a marked elevation of lipase (more than four times normal) with additional supportive evidence of pancreatitis. The additional supportive evidence included persistent elevation of lipase after the resolution of acute renal failure in four children, a marked increment in lipase in association with abdominal pain and an abnormal ultrasound of the pancreas after the initiation of oral feeding in a fifth child, and pancreatic exocrine and endocrine necrosis at autopsy in a sixth child.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gastrointestinal manifestations of hemolytic uremic syndrome: recognition of pancreatitis. 170 51

Nine children with acute typical post-diarrhea hemolytic uremic syndrome (HUS) were treated with intravenous gammaglobulin (IVIG). These children were compared to nine children with HUS who did not receive IVIG. The use of IVIG did not appear to have a beneficial effect on eight of the nine treated children. There were no significant differences found in the duration of hemorrhagic colitis, thrombocytopenia, elevation of the white blood count (WBC), anuria, dialysis, or hospitalization, or the presence of a central nervous system complication or pancreatitis. Although no significant difference was found in the duration of thrombocytopenia, there was a trend towards a longer duration of thrombocytopenia in children treated with IVIG (P = 0.13). One child demonstrated both an increase in her platelet count and a decrease in her WBC count within 24 h of receiving her first dose of IVIG.
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PMID:The use of intravenous gammaglobulin in the treatment of typical hemolytic uremic syndrome. 171 89

The authors studied the data concerning 101 patients who had undergone erroneous laparotomy for suspected acute surgical disease; these accounted for 0.4% of all the patients who were operated on for emergency indications in the same period. Eleven patients died. The operation was undertaken for an erroneous diagnosis of acute appendicitis (32 patients), acute cholecystitis (18), perforating gastric ulcer (15), peritonitis of unknown etiology (14), acute intestinal obstruction (5), strangulated hernia (3), destructive pancreatitis (3), tumor of the large intestine complicated by obstruction (3), abdominal abscess (2), thrombosis of the mesenteric vessels (1), ovarian apoplexy (1), closed abdominal trauma with injury to the viscera (4 patients). Diseases simulating the clinical picture of "acute abdomen" but not requiring an emergency operation were as follows: female reproductive (20 patients), pancreatic (11), renal diseases (11), hepatitis, cirrhosis of the liver (10), cardiovascular (9), pulmonary diseases (5), mesoadenitis (5), Crohn's disease (3), chronic colitis (3), carcinomatosis of the peritoneum (3), herpes zoster (3), and other diseases and injuries (20 patients). The main causes of the diagnostic and tactical errors were objective difficulties in the differential diagnosis due to similar symptomatology, as well as errors in the examination of the patient and haste in making a decision to make an operation.
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PMID:[Erroneous laparotomy in emergency surgery]. 177 33

In the literature an increasingly large body of evidence has revealed disturbances of zinc metabolism and a consecutive zinc deficit in a broad spectrum of chronic diseases. The authors call attention to the therapeutic benefit of zinc substitution mainly in chronic hepatic diseases, pancreatitis and colitis, as well as in diabetes and in several cases of immunodeficiency with various complications. Since suitable preparations are not available on the market 'possibilities concerning zinc substitution are rather limited. There is a real need for completing our therapeutic arsenal with an up-to-date zinc preparate, possibly in combination with a magnesium compound.
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PMID:[Clinical aspects of zinc]. 221 27

The rare instance of a gastrointestinal hemorrhage caused by a lithiasis of the duct of Wirsung is described. The world literature records only 13 other cases. Pancreatic calculi cause hemorrhage by either migrating through the pancreatic parenchyma to perforate the duodenum, ulcerating the vessels of the periductal parenchyma, or rupturing the pancreas. The usual sign of this complication of chronic calcifying pancreatitis, difficult to diagnose, is repeated gastrointestinal hemorrhages and sometimes pain, as in epigastric colitis. The immediate therapy is control of the hemorrhage. With transcatheter occlusive techniques, radical surgery can be postponed until it is more tolerable.
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PMID:Pancreatic lithiasis: a rare cause of gastrointestinal hemorrhage. 265 9

The list of extraintestinal manifestations of inflammatory bowel diseases does not classically include pancreatitis and pancreatic insufficiency. We report here six cases of unexplained pancreatitis associated with inflammatory bowel disease (five patients with Crohn's disease, one with indeterminate colitis). None of the classical etiologies for pancreatitis was found in our patients; moreover none of them had duodenal localization of Crohn's disease or sclerosing cholangitis, two conditions in which pancreatitis associated with inflammatory bowel disease has been previously described. Pancreatitis was painless (or was associated with moderate and atypical abdominal pain) in four of our six cases; no pancreatic calcification was found in any case; in three patients a total or subtotal exocrine pancreatic insufficiency was evidenced. Endoscopic retrograde pancreatography performed in four subjects showed normal or minimally altered pancreatic ducts even in those with severe pancreatic insufficiency. These cases emphasize the existence of a probably nonfortuitous association of inflammatory bowel disease with pancreatitis. Its recognition could make a significant contribution in the management of inflammatory bowel disease.
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PMID:Idiopathic pancreatitis associated with inflammatory bowel disease. 286 72

A spectrum of radiologic findings in cytomegalovirus (CMV) infection of the alimentary canal seen in 14 patients and correlated with pathologic examinations is described. Twelve patients had acquired immunodeficiency syndrome and two had no identified immunosuppression. Autopsies were performed on 12. Diffuse CMV colitis was present in eight patients, enteritis in seven, esophagitis in four, gastritis in two, cholangitis in one, and acute pancreatitis in one. Of 11 patients with enteritis and/or colitis seven had significant lower gastrointestinal bleeding and five died as a result of it. Radiologic findings in the gastrointestinal tract included superficial or deep mucosal ulcerations, perforation or fistula formation, luminal narrowing, rigidity and thickening of the intestinal wall, and inflammatory infiltration of the mesentery. These were seen on barium examinations and computed tomographic (CT) scans. Findings of pancreatitis were seen on CT scans in one patient. In another, a cholangiogram showed abnormal bile ducts caused by CMV cholangitis. The radiologist should be aware of the diverse manifestations of the disease and its likely occurrence in immunosuppressed individuals.
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PMID:Cytomegalovirus infection of the alimentary canal: radiologic findings with pathologic correlation. 303 23

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

A generalized debilitating disease in a horse was believed to be related to hypersensitivity to migrating strongyle larvae. The clinical signs included weight loss, diarrhea, and ulcers on all 4 coronary bands. The mare's condition deteriorated rapidly, so the mare was euthanatized and necropsied. The major histopathologic findings were chronic multifocal eosinophilic pancreatitis, hepatic portal fibrosis, biliary hyperplasia, and chronic ulcerative eosinophilic colitis. This case was similar to previously reported cases of chronic eosinophilic gastroenteritis in horses. Although the etiologic agent was not evident, the distribution and character of the lesions were consistent with a hypersensitivity response to migrating parasitic larvae, most probably Strongylus equinus.
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PMID:Chronic eosinophilic pancreatitis and ulcerative colitis in a horse. 399 43


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