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)

A new solid phase enzyme-linked immunosorbent assay (ELISA) was developed for the quantitation of human protein C antigen. Anti-protein C F(ab')2 fragments were adsorbed to polystyrene plates. The binding of serial dilutions of control or test plasma, containing protein C, was detected by incubation with peroxidase-labeled anti-protein. C-IgG followed by the addition of hydrogen peroxyde and 0-phenylenediamine. This ELISA is specific, sensitive (detection limit: 0.02%) and accurate (variation coefficient: 3 to 10%). When results are compared to those obtained by the Laurell technique (electroimmunodiffusion, EID), the correlation coefficient is 0.95 in all tested plasmas. Protein C antigen was measured by ELISA and EID in plasma from 40 controls, 14 patients with congenital protein C deficiency, 15 patients with liver cirrhosis and 40 dicoumarol-treated cases. In normal plasma, protein C ranged from 70 to 126%. In congenital deficiency, protein C was between 35 and 58% in 13 cases and 9% in one of them. In patients with liver cirrhosis and dicoumarol-treated cases, levels of protein C antigen were compared to those of other vitamin K dependent factors, i.e. Factors II and IX measured by EID and Factor X assayed by EID and ELISA. In liver cirrhosis, the amount of protein C was significantly lower than that of Factors II, IX and X. In short-term and long-term dicoumarol-treated patients, the highest correlation (r = 0.72) was observed between protein C and Factor X levels. In the plasma of patients undergoing oral anticoagulant therapy, protein C decreased more rapidly than Factors X or II and migrated in presence of calcium as a double peak, one with a normal mobility and one more anodal corresponding to the non carboxylated form of protein C.
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PMID:A new method for the estimation of protein C by ELISA. 608 75

A case is reported in which non-A, non-B posttransfusion hepatitis was followed serially by chronic persistent hepatitis, chronic active hepatitis, and liver cirrhosis that finally developed into hepatocellular carcinoma. The patient died after a 19-year clinical course. During the last 8 years, repeated attempts to identify serum hepatitis B surface antigen, antibody to hepatitis B surface antigen, and antibody to hepatitis B core antigen were consistently negative. Liver biopsy was performed five times during the clinical course, and at autopsy, liver tissue was obtained from four different nontumor regions. These specimens were investigated by a peroxidase immunoenzyme method which failed to detect hepatitis B surface antigen and hepatitis B core antigen. Non-A, non-B posttransfusion hepatitis may become chronic and sometimes may advance to hepatocellular carcinoma.
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PMID:Hepatocellular carcinoma after non-A, non-B posttransfusion hepatitis. 609 43

Primary hepatocellular carcinoma metastasizing to abdominal lymph nodes and to the left lung was observed in a 16-year-old male patient. No clinically apparent chronic liver disease preceded the carcinoma and no signs of cirrhosis were detectable in the nonneoplastic liver. Hepatitis B surface antigen, hepatitis B e antigen and antibody to hepatitis B core antigen were found to be positive in the serum. By immunohistochemistry (peroxidase-antiperoxidase technique) hepatitis B surface antigen could be demonstrated in the nontumorous liver parenchyma, but not in the primary hepatocellular carcinoma itself. Serum alpha-fetoprotein was only moderately elevated (75 ng/ml), but immunohistochemically primary hepatocellular carcinoma revealed a considerable number of alpha-fetoprotein-containing cells, whereas nontumorous parenchyma did not. Carcinoembryonic antigen could be demonstrated immunohistochemically in some tumor cells of a lymph node metastasis, but not in the primary tumor or in the nontumorous liver parenchyma. We propose that primary hepatocellular carcinoma developed in this case in a symptomless hepatitis B virus carrier without preceding cirrhosis, an we exclude a simultaneous acute hepatitis B.
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PMID:Primary hepatocellular carcinoma with hepatitis B virus infection in a 16-year-old noncirrhotic patient. 618 92

Tumor cell marker antibodies were used to analyze ten cases of hepatocellular carcinoma associated with cirrhosis. Clinically, eight of these cases gave a history of chronic alcoholism and the other two of hepatitis B virus infection. Formalin-fixed, paraffin-embedded sections from these cases were screened with antibodies against alpha fetoprotein (AFP), hepatitis B surface antigen (HBsAg) and carcinoembryonic antigen (CEA) using the peroxidase antiperoxidase and avidin-biotin immunoperoxidase procedures. Three cases were positive for AFP, four for HBsAg, and three for CEA; two cases had both HBsAg and CEA. Alpha fetoprotein was present only in the cytoplasm of tumor cells in three cases. Hepatitis B surface antigen, on the other hand, was present in the cytoplasm of hepatocytes in cirrhotic areas and, in one out of the four cases, was also present in hepatocellular carcinoma cells. Carcinoembryonic antigen was seen in three cases; it was present on the surface and in the cytoplasm of proliferating ducts within the cirrhotic areas and between cell surfaces of individual tumor cells in two cases. The presence of different markers was not related to the microscopic appearance of the tumors. In one case, positivity for AFP was of diagnostic help in a tissue sample obtained by needle biopsy. The avidin-biotin immunoperoxidase procedure was more sensitive than the peroxidase antiperoxidase (PAP technique in the pathological assessment of autopsy specimens. Our findings are in agreement with those of other reports and indicate that AFP and HBsAg are the most commonly found markers in hepatoma associated with cirrhosis, and that CEA staining is variable and hepatoma associated with cirrhosis, and that CEA staining is variable and probably non-contributory.
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PMID:Immunohistochemistry of hepatocellular carcinoma associated with cirrhosis. 621 34

10 cases of congenital deficiency of alpha 1-antitrypsin with liver involvement were identified on clinical grounds; 10 cases of liver cirrhosis were selected by way of the diastase-PAS-reaction. In these 20 cases alpha 1-antitrypsin was demonstrated in paraffin sections by a modification of the indirect peroxidase-antiperoxidase method. In all these cases the immunoreactive inclusions could be demonstrated in the hepatocytes, even when the paraffin sections were several years old. 399 cases of cirrhosis of the liver were investigated in this retrospective study; only 10 of these cases had, as mentioned above, inclusions in the hepatocytes, which were immunoreactive, PAS-positive, and resistant against diastase.
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PMID:[Diagnosis of congenital deficiency of alpha 1-antitrypsin by the immune peroxidase technique (author's transl)]. 625 26

Liver glutathione-peroxidase (L-GSH-Px) and glutathione-reductase (GSSG-Red) activities were measured in supernatants of liver tissues obtained from a total of 36 subjects. Sixteen of these patients had a functionally normal liver (control group), whereas of the remaining 20 patients, 10 were cirrhotic and 10 had a liver disease other than cirrhosis. The mean value of L-GSH-Px of the control group was 33.12 +/- 12.66 U/g protein, a value similar to that found in patients with liver disease. The L-GSH-Px of the control group was positively correlated with the age of the subjects (r = 0.620; p less than 0.02). In contrast, in patients with liver disease an opposite behaviour of the two parameters was noted (r = -0.497; p less than 0.05). L-GSH-Px activity tended to be higher in males than in females, whereas the erythrocyte glutathione-peroxidase (E-GSH-Px) of the same patients was higher in females, albeit not significantly. L-GSH-Px and E-GSH-Px were not correlated either in normal or in liver disease. The mean GSSG-Red of the control group was 40.63 +/- 11.10 U/g protein, which is not different from that of the group of liver patients. GSSG-Red was not correlated with L-GSH-Px or with the age of patients. In two patients with hepatoma, the GSH-Px activity of the cancer tissue was low and the GSSG-Red activity high.
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PMID:Glutathione-peroxidase and glutathione-reductase activities of normal and pathologic human liver: relationship with age. 625 11

In many geographical areas especially in African and South-east-Asian countries hepatitis B virus infection is considered to be a major etiological factor in the development of primary hepatocellular carcinoma. 107 autopsy- and 15 biopsy-specimens were studied by means of immunohistochemistry [peroxidase-antiperoxidase-(PAP-)method] to demonstrate the association between primary hepatocellular carcinoma and hepatitis B surface antigen (HBsAg). HBsAg was found in 8 of 107 tumour specimens (7.4%) and liver cirrhosis in 102 of the 107 autopsy specimens with hepatocellular carcinoma (95%). 10 of the 15 biopsy-specimens showed neoplastic and non-neoplastic liver tissue, and in 2 of these 10 cases HBsAg was found. Liver cirrhosis could be seen in 9 of those 10 specimens. HBsAg was also studied in 90 cases with liver cirrhosis and was found to be positive in 2 of them (2,2%). HBsAg associated with primary hepatocellular carcinoma was only found in non-neoplastic liver cells of cirrhotic livers. Our studies indicate that in our geographical area the association of HBsAg with primary hepatocellular carcinoma is much less conspicuous than in Asian, African and even Southern European communities.
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PMID:[Immunohistochemical studies on the association between hepatitis B surface antigen and primary hepatocellular carcinoma (author's transl)]. 628 95

Alpha 1-antitrypsin has been examined in formalin-fixed, paraffin-embedded liver specimens from Greek patients with cirrhosis (35 cases) and hepatoma (55 cases) by peroxidase-antiperoxidase (PAP) method. Ring-like AAT globules were found in the non-neoplastic cells in 12% of the cases of hepatoma and in 11% of the cases of cirrhosis. Atypical globules were seen in neoplastic cells in 5.4% of the cases of hepatoma and in 17% of the cases of liver cirrhosis. A diffuse fine granular pattern of AAT distribution was present in 31% of the cases of hepatoma in the neoplastic cells and in 27% of those in the non-neoplastic cells. The relatively high incidence of ring-like AAT-globules, and of atypical globules in cases of hepatoma and cirrhosis is not in agreement with the extremely low gene frequency of Z allele in a Greek population of patients with cirrhosis and hepatoma. Thus, there is some doubt whether AAT-globules in the liver represent a histopathologic marker of genetically determined AAT deficiency. A relationship between AAT deposits and the degree of differentiation of hepatoma was noted in this series. AAT-positive cells were found in 55% of moderately differentiated, in 29% of highly differentiated and in 20% of poorly differentiated hepatomas.
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PMID:Demonstration of alpha 1-antitrypsin in paraffin sections of hepatoma and cirrhosis. 629 75

The relationship between glutaraldehyde-treated polymeryzed human serum albumin (pHSA) and HBe antigen (HBeAg)-positive serum was examined by the use of a new enzyme-linked immunosorbent assay (ELISA). The author succeeded in measuring the pHSA binding activity (pHSA-BA) of HB surface antigen (HBsAg) particles in the present ELISA method using horseradish peroxidase-labelled pHSA after fixation of HBsAg on an anti-HBs-coated well of polystyrene microplates. In HBeAg-positive group, the pHSA-BA of sera of 40 asymptomatic carriers and 2 chronic persistent hepatitis (CPH) patients were higher than those of 8 chronic active hepatitis (CAH) (p less than 0.01) and 8 liver cirrhosis sera (p less than 0.05). On the contrary, in the anti-HBe-positive group the pHSA-BA of 17 asymptomatic carriers and 3 CPH sera were lower than those of 8 CAH (p less than 0.005) and 10 liver cirrhosis patient sera (p less than 0.005). In the both-negative group the pHSA-BA of 8 asymptomatic carrier and 3 CPH sera were also lower than that of 8 CAH (p less than 0.05). In acute exacerbation of HBsAg-positive CAH the pHSA-BA elevated one to two months before the peak of S-GPT level, being correlated with the DNA-polymerase activity. Because of its apparent reproducibility, it is concluded that low cost and some advantages may have clinical utility in the same setting as the HBeAg is now used.
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PMID:Detection of serum albumin receptor in hepatitis B virus carriers by enzyme-linked immunosorbent assay. 629 49

An autopsy case of pulmonary hypertension in a 29-year-old Japanese female with macronodular, posthepatic liver cirrhosis and hepatitis-B antigenemia was presented. No recognizable known cardio-pulmonary disease or portal thrombosis was obtained. Hepatitis-B antigen was demonstrated in the cirrhotic hepatocytes by a specific peroxidase antiperoxidase method. Characteristic pulmonary arterial changes including plexiform lesions with varying developmental stages were widely observed throughout the lungs. Complication of these two distinct disease processes seems to be rarely encountered in the literature. Discussion was focused on the possible interrelationship between the liver cirrhosis with hepatitis-B antigenemia and pulmonary hypertension. Proposed were presumptive underlying humoral, particularly immunological, abnormalities common to these diseases rather than mere incidental complications.
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PMID:Pulmonary hypertension associated with liver cirrhosis and hepatitis-B antigenemia. 634 Feb 45


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