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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Asia, Africa, and other tropical areas, primary hepatic carcinoma (PHC) is associated with liver cirrhosis of the postnecrotic (macronodular) type. Chronic viral hepatitis is likely to be the cause of this cirrhosis in many patients from regions where chronic infection with the hepatitis B virus (HBV) is common. More than 95% of patients with hepatoma (in Mali and Senegal) have evidence of infection with HBV, a much higher frequency than in controls. Thirty-nine of 62 patients with PHC had hepatitis B surface antigen (HBsAg) (controls, 8 of 98) and 56 of 63 (controls, 26 of 100) had antibody against hepatitis B core antigen (anti-HBc). In earlier studies, we demonstrated a maternal effect of HBsAg. If the mother has the antigen and the father does not, the children are much more likely to also have HBsAg than if the father has the antigen and the mother does not (93/161 = 57.8% when mother is positive vs. 28/135 = 20.7% when father is positive; P = 0.6 X 10(-10)). Studies in Greece and in the Solomon Islands show that presence of HBsAg in parents affects the sex ratio of the offspring of the mating. This implies that the presence of the agent in a parent can affect the fetus early in life. Parental studies in the west African hepatoma patients showed that there is a very high frequency of HBsAg in mothers (71.6%), while the frequency in fathers (18.5%) is significantly less. This suggests that the development of hepatoma in offspring is related to infection in parents. Several years ago, we described a vaccine which may be useful in preventing infection with hepatitis B. Strategies are discussed which might be effective in preventing the development of carriers with, it is hoped, a consequent decrease in the frequency of HBV carriers, chronic hepatitis, and primary hepatic carcinoma. The strategy would employ methods for decreasing the frequency of the agent in the environment by the application of public health methods including the vaccination of appropriate newborns and other members of the population.
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PMID:The relation of infection with the hepatitis B agent to primary hepatic carcinoma. 17 34

In Asia, Africa and other tropical areas primary hepatic carcinoma (PHC) is associated with liver cirrhosis of the post-necrotic (macronodular) type. Chronic viral hepatitis is likely to be the cause of this cirrhosis in many patients from regions where chronic infection with the hepatitis B virus (HBV) is common. More than 95% of patients with hepatoma (in Mali and Senegal) have evidence of infection with HBV, a much higher frequency than in controls. Thirty-nine of 62 PHC patients had hepatitis B surface antigen (HBSAg) (controls: 8 of 98) and 56 of 63 (controls: 26 of 100) had antibody against hepatitis B core antigen (anti-HBC). In earlier studies we demonstrated a maternal effect of HBSAg. If the mother has the antigen and the father does not, the children are much more likely to also have HBSAg than if the father has the antigen and the mother does not (93/161 = 57.8% when mother is positive vs. 28/135 = 20.7% when father is positive; p = 0.6 X 10(-10)). Studies in Greece and in the Solomon Islands show that presence of HBSAg in parents affects the sex ratio of the offspring of the mating. This implies that the presence of the agent in a parent can affect the fetus early in life. Parental studies in the African hepatoma patients showed that there is a very high frequency of HBSAg in mothers (71.6%) while the frequency in fathers (18.5%) is significantly less. This suggests that the development of hepatoma in offspring is related to infection in parents. We described a vaccine several years ago which may be useful in preventing infection with hepatitis B. Strategies are discussed which might be effective in preventing the development of carriers with, it is hoped, a consequent decrease in the frequency of HBV carriers, chronic hepatitis and primary hepatic carcinoma. The strategy would employ methods for decreasing the frequency of the agent in the environment by the application of public health methods including the vaccination of appropriate newborns and other members of the population.
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PMID:[The relation of infection with the hepatitis B-agent to primary hepatic carcinoma (author's transl)]. 19 Apr 99

Dramatic advances in the understanding of the pathogenesis, pathophysiology, prevention, and treatment of the major viral diseases of the liver have been made. Hepatitis B and A viruses have been identified, with specific diagnostic serologic assays commercially available for these infections. The diagnosis of non-A, non-B hepatitis is currently made by exclusion. Morphological alterations in viral hepatitis are similar, regardless of the etiologic agent. Chronic viral hepatitis may be associated with hepatitis B and non-A, non-B, but not with hepatitis A. Persistent infection with hepatitis B virus is associated with an increased incidence of primary hepatocellular carcinoma. Viruses similar to the hepatitis B virus cause the same spectrum of liver disease in certain animals. With the development of a vaccine against hepatitis B virus infection, it may be possible to prevent a large proportion of worldwide chronic liver disease, as well as primary hepatocellular carcinoma.
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PMID:The biology of viral hepatitis. 628 89

Chronic viral hepatitis is prevalent worldwide in the pediatric population and can be associated with significant morbidity and mortality. Acquisition of disease in early childhood may predispose children to long-term complications, including cirrhosis and HCC. Efforts should be made to recognize, control, and prevent further spread of these infections, especially in areas where hepatitis is endemic. Alpha interferon therapy hastens disease remission in a proportion of patients with chronic hepatitis B. Further studies are needed to define the role of interferon in chronic HDV and HCV infection in children.
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PMID:Management of chronic viral hepatitis in children. 763 78

Chronic viral hepatitis caused by hepatitis B, C or D may lead to cirrhosis, hepatocellular failure and hepatocellular carcinoma. The morbidity of these diseases has necessitated a prolonged search for effective therapy. Interferon-alpha has been studied widely, and remains the mainstay of treatment. Therapy for hepatitis B has now become possible with the demonstration that alpha-interferons inhibit hepatitis B virus (HBV) replication and that prolonged therapy can lead to a remission in disease. A number of other cytokines, including thymosin, are being evaluated. Currently used nucleoside analogues and anti-retroviral therapies used in human immunodeficiency virus infection have not proven useful in chronic hepatitis B. There are a number of new experimental nucleoside analogues with activity against HBV. Unfortunately, fialuridine has been associated with severe mitochondrial damage and hepatotoxicity. Other stereoisomers may be more active and less toxic, but the potential danger of these drugs indicates that large scale clinical trials should proceed cautiously. Experimental test systems for the preliminary investigation of antiviral compounds in hepatitis B and C will be required. Antisense oligodeoxyribonucleotides may inhibit the expression of the HBV genes. The natural history of hepatitis C is uncertain. Therapeutic trials of interferon-alpha indicated that a proportion of patients may respond to treatment with this agent. There is most information about 3 mU t.i.w. administered for 6 months. It is not yet clear whether this dose is optimal. Multivariate analysis of several pretreatment parameters indicate that patients without cirrhosis are more responsive to interferon. The influence of genotypes of hepatitis C is the subject of considerable interest at present. Patients with diverse circulating quasispecies may be less responsive to therapy than those with a single major species. Improved responses have been observed in patients with lower levels of circulating hepatitis C virus RNA.
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PMID:Treatment and prevention of chronic viral hepatitis. 771 82

Chronic viral hepatitis, frequently an asymptomatic disease, can persist for decades. Despite the lack of symptoms, prolonged infection can lead to the complications of cirrhosis, liver failure and hepatocellular carcinoma. The goal of therapy is to reduce the risk of developing these complications and to eradicate the infectious pool. Patients with ongoing viral replication appear to be at greatest risk for developing complications. These patients have been targeted for treatment. Numerous randomized studies of interferon treatment of chronic hepatitis B and C have been published in the last 8 years. The experience from these studies and more recent developments will be reviewed.
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PMID:The role of interferon in the treatment of viral hepatitis. 780 78

Chronic viral hepatitis is caused mainly by chronic infection with hepatitis viruses B (HBV), C (HCV), or delta (HDV). Persons chronically infected with one or more of these viruses may develop chronic progressive hepatitis, cirrhosis, and liver failure. In addition, chronic HBV and HCV infections are major causal risk factors for hepatocellular carcinoma. Alcohol consumption accelerates the development of chronic liver disease among HCV-infected individuals and may have similar effects on persons chronically infected with HBV alone or HBV and HDV, but the reported studies are inconsistent.
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PMID:The epidemiology of hepatitis viruses B, C, and D. 879 71

An estimated 400 million people are chronically infected with the hepatitis B virus (HBV). Chronic viral hepatitis infection incurs serious sequelae such as liver cirrhosis and hepatocellular carcinoma. Prevention and treatment, thus, represent an important target for public health. Preventive vaccines using HBsAg alone or combined with other antigens allow for the generation of neutralizing antibodies which effectively prevent infection in immunocompetent individuals. Cell-mediated immunological mechanisms are thought to be crucial in determining viral persistence or viral elimination. Therapeutic approaches aiming to shift cellular immunity towards viral elimination have been on the research agenda for many years. This paper summarizes pre-clinical and clinical results obtained with the use of immunogenic peptides formulated as vaccines to selectively boost cellular immune responses. Such vaccines are capable of generating cellular immune responses in animal models as well as in humans and represent an important step towards the development of a therapeutic vaccine against chronic hepatitis.
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PMID:Peptide vaccines against hepatitis B virus: from animal model to human studies. 1174 95

In spite of great efforts in the research relating to human hepatocarcinogenesis, its mechanism on the molecular level is yet to be determined. Chronic viral hepatitis may increase the chances of genetic events in hepatocytes of the host, by increasing the number of target cells or through proliferation of initiated hepatocytes, toward the eventual development of hepatocellular carcinoma. These conditions are referred to comprehensively as the 'hypercarcinogenic state'. Our goal, then, should be directed to the reversion of the 'hypercarcinogenic state' to the 'normo- or hypocarcinogenic state' so as to hopefully prevent or at least postpone the development of hepatocellular carcinoma.
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PMID:Molecular aspects of human hepatocarcinogenesis mediated by inflammation: from hypercarcinogenic state to normo- or hypocarcinogenic state. 1186 83

Chronic viral hepatitis is a common disease. More than 500 million people have chronic viral hepatitis worldwide. These diseases are due to chronic infection with hepatitis B virus, hepatitis D virus or hepatitis C virus. Chronic viral hepatitis is responsible for severe complications: cirrhosis and hepatocellular carcinoma, which are responsible for major morbidity and mortality worldwide. The prognosis of chronic viral hepatitis depends on the rate of progression of fibrosis, which varies widely from one patient to another. Some factors, such as gender, age, alcohol consumption and immune status, influence the progression of fibrosis. In recent years, treatment of chronic viral hepatitis has markedly improved-especially in chronic hepatitis C, with more than 50% of patients having a sustained response with the combination of pegylated interferon and ribavirin. Also, in chronic hepatitis B, new drugs are available, or being evaluated, and combination therapy could dramatically change future therapeutic strategies.
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PMID:Transition of care between paediatric and adult gastroenterology. Chronic viral hepatitis. 1267 18


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