Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 133 children aged between less than a month to 14 years presenting consecutively with hepatitis were prospectively studied over a 6-year period. Most cases were acute and presented at the icteric phase. The peak incidence was in very young infants whose illness had to be differentiated from congenital biliary tract obstruction. The older children exhibited the usual manifestations of lethargy, anorexia and tenderness over the liver area to varying degrees. There were 2 cases of chronic active hepatitis in children aged 13 and 14 years, one a female and the other a male. Their illness was controlled with steroid therapy. The serum biochemistry was characteristic in all cases. Serological tests revealed that about 55% of the children had antibody to hepatitis A virus but only 4% demonstrated HAV-specific IgM, while 15% had hepatitis B surface antigen (HBsAg) and 23% demonstrated antibody to core antigen (HBcAg). While most of the children with acute hepatitis made a full clinical and biochemical recovery, 2 have persistent HBs antigenaemia. There were 3 deaths in children who had fulminant hepatitis. Our results show that exposure to hepatitis A virus appears to be prevalent in Nigerian children and probably occurs quite early in life, and infections with hepatitis B virus and perhaps other hepatotropic viruses are also not uncommon. The surveillance of such children and long-term follow-up are necessary. There is already compelling evidence to indicate that hepatocellular carcinoma, prevalent among young adults in our environment, may be related to hepatitis B antigenaemia persisting over several years. The need for an effective vaccine against hepatitis B virus infection cannot, therefore, be over-emphasized.
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PMID:Patterns of childhood hepatitis in the Nigerian African. 653 16

Hepatitis B viral (HBV) DNA was detected in a hepatoma cell line which produces hepatitis B surface antigen (HBsAg) and in patients with acute hepatitis B. The serum of one patient with acute hepatitis B was found to be infectious when injected i.v. into a chimpanzee up to a dilution of 10(-8). Hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were detectable in the same serum sample by radioimmunoassay up to a dilution of 10(-5) and of 10(-3), respectively. Using DNA: DNA hybridization on nitrocellulose membranes, HBV DNA sequences were detectable up to 10(-8) dilution corresponding to the infectivity level. Based on this finding, it appears that DNA: DNA hybridization is the most sensitive method for detecting hepatitis B virus (HBV) infection. In situations with low virus levels it may be the only indicator of the presence of infectious hepatitis B virus. The use of a tritium-labelled probe makes the method economical and adaptable to hospital laboratories.
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PMID:DNA: DNA hybridization method for the diagnosis of hepatitis B infection. 674 40

THREE FORMS OF VIRAL HEPATITIS CAN BE RECOGNIZED: hepatitis A, hepatitis B, and hepatitis non-A, non-B. Hepatitis A is caused by a picornavirus, is transmitted by the faceal-oral route, does not become chronic, and no chronic virus carriers exist. The virus can be grown in cell cultures, and killed as well as live attenuated virus vaccines are under development. Hepatitis B is caused by an enveloped virus containing a circular, double-stranded form of DNA. The disease is transmitted parenterally through inoculation of blood or blood products containing virus or through close personal contact with a virus-positive person. Hepatitis B becomes chronic in a certain number of cases and can lead to cirrhosis and primary liver cell carcinoma. The blood and certain body secretions of individuals with a persistent or chronic infection may remain infectious for many years. The hepatitis B virus cannot be grown in cell cultures but the entire genome has been sequenced and cloned in bacterial and eukaryotic cells. An inactivated virus vaccine has been prepared from hepatitis B surface antigen present in the plasma of hepatitis B virus carriers and further vaccines are under development. The agents of hepatitis non-A, non-B have not been identified. It is possible to distinguish between a predominantly parenterally transmitted and an orally transmitted form of hepatitis non-A, non-B. The latter is reported to be caused by a picornavirus that does not, however, have any antigenic relationship with hepatitis A virus.
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PMID:Viral hepatitis. 681 33

The PLC/PRF/5 human hepatoma cell line producing hepatitis B surface antigen (HBsAg) was studied to determine whether infectious hepatitis B virus (HBV) was also being produced. 2 chimpanzees with no previous exposure to HBV and no serologic markers of past or active HBV infection were inoculated intravenously with 50 ml of either tissue culture supernatant fluid (357 ng/ml HBsAg) or a suspension of cells disrupted by repeated freeze-thaw cycles (57 ng/ml HBsAg). No evidence of HBV infection was detected in either chimpanzee during 6 months of evaluation. This study suggests that the expression of a portion of the HBV genome, when a portion or all of that genome has been incorporated into a host cell, can result in the production of HBsAg without infectious HBV. If it becomes possible to produce a similar expression of this portion of the genome by itself in nonmalignant cells, HBsAg without HBV may be produced in vitro for use in hepatitis B vaccines.
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PMID:Nondetection of infectious hepatitis B virus in a human hepatoma cell line producing hepatitis B surface antigen. 729

At the 4th National Foundation for Digestive Disease (NFDD) Day in 1991 where public lectures on prevention of hepatitis and early detection of hepatocellular carcinoma were given, screening of sera obtained from 364 registrants for antibodies to Hepatitis A (IgG) was undertaken. The overall sero-prevalence rate was 50%, with 55% for males and 46% for females with antibodies for HAV. None of the subjects below 20 years old had antibodies to HAV. This rose to 16% for those 21-30 years old and 92% for those above 61 years. This study shows that in Singapore, prevalence of anti-HAV antibodies rise with age and is approaching the low endemicity pattern that is seen in developed countries.
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PMID:Seroprevalence of antibodies against hepatitis A (anti-HAV) in Singapore: the NFDD experience. 757 Jan 29

Antibody to hepatitis C virus (Anti-HCV) was examined in sera of 416 patients with hepatocellular carcinoma (HCC). The prevalence of anti-HCV was 11.1% (46/416), among them, the dual infection rate with HCV and HBV was 5.8% (24/416), in contrast to 2.0% (2/100) in blood donors. Moreover, sera of 38 patients with HCC accompanying with acute hepatitis were tested for anti-HAV, HBsAg and anti-HCV. Their positive rates were: hepatitis A 5.3% (2/38), hepatitis B 76.3% (29/38), hepatitis C 10.5% (4/38), and other hepatitis 7.9% (3/38), respectively. These results indicate that HBV infection seems to be more important than HCV infection in the etiology of HCC in our country. The role of HCV in the development of HCC remains to be further investigated.
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PMID:[Prevalence of anti-HCV in sera of patients with hepatocellular carcinoma]. 768 32

Specific and sensitive diagnostic tests are now available to identify type A, B, C, D and E hepatitis. Hepatitis A and E which cause only acute, very rarely fulminant, hepatitis are spread largely by the faecal-oral route, having a brief viraemic phase. Hepatitis B, C and D which are transmitted parenterally and via secretions are often associated with chronic viraemia. Patients with chronic renal disease are at particular risk. Impaired immunity due to disease or drugs increases the propensity to develop a chronic carrier state which may progress to cirrhosis and hepatocellular carcinoma. Limited reports indicate that hepatitis C infection may cause cirrhosis more rapidly than hepatitis B. The emergence of mutants to both hepatitis B and C is a cause for concern. Treatment with interferon is of limited efficacy. Screening of blood products for viral markers and prudent handling of potentially infected materials to avoid contamination of damaged skin or mucous membrane are the best strategies to prevent infection. Hepatitis B vaccination of all newborns, young adolescents and those at risk is the most effective means of reducing the carrier frequency.
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PMID:Viral hepatitis in children with renal disease. 781 14

The major cause of liver diseases world-wide are the infectious hepatitis A-E which are due for different viruses. Most of the cases are clinically asymptomatic and without jaundice with a high rate of cure. The diagnosis and the differentiation of the various clinical syndromes are based mainly on serological markers of the involved antigen-antibody-systems. For insurance purposes the chronic hepatitis B, C and D are of great importance. Where chronic persistent hepatitis has a nearly normal life expectancy, chronic active hepatitis which may develop into cirrhosis and/or hepatocellular carcinoma has an increased mortality.
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PMID:[Viral hepatitis. Insurance medicine observations]. 782 66

Viral causes of acute or chronic hepatitis are the hepatitis A virus [HAV], the hepatitis B virus [HBV], the hepatitis C virus [HCV], the hepatitis delta virus [HDV], and the hepatitis E virus [HEV]. These viruses haven been characterized in great detail and can be detected by specific and sensitive serological or molecular assays. While HAV and HEV cause only acute hepatitis, infection with HBV, HCV or HDV frequently takes a chronic course. With time chronic viral hepatitis can progress to liver cirrhosis and its clinical sequelae as well as to hepatocellular carcinoma [HCC]. Apart from prophylactic measures aimed at the prevention of these viral infections, for those chronically infected natural or recombinant alpha-interferon may be a therapeutic option with the potential to prevent the development of liver cirrhosis and HCC.
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PMID:[Viral hepatitis A to E--diagnosis, clinical aspects and therapy]. 794 Apr 9

Two recombinant interferons-alpha (IFNs-alpha) were assayed for their antiviral effect on hepatitis A virus (HAV) replication in the human hepatoma cell line PLC/PRF/5. IFN alpha-2a and IFN alpha-2b resulted in concentration-dependent inhibition of HAV antigen expression and HAV infectivity at non toxic concentrations. Their selectivity indices, calculated as the ratio of the dose that reduced the number of viable cells to 50% (CD50) to the effective dose that inhibited 50% of viral antigen expression (ED50) were > 1000. Recombinant IFN-alpha emerged, from the present study, as a promising candidate for chemotherapy of hepatitis A.
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PMID:[Antiviral effect of recombinant interferon-alpha on hepatitis A virus replication in human liver cells]. 798 98


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