Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Raised serum alpha-fetoprotein levels measured by radioimmunoassay were found in 19 out of 24 (79%) patients with primary liver cancer and in 32 out of 311 (10%) patients with other liver diseases. The rise was transient in cases of hepatitis and a transient rise was also seen after alcohol intake ceased in two patients with cirrhosis. alpha-Fetoprotein levels exceeding 500 ng/ml were 30-50 times more common in primary liver cancer than in other liver diseases. A rise in level seems to reflect the extent of liver regeneration in liver diseases other than primary cancer.
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PMID:Serum alpha-fetoprotein: diagnostic significance in liver disease. 440 83

The precise nature of the relationship between cirrhosis and HCC remains to be elucidated. However, it seems likely that no single explanation will cover the various forms the association takes in different parts of the world. In the high HCC incidence regions of sub- Saharan Africa and the Far East, an etiology common to the two disorders, HBV and possibly other hepatitis viruses, seems to account for the majority of cases. The role of aflatoxin in these areas is uncertain because it appears not to cause cirrhosis in man. In populations in which HCC is uncommon, alcoholic cirrhosis is the most frequent association of HCC. There is no convincing evidence to support a shared etiology in this situation because alcohol has not thus far been proved to be directly oncogenic for the liver. Possibly, cirrhosis renders the hepatocytes more susceptible to environmental carcinogenic factors. The same explanation may apply to hemochromatosis. There is at present little evidence for the postulate that HCC is an inevitable consequence of the hyperplasia of cirrhosis.
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PMID:Relationship between hepatocellular carcinoma and cirrhosis. 608 59

The Liver Cancer Study Group of Japan statistically analyzed 2396 cases of primary liver cancer diagnosed from January 1, 1978 to December 31, 1979 in over 500 hospitals throughout the country. They comprised 1047 cases of hepatocellular carcinoma, 93 of cholangiocarcinoma, 9 of mixed carcinoma, 16 of hepatoblastoma, and 33 others. In 1198 cases (50%) a histologic diagnosis was available. The survey and analysis, based mostly on the histologically proven cases, describe the gross anatomic and histologic features of the tumors, grade of anaplasia and growth patterns of the tumor cells, pathology in noncancerous portions of the liver, distant metastases, past medical history, frequency of hepatitis in the past history, frequency of positive HBsAg and anti-HBs, age distribution, subjective symptoms, radiographic features (angiogram, scintiscan, computed tomography), ultrasonography, surgical procedures, extent of hepatic resection, and survival.
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PMID:Primary liver cancer in Japan. The Liver Cancer Study Group of Japan. 608 97

Statistical analyses have been made by the Liver Cancer Study Group of Japan of 4031 cases of primary liver cancers diagnosed at 155 institutes during the period of Jan. 1, 1968-Dec. 31, 1977, based on the questionnaire in the form of individual file. They comprised 2411 cases of hepatocellular carcinoma, 268 of cholangiocellular carcinoma, 58 of the mixed type, 69 of hepatoblastoma, 23 of others, and 1202 cases with only clinical diagnosis. The survey and analyses mostly based on the histology-proven cases included gross anatomical and histological features of tumors, grades of anaplasia and growth patterns of tumor cells, pathology of noncancerous liver portion, frequency of accompanying cirrhosis or fibrosis, distant metastases, past history, frequency of hepatitis in the past history, frequency of positive HBsAg and anti-HBs, familial clustering of positive HBsAg tests, age distribution, subjective symptoms, objective signs, serum alpha-fetoprotein, celiac angiography findings, number of operations performed, kinds of surgical approaches made, extents of hepatic resection, prognosis in terms of survival in relation to various surgical treatments, chemotherapeutic agents used and routes of administration, prognosis as related to the accompanying parenchymal liver disease, and overall survival.
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PMID:Primary liver cancers in Japan. 615 97

Lectin affinities of AFP were analyzed using Con A sepharose chromatography and crossed immuno-affino-electrophoresis. With Con A, AFP was divided into three subfractions, nonbound, loosely-bound and tightly-bound by chromatography, or two subfractions, nonbound and bound by electrophoresis. Con A nonbound subfraction was small in percentage in hepatocellular carcinoma (HCC), neonatal hepatitis, congenital biliary atresia (CBA), liver cirrhosis (LC) and cord sera. In contrast with these, the increase of Con A non-bound AFP was observed in yolk sac tumor (YST) and metastatic liver cancer (Meta). With LCA, AFP was divided into three subfractions: nonbound, loosely bound and tightly bound. Loosely bound fraction was very small in every specimen. AFPs from cord sera and LC showed uniform LCA affinity pattern, but AFPs from HCC were not uniform. Our data suggest that the analyses of lectin affinity of AFP serve as a diagnostic tool in differentiating (1) HCC from YST, (2) HCC from Meta, (3) CBA or neonatal hepatitis from YST and (4) LC from some cases of HCC.
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PMID:[Analysis of lectin-affinity of alpha fetoprotein-diagnostic approach]. 619 65

It has been 30 years since the Third World Health Assembly convened a WHO Expert Committee to consider investigation, control, and prevention of viral hepatitis. During that time, significant advances have been made in understanding the etiology and epidemiology of viral hepatitis. Technological advances of the 1970s enabled widespread rapid diagnosis and the development of vaccines of high efficacy. These advances have allowed the implementation of control programs on a global scale. Because liver cancer (PHC) is among the 10 most common cancers in the world, the link between PHC and viral hepatitis is important. Up to 80% of these cancers are attributable to the hepatitis B virus. Although the development of PHC is not associated with acute hepatitis B virus itself, the chronic HBV carrier state may be classified as a precancerous lesion. Task forces have been convened consider implementation of hepatitis control programs, especially in countries where the infection is hyperendemic. The most important prevention method is active immunization, but vaccination strategies must consider differences in geographical patterns of prevalence. In areas of low endemicity, such as North America, Western Europe, and Australia, immunization of selected high risk groups is suggested. In areas of high endemicity, such as sub-Saharan Africa, southeast Asia, and China, large-scale vaccination of infants is recommended, similar to DPT and polio vaccination programs. Current hepatitis B vaccines are favorable to mass infant immunization because of their high tolerability, excellent immunogenicity, and their ability to induce primary humeral antibody response. However, these vaccines are available in insufficient quantities and the costs are too high for use on a large scale. Newer vaccines, based on recombinant DNA techniques (rather than plasma-derived vaccines) show promise in increasing the quantity and reducing the cost of hepatitis B vaccines.
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PMID:World-wide control of hepatitis B. 624 Apr 73

Hepatitis derived from hepatitis B virus (HBV) infection is endemic throughout the world, but it is particularly prevalent in Asia and Africa. In these areas, demographic studies show a strong coincidence between HBV infection (assayed by HBV antigenic markers) and the incidence of primary liver cancer. On these grounds, a causal link between HBV infection and primary hepatocellular cancer has been proposed. Recently, a human hepatoma cell line (PLC/PRF/5; Alexander cells) has been shown to produce hepatitis B surface antigen (HBsAg). We show here that the Alexander cell line contains at least six (four complete and two partial) hepatitis B viral genomes integrated into high molecular weight host DNA. An analysis using specific probes to fragments of the HBV genome suggests that integration of the virus in most cases occurs at the nicked cohesive end region of the virus. Expression of viral sequences using Northern blots demonstrates the presence of RNA transcripts specific for the surface antigen sequences of HBV DNA and the absence of detectable transcripts corresponding to the hepatitis B core antigen.
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PMID:Integration of hepatitis B virus sequences and their expression in a human hepatoma cell. 625 75

Assay conditions of human liver glutathione S-transferase and its activity in human serum from liver disease patients were investigated. One mmol/l reduced glutathione, and 1 mmol/l-1-chloro-2,4-dinitrobenzene, pH 6.5, were used for the measurement, because of the very low non-enzymatic conjugation. Glutathione S-transferase activity was inhibited by bilirubin, but this inhibition was counteracted by the presence of a low concentration of albumin. The normal human serum glutathione S-transferase activity was 5.2 +/- 2.4 I.U./l (mean +/- S.D.), and was not influenced by any differences of age, sex or leukocyte count. A significant increase in serum enzyme activity was noted in cases of acute hepatitis with GPT exceeding 200 I.U./l, primary hepatoma and metastatic liver cancer. Some of the cases with fulminant hepatitis showed extremely high values. The degree of correlation between serum glutathione S-transferase and GOT or GPT was high in acute hepatitis, with GOT or GPT exceeding 200 I.U./l, in fulminant hepatitis, primary hepatoma and gall stones, while in chronic hepatitis and liver cirrhosis it was low. In cases of acute hepatitis and fulminant hepatitis, the disappearance of serum glutathione S-transferase from the blood was much faster than that of GOT and GPT. Serum glutathione S-transferase measurements will provide new and unique information for the diagnosis of acute liver diseases.
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PMID:Serum glutathione S-transferase activity in liver diseases. 625 85

The aflatoxin B1 content of liver tissue was measured in patients who died from chronic liver disease [hepatocellular carcinoma (HCG) (5), schistosomal liver fibrosis (1), chronic aggressive hepatitis (1)] and compared with fifteen controls who died of motor traffic accidents (10), drowning (1), malnutrition (1), idiopathic cardiomegaly (1) and lung infection (2). Significant levels of aflatoxin B1 were found in hepatocellular carcinoma patients who were also hepatitis B surface antigen (HBsAg) negative. Histology showed HCC arising in macronodular cirrhosis.
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PMID:Aflatoxin B1 in hepatocellular carcinoma. 625 85

Developments in viral hepatitis have been traced from Saul Krugman's distinction of two types, MS1 and MS2 (A and B), and Baruch S. Blumberg's discovery of Australia antigen. Hepatitis A has been grown in tissue culture, the structure of the virus is known, and the acute disease can be diagnosed. Knowledge of the molecular biology of the more complex hepatitis B virion has allowed the development of an effective vaccine and distinction of replicative and nonreplicative stages of infection. Integration, in the hepatocyte, of hepatitis B viral DNA into host DNA is the precursor of liver cancer. The infection of hepatitis B carriers with another infectious agent, delta, has added a new dimension to the problem. Other unidentified causes of hepatitis have been lumped together as non-A, non-B, and these remain to be defined and accurately diagnosed.
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PMID:Landmark perspective: Landmarks in viral hepatitis. 642 56


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