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 rapid multisite radioimmunoassay for measurement of human alpha-fetoprotein (AFP) that uses two high-affinity monoclonal antibodies directed against distinct and separate determinants on the protein was developed and designated M-RIA. The sensitivity of the "simultaneous-sandwich" M-RIA is approximately equal to 0.5 ng/ml of serum after a 1-hr incubation period. Serum AFP levels have been measured in 1747 individuals with hepatocellular carcinoma (HCC), acute and chronic hepatitis B virus infection, chronic hepatitis B surface antigen (HBsAg)-carrier states, cirrhosis, other malignant tumors, and normal and disease controls to determine the specificity of the assay. Eighty percent (68/85) of patients with HBsAg-positive HCC had AFP levels of greater than 200 ng/ml (range, 260 to greater than 200,000 ng/ml). In contrast, all 450 normal subjects and 477 chronic HBsAg-positive carriers had levels of less than 20 ng/ml. More importantly, in acute and chronic hepatitis B, cirrhosis, and other malignant tumors and in the remaining disease controls, AFP levels were less than 20 ng/ml in 99.3% of the subjects, the great majority (greater than 96%) being less than 5 ng/ml. Indeed only two of 1635 individuals, one with acute hepatitis and the other with carcinoma of the esophagus had AFP levels of greater than 100 ng/ml. These observations are at variance with previous studies with conventional polyvalent RIAs of AFP levels of greater than 20 ng/ml in approximately equal to 40% of acute and chronic hepatitis and in 30% of cirrhosis. This striking specificity of the M-RIA is probably due in part to recognition of epitopes unique to AFP and suggest that such an assay may be used in the detection, early identification, and monitoring of AFP-producing tumors in high-risk populations.
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PMID:Serum alpha-fetoprotein levels in human disease: perspective from a highly specific monoclonal radioimmunoassay. 620 28

Sera from persons infected with hepatitis B virus were fractionated into 19s and 7s moieties by high performance liquid chromatography and then tested for the antibody to hepatitis B core antigen (anti-HBc) of immunoglobulin M (IgM) class by radioimmunoassay. Sera from 17 patients with acute or fulminant hepatitis invariably showed a high activity of 19s IgM anti-HBc (sample/normal ratio 30.6 +/- 13.6). In addition, they all revealed a much lower activity of 7s IgM anti-HBc (4.1 +/- 3.4). In remarkable contrast, 7s IgM anti-HBc activity was higher than 19s IgM anti-HBc activity in the sera from 5 asymptomatic carriers (10.4 +/- 2.4 vs. 1.0 +/- 0.1), 4 patients with chronic persistent hepatitis (11.7 +/- 1.4 vs. 2.1 +/- 1.4), 13 with chronic active hepatitis (13.6 +/- 3.0 vs. 6.0 +/- 5.6), and 10 with liver cirrhosis (8.9 +/- 3.4 vs. 5.4 +/- 2.4). Among these 32 cases of persistent hepatitis B virus infection, there were only 2 (6.3%) in which the 7s IgM anti-HBc was lower than the 19s IgM anti-HBc. The proportion of patients who showed the value of 7s IgM anti-HBc exceeding that of 19s IgM anti-HBc was significantly higher for persistent (30 of 32) than for acute (0 of 17) hepatitis B virus infection (p less than 0.001). On the basis of these results, the determination of IgM anti-HBc in terms of 19s and 7s subpopulations would be useful for differentiating acute from chronic hepatitis B virus infection, especially when the titer of IgM anti-HBc is not high enough to exclude a persistent hepatitis B virus infection.
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PMID:Low molecular weight (7s) immunoglobulin M antibody against hepatitis B core antigen in the serum for differentiating acute from persistent hepatitis B virus infection. 672 59

The hepatitis B virus is a member of an unusual family of noncytopathogenic, hepatotropic DNA viruses--the hepadnaviruses. The complete virus comprises a lipoprotein coat, the hepatitis B surface antigen, enveloping a nucleocapsid core that contains a small, circular DNA molecule. Four open reading frames have been identified on the hepatitis B virus DNA genome. They encode seven proteins, including a hepatitis B virus DNA polymerase molecule with reverse transcriptase activity. The replication of the virus resembles that of retroviruses and occurs predominantly but not exclusively in hepatocytes. Virus variants involving genomic mutations have been identified. Testing for hepatitis B surface antigen permits detection of many but not all acutely infected patients. Diagnosis of acute infection rests on the identification of IgM antibodies to the hepatitis B core antigen. Antibody to hepatitis B surface antigen appears in serum during the convalescent phase of hepatitis B virus infection. It is the neutralizing, protective antibody largely responsible for immunity to reinfection. In persistent infection hepatitis B surface antigen is present, antibody to hepatitis B core antigen is predominantly an IgG antibody, antibody to hepatitis B surface antigen is not detectable or is present in very low titers and viral replication may be active. Persistent infection leads to an asymptomatic carrier state, chronic hepatitis, cirrhosis and hepatocellular carcinoma. No specific treatment exists for acute hepatitis B virus infection. Current data indicate that approximately 50% of adults who have chronic infection achieve virologic, biochemical and histologic remission from treatment with alpha-2b-interferon.
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PMID:Hepatitis B today: clinical and diagnostic overview. 832 12

Liver cirrhosis is one of the main causes of death in Mediterranean countries. A trend towards a global reduction in the mortality rate has been recently reported. In order to clarify better this trend and in an attempt to hypothesize the future pattern of mortality, we analysed data from 254,834 Italian subjects aged 30-79 who died from liver cirrhosis during the period 1972-1986. We used a log-linear Poisson model to examine the effects of age, calendar period of death and birth cohort. Our data confirm that both in the population as a whole and after stratification for three geographical areas (Northern, Central and Southern Italy) the mortality rate is decreasing. The age-effect analysis showed an exponentially rising effect in the Southern population, in accordance with the viral aetiology of cirrhosis, whereas an increased effect followed by a decreased effect was observed in the Northern and Central population, suggesting the alcoholic aetiology for the disease. The results from the birth-cohort effect suggested that in the Northern and Central populations mortality should continue to decrease over the next decade, possibly due to the implementation of better prevention programmes for cirrhotics and to decreased alcohol consumption in Italy. In the Southern population, however, mortality is still rising and this will probably continue for the next decade, as the generations born between 1940 and 1950 who are at high risk of carrying chronic hepatitis B virus infection, reach the age of higher risk of death from liver cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of age, birth cohort and period of death on Italian liver cirrhosis mortality, 1972-1986. 835 64

An estimated 200,000 to 300,000 hepatitis B virus infections occur annually in the United States. With acute infection, symptoms develop in fewer than 5% of infants, 5 to 15% of children between the ages of 1 and 5 years and 33 to 50% of older children and adults. However, the risk of chronic infection after acute infection is inversely proportional to age. The risk of chronic infection is highest for infants who acquire infection during the perinatal period (70 to 90%), lower for children younger than 5 years (20 to 50%) and lowest for older children and adults (5 to 10%). Therefore although only approximately 8% of acute infections in the United States occur in children younger than 10 years, these infections account for 20 to 30% of all chronic infections. Children usually acquire infection from infected mothers at the time of birth or from infected household contacts. The risk of hepatitis B virus transmission between children in day-care centers and schools is very low. Among adults and adolescents sexual activity and injecting drug use are the most common risks for acquisition of infection, yet at least 30% of reported hepatitis B among adults cannot be associated with an identifiable risk factor. Because chronic hepatitis B virus infection is associated with long term consequences of cirrhosis and primary hepatocellular carcinoma, prevention of chronic infection is the most important reason for vaccination against hepatitis B. Routine infant immunization is the most feasible, cost-effective means to control hepatitis B virus transmission.
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PMID:Epidemiology of hepatitis B. 839 67

One of the major antecedent factors preceding the development of hepatocellular carcinoma is chronic hepatitis B virus infection. Also, recent molecular studies have shown that activation of c-oncogenes might be responsible for the malignant transformation in some cases of hepatocellular carcinoma. We used immunohistochemical methods to investigate the correlation of ras and c-myc oncogene expression with the presence of HBsAg in human liver disease. Our material consisted of 23 chronic active hepatitis B needle liver biopsies and surgical specimens from 11 cases of cirrhosis, 23 hepatocellular carcinoma and 10 normal adult livers. Direct, three-step and streptavidin-biotin-complex immunoperoxidase techniques using polyclonal (anti-HBsAg) and monoclonal antibodies (anti-ras p21, anti-myc p62), were performed. Normal liver tissues were negative for all antibodies used. In HBsAg+ chronic active hepatitis B cases enhancement of c-myc, and less frequently of ras oncogene expression, was a common observation. Increased myc p62 and ras p21 expression was a finding not restricted to HBsAg+hepatocytes, which occasionally were negative for oncoprotein immunostaining. All HBsAg-chronic active hepatitis B cases were negative for ras p21 and myc p62 specific staining. Cirrhotic livers showed more frequently enhanced c-myc expression. Most of the immunostained cells were negative for HBsAg. HBsAg- cases of hepatocellular carcinoma more often showed ras p21 than myc p62 overexpression. HBsAg+ hepatocellular carcinomas presented only ras p21-positive immunostaining, which was not detected in HBsAg+ hepatocytes. Our recent data supports the view that continued expression of HBsAg in human liver disease is not necessary for the enhancement of ras and c-myc oncogene expression.
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PMID:Expression of ras and c-myc oncoproteins and hepatitis B surface antigen in human liver disease. 846 26

We studied the relationship between hepatocyte proliferation and hepatitis delta virus (HDV) replication at the single cell level. The proliferating cell nuclear antigen (PCNA) (by immunohistochemistry) and the HDV RNA (by in situ hybridization) were stained in neoplastic and non-neoplastic liver tissues of 19 patients with chronic HDV infection, including four cases of cirrhosis with superimposed hepatocellular carcinoma (HCC). As controls, we assessed the hepatocyte proliferation of liver tissues from 16 patients with chronic hepatitis B and on three normal livers. The hepatocyte PCNA labelling index of HDV-infected tissues was comparable with that seen in chronic hepatitis B-infected livers but was significantly higher than that observed in normal livers. Although cirrhotic tissues had lower hepatocyte proliferating fractions than non-cirrhotic tissues, the difference was not statistically significant. The hepatocyte proliferation rate did not correlate with the level of intrahepatic HDV replication or with the histological activity. In double-labelling experiments, PCNA and HDV RNA staining did not co-localize, with the exception of two of three cirrhotic tissues associated with HCC, where the association between the two markers was statistically significant. This co-localization was not observed, however, in the adjacent tumorous tissues. In patients with chronic HDV infection the hepatocyte proliferation was increased with respect to normal liver tissue, but was comparable with that observed in patients with chronic hepatitis B virus infection and did not correlate with the level of HDV replication or the histological activity. In the cirrhotic tissue of patients with HCC (but not in the tumour counterpart), HDV RNA may occasionally co-localize with the marker of hepatocyte proliferation. Whether this association between viral replication and cell division is related to liver carcinogenesis remains to be established.
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PMID:Relationship between hepatocyte proliferation and hepatitis delta virus replication in neoplastic and non-neoplastic liver tissues. 909 64

While the cytological features of hepatocellular carcinoma on fine needle aspiration cytology are well described, cases of hepatocellular carcinoma with malignant cells in ascitic fluid and their characteristics are not. A patient is described with cirrhosis resulting from chronic hepatitis B virus infection, ascites, and hepatocellular carcinoma diagnosed by effusion cytology. The malignant cells in the effusion were shown to be positive for alpha fetoprotein using immunocytochemistry, and for human albumin using in situ hybridisation, confirming the diagnosis of hepatocellular carcinoma. Further investigations in a terminally ill patient were thus avoided.
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PMID:Effusion cytology of hepatocellular carcinoma with in situ hybridisation for human albumin. 921 33

Hepatitis B viruses can cause chronic liver diseases in both children and adults. In hyperendemic areas, although most related complications occur during adulthood, nearly half of the primary infection in chronic hepatitis B virus carriers occurs in perinatal period through maternal transmission and the other half are from horizontal transmission mainly through intrafamilial spread or injection using unsterilized needles. Children with chronic hepatitis B virus infection are mostly asymptomatic. They are generally active and growing well with very rare exceptions. Even with acute exacerbation of liver function and active inflammation, jaundice or growth failure is uncommon. Mild histologic abnormalities in the liver begins early in life and may progress to severe liver impairment in later life. Severe liver damage, with bridging hepatic necrosis or fibrosis, or cirrhosis of the liver may occur, but is rare during childhood. Universal immunization program of hepatitis B virus has been proved to be effective in reducing hepatitis B carrier rate for more than 10 folds, and the incidence of hepatocellular carcinoma in children has also been reduced significantly.
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PMID:Hepatitis B: long-term outcome and benefits from mass vaccination in children. 965 11

The objective of this study was to investigate the epidemiology, etiology, and long-term outcome of an extended outbreak of acute hepatitis that occurred in an area of Sweden between 1969 and 1972. The outbreak was analyzed retrospectively by retesting stored frozen serum samples for the presence of hepatitis A, B and C markers. The results were compared with the diagnoses that had been determined during the outbreak. Of 180 patients, 29 (16%) had acute hepatitis A, 126 (70%) had acute hepatitis B, and eight (4.4%) had acute hepatitis C. The Australia antigen test used during the outbreak had failed to identify 21 patients with acute hepatitis B virus infection. Genotyping of the hepatitis B virus strains showed that genotype D was the most prevalent, irrespective of the transmission route. An attempt was made to follow up patients with unresolved hepatitis B virus infection, 25-27 years after the acute infection. None of the 100 patients with acute hepatitis B infection who were traced had become chronic carriers. In ten patients with hepatitis C virus infection, the follow-up showed considerable variation in the outcome, ranging from spontaneous resolution to death through liver cirrhosis. Intravenous drug users had a high prevalence of hepatitis C virus infection, with 52% testing positive for hepatitis C antibodies.
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PMID:Long-term outcome of acute hepatitis B and C in an outbreak of hepatitis in 1969-72. 1070 75


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