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)

Alpha1-fetoprotein (AFP) is an alpha1-glycoprotein which can be found in high concentration during fetal development in many mammals, birds, sharks and, also, man. The alpha-fetoproteins of various species have similar physico-chemical properties and often common antigenic determinants. Differences of microheterogeneity depend on a different content of sialin-acid. During human fetal development the serum AFP concentration falls with increasing gestational age. 4-5 weeks after birth AFP can be detected usually in low serum concentrations. Using more sensitive immunulogic techniques e.g. radioimmunoassay there was shown that AFP is present in sera of normal adults in concentrations of 10-20 ng/ml. AFP serum concentrations rise physiologically during pregnancy up to 500-550 ng/ml. During fetal development liver, yolk sac and gastrointestinal tract are the major sites of synthesis. In primary liver cell carcinoma, hepatoblastoma and in teratoblastoma containing yolk sac tissue AFP synthesis rises in tumor cells; the AFP serum concentration increases above 2 microgram/ml. In patients with benign liver diseases e.g. virus hepatitis, a transient rise of AFP serum concentrations was seen. Moreover, increased levels of AFP were found in hereditary diseases e.g. congenital tyrosinemia, ataxia-telangiectasia and in the amniotic fluid in congenital nephrosis of Finnish type. AFP assay in serum is clinically important for the control of course and treatment of primary liver cell carcinoma and teratoblastoma. AFP assay in amniotic fluid is a method for the prenatal detection of neural tube defects and the fetal distress syndrome, especially.
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PMID:[Alpha1-fetoprotein: physiology, pathology and diagnosis especially in childhood (author's transl)]. 7 May 46

The human hepatoblastoma-derived cell line HB611 secretes hepatitis-B surface antigen (HBsAg) and hepatitis-B e antigen (HBeAg) into the medium. Hepatitis-B-virus (HBV) DNA integrated into the cellular genome was found to be hypermethylated. When the cells were treated with 5-azacytidine for 3 days, the level of HBsAg in the medium increased, while the level of HBeAg remained constant. The level of alpha-fetoprotein (AFP) decreased with the 5-azacytidine treatment. Southern blot analysis of DNA digested with HpaII or MspI showed that 5-azacytidine treatment resulted in hypomethylation of the integrated HBV DNA, suggesting that 5-azacytidine increased HBsAg production in the cells through hypomethylation of the HBV genomic DNA.
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PMID:Enhancement of hepatitis-B surface-antigen expression by 5-azacytidine in a hepatitis-B-virus-transfected cell line. 137 94

Hep G2-derived hepatoblastoma cells (2.2.15), which actively produce hepatitis B virus (HBV), were cultured in the presence of 2',3'-dideoxyguanosine (ddG), 2',3'-dideoxyinosine, or 3'-azido-2',3'-dideoxythymidine (AZT). ddG was the most potent agent. It diminished viral replication by up to 95%, as assessed by the amount of episomal HBV DNA, without impairing cellular growth. AZT was the least effective against HBV. Northern blot analysis revealed no apparent difference in the pregenomic viral RNA profile, suggesting that these dideoxynucleosides suppress reverse transcription in the replicative cycle of HBV. The effect of varying the time of drug exposure showed that these agents can suppress HBV replication even when added late in culture. HBV replication in another 2.2.15 cell population of the same lineage was affected by ddG differently, which may enable the investigation of phenotypic or genetic alterations during culture. The present data suggest that some 2',3'-dideoxynucleosides can exert a potent antiviral activity against HBV in vitro, at least under certain circumstances, although the data do not prove that any of these agents have utility in patients with hepatitis.
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PMID:In vitro inhibition of hepatitis B virus replication by 2',3'-dideoxyguanosine, 2',3'-dideoxyinosine, and 3'-azido-2',3'-dideoxythymidine in 2.2.15 (PR) cells. 194 Apr 65

To establish stable cell clones allowing continuous replication of hepatitis delta virus (HDV), Hep G2, a hepatoblastoma cell line containing no hepatitis B virus (HBV) DNA sequences, was transfected with a recombinant plasmid containing a tandem trimer of HDV cDNA (driven by the simian virus 40 late promoter) and a neomycin-resistance gene. After selection with the neomycin analogue G418, at least two of the resistant clones were shown to have intact delta antigen by specific immunoblotting, and the delta antigen was located in the cell nucleus by immunofluorescence. Transfected cloned viral DNAs were found to be integrated into cell chromosomes. Replication of the HDV genome was demonstrated by the presence of not only genomic and antigenomic HDV RNAs but also HDV RNAs in multimeric and circular forms. In addition, a 0.8-kilobase antigenomic RNA containing a poly(A) tail and encoding the delta-antigen open reading frame was documented. Continuous replication and transcription of the HDV genome was thus achieved in these transfected cell lines. The results confirmed that replication of HDV was unassisted by HBV. Stable passage of such cell lines strongly suggests that HDV lacks direct cytopathicity in hepatocytes. These clones should be useful in studying the details of the HDV life cycle and the relationship between HDV and its helper virus, HBV.
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PMID:Continuous expression and replication of the hepatitis delta virus genome in Hep G2 hepatoblastoma cells transfected with cloned viral DNA. 216 71

Hepatoblastoma differs from the adult type of hepatoma in clinical and pathologic features. The ratio of fucosylation of serum alpha-fetoprotein (AFP) was determined in seven patients with hepatoblastoma and in 21 infants and children with otherwise elevated serum AFP, using the improved technique of lentil agglutinin-affinity immunoelectrophoresis. The clinical data for the seven patients with hepatoblastoma were also reviewed. The ratio of fucosylation of AFP was significantly higher in all seven patients with hepatoblastoma, whereas it was minimal in all other cases of benign hepatic conditions such as neonatal hepatitis or biliary atresia, as well as in normal newborns. The ratio of fucosylation in hepatoblastoma, however, definitely decreased with the age of the patient at presentation. This finding suggests a correlation between fucosylation and a rapid rate of tumor growth, because all hepatoblastomas are believed to originate early in fetal life.
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PMID:The ratio of fucosylation of alpha-fetoprotein in hepatoblastoma. 247 Apr 90

A sensitive new technique for lectin-affinity immunoelectrophoresis was applied to samples from 28 infants and children in order to distinguish the origin of elevated alpha-fetoprotein (AFP) in sera. This new immunoelectrophoresis was successfully performed within 24 hours in sera with AFP as small as 910 ng/mL. With combined use of concanavalin A (Con A) and lentil agglutinin (LCH) binding tests, AFPs were classified into three subtypes: benign hepatic condition type (six patients), hepatocellular carcinoma type (nine patients) and yolk sac type (12 patients). AFP was of hepatocellular carcinoma type in all seven patients with hepatoblastoma, and of benign hepatic condition type in six of seven patients with elevated AFP due to conditions such as hepatitis, biliary atresia, and normal newborn. The question as to whether AFP produced in "hepatoblastoma" is of benign hepatic condition type or hepatocellular carcinoma type was first answered by the information in this present report. The differentiation between yolk sac and general hepatic AFPs was completed with the Con A binding test.
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PMID:Three different types of alpha-fetoprotein in the diagnosis of malignant solid tumors: use of a sensitive lectin-affinity immunoelectrophoresis. 247 22

Chemotherapy was used to treat 11 children with hepatoblastoma that was judged to be unresectable because of tumor tissue in both lobes of the liver (eight patients) or because of size of the primary tumor (three patients). Three with bilobar involvement also had metastatic disease. Adriamycin was used in all patients. In nine, it was used in combination with cisplatin. A combination of other agents was used in four of these children. After two to six cycles (mean, 4 cycles), eight primary tumors exhibited marked response with greater than 50% reduction in size. Metastases disappeared in two patients. Complete resection of residual tumor was attempted in eight cases, and was successful in seven. One patient died at the time of surgery during an extended right hepatectomy. Two children had anaplastic hepatoblastomas that did not respond to chemotherapy, and the children died. One responder with giant cell hepatitis died from a severe coagulopathy and bleeding during chemotherapy before surgery. With preoperative chemotherapy, seven of 11 children with "unresectable" hepatoblastoma are now alive without disease 4 to 42 months following successful resection.
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PMID:Preoperative chemotherapy in 'unresectable' hepatoblastoma. 254 11

Parents of 75 children with hepatoblastoma, registered with the Childrens Cancer Study Group, and 75 age-matched controls, who had been identified through random digit dialing were interviewed. No evidence was found to support the primary study hypotheses relating to hepatitis infection, maternal estrogen exposure, alcohol consumption, smoking, or potential sources of nitrosamines. Case mothers were more likely to report occupational exposure to metals (odds ratio [OR] = 8.0, P = 0.01), petroleum products (OR = 3.7, P = 0.03), and paints or pigments (OR = 3.7, P = 0.05). Metal exposures were commonly to welding or soldering fumes, and most occurred daily, before and during the index pregnancy. Petroleum product exposures were predominantly to lubricating oils or protective greases. The only significant paternal exposure was to metals (OR = 3.0, P = 0.01) and the risk with exposure to petroleum products was marginally significant (OR = 1.9, P = 0.06). These findings provide further evidence that occupational exposures may increase the risk of cancer in offspring.
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PMID:A case-control study of risk factors for hepatoblastoma. A report from the Childrens Cancer Study Group. 254 9

The Liver Cancer Study Group of Japan statistically analyzed 4658 cases of primary liver cancer diagnosed from January 1, 1980 to December 31, 1981 in over 400 hospitals throughout the country. The study group comprised 2038 cases of hepatocellular carcinoma, 146 of cholangiocarcinoma, 33 of mixed carcinoma, 30 of hepatoblastoma, six of sarcoma, and 33 others. In 2286 cases (49.1%) a histologic diagnosis was available. The survey, based mostly on the histologically proven cases, describes histologic features of the tumors, grade of anaplasia and growth patterns of the tumor cells, pathology in noncancerous portions of the liver, distant metastases, medical history, frequency of hepatitis in the 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. Sixth report. The Liver Cancer Study Group of Japan. 304 Feb 16

The liver in an infant or child is as liable to the same pathologies afflicting the adult liver but with certain differences in prevalence and causes. Genetic disorders are more likely to present in the paediatric age group where many involve metabolic processes such as galactosemia, phenylketonuria, glycogen storage disease and others. Many of these present in the newborn period. However, neoplasms and hamartomas also present in the newborn period, such as congenital neuroblastoma with an enormously enlarged liver, hepatoblastoma and haemangioma. The latter may present with intractable cardiac failure as a result of considerable shunting of blood. Acquired liver lesions often present in the newborn period or early infancy and this includes hepatitis and biliary atresia. The difficulties in the differentiation of the two lesions will be discussed together with the management of biliary atresia. As the child grows older, Reyes encephalopathy with microvesicular fat in the liver is not uncommon. The pathophysiology of Reyes encephalopathy as seen locally will be described. The choledochal cyst with direct (Caroli's disease) or indirect effect on the liver will be described. Problems of childhood portal hypertension as well as congenital hepatic fibrosis will be described. Hemosiderosis of the liver is chiefly seen in homozygous beta-thalassaemia patients who have been kept alive with repeated blood transfusions. Amoebic and pyogenic hepatitis, fatty liver due to protein malnutrition, biliary ascariasis, etc, which are common in tropical and subtropical countries are rarely seen now in Singapore children.
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PMID:Paediatric liver disorders in Singapore. 346 38


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