Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated circulating CEA levels occur in patients with benign gastrointestinal and hepatic disorders. These are usually less than 10 ng/ml. Of clinical importance is the influence of liver disease on the interpretation of CEA. At least 50% of patients with severe benign hepatic disease have elevated CEA levels, most often active alcoholic cirrhosis, and also chronic active and viral hepatitis, and cryptogenic and biliary cirrhosis. Patients with benign extrahepatic biliary obstruction may have increased plasma CEA, the highest in patients with co-existent cholangitis and especially liver abscess. The liver appears to be essential for the metabolism and/or excretion of CEA. Hence, liver work-up is needed to assess any patient with an elevated CEA. A damaged liver may further augment elevated CEA levels due to cancer. The increased circulating CEA observed in some patients with active ulcerative colitis tends to correlate with severity and extent of disease and usually returns to normal with remission. CEA levels also may be mildly elevated in patients with pancreatitis and in adults with colonic polyps. Smoking may contribute to the increased CEA levels seen in patients with alcoholic liver disease and pancreatitis. Therefore, in interpreting mildy elevated circulating CEA levels in patients with GI tract diseases, one must consider benign as well as malignant etiologies.
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PMID:Carcinoembryonic antigen (CEA) levels in benign gastrointestinal disease states. 36 Dec

The authors have used an original method of direct radioimmunoassay of plasma CEA for testing plasma of 1704 patients affetected by various neoplastic and non-neoplastic diseases. The percentage of positive results in blood from patients with adenocarcinoma of the gastroenteric tract was 66.8%. The positivity in other non-neoplastic diseases was 2.7%, except for liver cirrhosis and other chronic hepatopathies, which showed 29.6% of positive reactions. The test should be clinically useful in the differential diagnosis of gastro-enteric carcinoma.
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PMID:A study of plasma CEA by a direct radioimmunoassay method in 1704 cases. 89 44

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

Benign liver diseases are a cause of increased serum levels of CEA. We studied the behavior of CEA in 86 patients with liver cirrhosis who underwent extensive clinical and laboratory evaluation. We found abnormal CEA levels in 38.4% of the patients (28.6% Child's grade A, 40.6% Child's B, and 42.4% Child's C) with a mean of 4.75 ng/ml. Significant differences were found between patients and controls. There was a trend towards higher levels of CEA in more severe cirrhosis according to Child's classification, although this was not significant. We found significant correlations between CEA and some liver tests, including glycocholic acid (r = 0.264., p = 0.012), a marker of severity in liver diseases. The increase of CEA in these patients is probably due to alterations in its metabolic processing caused by hepatocellular dysfunction. Moderate elevations of serum CEA can be expected in cirrhotic patients independently of malignancy.
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PMID:Evaluation of the behavior of carcinoembryonic antigen in cirrhotic patients. 149 Nov 81

In some cases of ascitic fluid due to cirrhosis, benign mesothelial clusters may be observed, accompanied by markedly atypical cells that have been proposed to be abnormal macrophages, mesothelial cells or necrotic cells of hepatic origin. The aim of this study was to determine the origin of these cells with the use of a panel of monoclonal antibodies (MAbs) against cell surface antigens. Furthermore, the lymphocyte subpopulations were analyzed for a possible correlation with the presence of abnormal cells. Markedly atypical cells were found in 4 of 12 cases. They showed no phagocytosis of latex particles and were negative for MAbs My4 (CD14), HLE-1 (CD45), Leu M1 (CD15), CEA 3-13 and HEA-125. They reacted positively with BMA-120 and HLA-1. This staining pattern demonstrated the mesothelial origin of the markedly atypical cells. The profile of the lymphocyte subpopulations in the cases with markedly atypical cells was not different from the other cases. We propose that these cells are abortive cluster formations of mesothelial cells.
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PMID:Immunocytochemical analysis of ascitic fluid due to cirrhosis. A contribution to understanding the origin of markedly atypical cells. 154 8

The present study is based on the assay of four markers (AFP, CEA, TPA, Ca 19-9) using IRMA methods in 36 normal subjects, 44 cirrhosis and 66 HCC patients. Parametric and non parametric tests were used to test differences and correlations. ROC curves and discriminant functions were also elaborated. Normal 95% "cut-off" was determined by the "boostrap" method yielding: CEA 3.4 ng/ml; Ca 19-9 55 U/ml; TPA 58U/l and AFP 5.2 ng/ml. In HCC patients the values of the four markers were, on average, significantly different from those of normal subjects. However, only AFP and TPA exhibited high diagnostic accuracy (90%) for detection of the tumor. Higher than normal mean values for all markers were, also observed in cirrhotic patients. Only AFP yielded effective discrimination between HCC and cirrhosis. The positive prediction for the presence of the tumor on cirrhotic ground was 95% for AFP values higher than 18.5 ng/ml, with a 78% negative predictive value with a 6 ng/ml threshold. Association of AFP with TPA showed only a marginal diagnostic improvement. Results were not improved at all by combining CEA and Ca 19-9 with AFP and/or TPA. In conclusion, AFP is and remains the best marker for HCC and the only one effective in discriminating of HCC from cirrhosis. TPA may be considered a valid alternative if cirrhosis is not present. CEA and Ca19-9 are of no use.
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PMID:AFP, CEA, CA 19-9 and TPA in hepatocellular carcinoma. 170 5

We have evaluated tumor-associated trypsin inhibitor (TATI) as a marker for pancreatic and hepatic cancer. Of the patients studied 52 had pancreatic cancer, 30 primary liver cancer, 32 chronic pancreatitis, 25 biliary tract inflammatory disease, and 28 liver cirrhosis. A considerable number of falsely elevated values were observed in benign biliary diseases and in chronic relapsing pancreatitis. In pancreatic cancer the sensitivity of TATI was 63% while that of CEA was 40% and of CA19-9 77%. TATI is a marker of pancreatic disease but it does not differentiate between pancreatitis and pancreatic cancer. In liver cancer TATI and AFP has similar sensitivity and specificity.
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PMID:Tumor-associated trypsin inhibitor in pancreatic diseases. 172 34

MCA serum levels were determined in 27 healthy subjects, 136 with benign pathology (42 breast) and in 289 patients with cancer (247 active). The last group includes 223 patients with breast cancer (96 without metastases, 89 with metastases and 38 no-evidence of disease). CEA and CA15-3 serum levels were determined in all the patients with breast diseases. The mean levels of MCA were 4.7 + 2.4 U/ml in the control group, considering less than 11 U/ml as normal. MCA values were abnormal in 15.4% of patients with benign pathology, mainly in those with liver cirrhosis (8/20) and lung diseases (4/20). In the majority of these cases, the rise was only moderate, lower than 15 U/ml in 97.5% of patients. In malignant diseases, important increments were found in breast cancer (19.8% Mo, 77.5% M1) and ovarian cancer stages III-IV (44.4%). When we compared MCA serum levels with CA15-3 and CEA in breast pathology, a similar specificity was observed: 92.3%, 92.3% and 100% in cases with benign pathology and 92.1%, 94.7%, and 97.4% in NED patients, respectively. MCA and CA15-3 sensitivity was similar in breast cancer without metastases (19.8%) and lower for CEA (16.7%). In patients with breast cancer without metastases, we found a relation between positivity of these tumor markers and prognostic factors (tumor size, nodal involvement). The disease free interval in patients with locoregional breast cancer was shorter in cases with abnormal presurgical levels of some of the tumor markers, but only the difference from MCA was significant (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:MCA in patients with breast cancer: correlation with CEA and CA15-3. 223 Mar 47

Levels of serum Span-1, a new tumor marker for pancreatic cancer, were assayed in 64 patients with pancreatic cancer, 90 with nonpancreatic cancer, and 254 with nonmalignancies, involving 55 healthy controls. Furthermore, Span-1 was compared with other tumor markers (CA19-9, carcinoembryonic antigen [CEA], and DU-PAN-2). Frequency of elevated Span-1 levels was 81.3% in pancreatic cancer. False-positive elevations of serum Span-1 levels were rather common in liver cirrhosis (53.8%) and chronic hepatitis (26.3%). The sensitivity, specificity, and efficiency of this assay for pancreatic cancer, was 81.3%, 75.6%, and 76.5% against all subjects without pancreatic cancer, respectively. In comparison with other markers, sensitivity of Span-1 tended to be highest with similar specificity to those of CA19-9 and CEA. The Span-1 assay has a high sensitivity and specificity for pancreatic cancer. It is almost equivalent to CA19-9 assay. However, this assay is not specific for chronic liver diseases.
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PMID:Usefulness of a new tumor marker, Span-1, for the diagnosis of pancreatic cancer. 231 Oct 67

Primary liver carcinoma (PLC) may express a certain number of markers. Here we communicate results of an analysis of five such markers (alpha-1-antitrypsin--AAT--, carcino-embryonic antigen --CEA--, alpha-fetoprotein --AFP--, and superficial --HBsAg-- and core --HBcAg-- antigens of hepatitis B virus) by means of PAP techniques in 130 cases of PLC, comparing the neoplastic tissue and the non-tumorous liver. Three variants of PLC are distinguished: hepatocarcinoma (HC) (108 cases); cholangiocarcinoma (CC) (19 cases); and three cases of hepatocholangiocarcinoma (HCC). AAT was positive in 29 HC, 2 HCC, and negative in all 19 CC. CEA appeared positive in 16 HC, 16 CC and only one HCC. AFP was positive in two HC, and negative in all CC and HCC. HBsAg displayed positivity in 15 HC and one HCC, being negative in all 19 CC. HBcAg was positive in 4 HC, and negative in all CC and HCC. HBsAg was also positive in two neoplastic emboli associated with HC. On the non-tumorous liver tissue the immunohistochemical results showed positivity for AAT and CEA, but not for AFP. Therefore the present results confirm that in the geographical area from which these tumors proceed, PLC is closely correlated with HBsAg positivity and with cirrhosis.
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PMID:Immunohistochemical characterization of 130 cases of primary hepatic carcinomas. 244 80


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