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)

Chronic hepatitis C is the leading cause of decompensated liver disease requiring liver transplantation and a major cause of hepatocellular carcinoma (HCC). In liver clinic series, about 20% of those chronically infected with hepatitis C virus (HCV) develop cirrhosis over 20 years. From epidemiological data, however, it is clear that certain subgroups of patients are more likely to develop liver-related complications than others. Both host and viral factors have been implicated in individual susceptibility to adverse outcomes. The impact of host factors, such as alcoholism, is now well defined, and viral factors, such as genotype and viral load, appear to be less influential than previously considered. Coinfections with HIV, hepatitis A virus (HAV) and hepatitis B virus (HBV) may influence the rate of fibrotic progression and the subsequent development of complications in patients with chronic hepatitis C. The stage of fibrosis on biopsy and biochemical markers, such as a low serum albumin, can help identify patients who are more likely to develop complications. The role of the immune system in modifying the course of HCV is only now being defined. This editorial explores the role of host and viral factors in the development of liver-related complications in HCV-infected individuals.
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PMID:Predictors of liver-related complications in patients with chronic hepatitis C. 1120 65

So far seven hepatotropic viruses were identified. They are described by letters A,B,C,D,E, G and TTV. The virus of hepatitis F is so far speculative. Virus of hepatitis A and E are transmitted by the orofaecal route and cause only acute hepatitis. The remaining hepatotropic viruses are transmitted by the parenteral route and have a longer incubation period than viruses A and E. The infection with the virus of hepatitis B develops into the chronic stage in about 10% and that of virus C in 50-90%. At least one third of chronic carriers of the virus of hepatitis B or C develop within 10-20 years liver cirrhosis or hepatocellular carcinoma. The objective of therapeutic regimes is eradication of the viruses or at least arrest or retarding of the activity of the disease. Corticoids are not used. The basis of therapeutic regimes is interferon alpha or lamivudine in hepatitis B and interferon alpha with ribavirine in hepatitis C. There is a permanent therapeutic response only in cca 40-50%. Active immunisation is possible against virus of hepatitis A and B. The virus of hepatitis D is a false virus, i.e. a so-called virold, and the cause is a super- or co-infection with the virus of hepatitis B. In this country it is practically not encountered, similarly as the virus of hepatitis E. The assembled findings on virus of hepatitis G are not applied so far very much in practice.
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PMID:[Characteristics of still unknown hepatotropic viruses and a clinical picture of the disease]. 1122 77

Hepatitis C virus (HCV) is one of the leading causes of chronic liver disease. It was first identified in 1989, as being distinct from hepatitis A and hepatitis B. The HCV does not attack the immune system, but rather causes an inflammatory reaction that is localized within the liver, involving the entire organ. About 80% of patients with acute hepatitis C will develop chronic HCV, of which about 20-30% will progress to cirrhosis and its consequences, over 10-20 years. After 20-40 years, a smaller proportion of patients with chronic disease will develop hepatocellular carcinoma. The course and outcome of the disease vary considerably. In some individuals, spontaneous remission occurs over a few years; in others, the disease is more severe, progressing to cirrhosis and end-stage liver disease. Despite biochemical and pathological confirmation of the diagnosis, patients are often asymptomatic for many years. Hepatic failure occurs late in the disease. Factors suggesting a poor prognosis include high serum transaminase levels, active cirrhosis on liver biopsy, and an increased viral load (HCV RNA), as well as associated medical conditions such as alcoholic liver disease, hepatitis B viral (HBV) infection, or human immunodeficiency virus (HIV). Nutrition has been recognized as a prognostic indicator in patients with chronic liver failure. However, standardized approaches for the diagnosis and classification of malnutrition in this population have not been consistently applied before implementing nutrition intervention. Common criteria for the assessment of malnutrition, weight and body mass index (BMI) for example, do not give accurate data in patients with chronic liver disease, complicated by ascites and edema. In addition, the chronic inflammatory reaction of liver failure progresses slowly, so that subtle nutritional deficits are not obvious at early stages of the disease. A review of the literature has been undertaken to identify current nutritional guidelines for patients with hepatitis C as well as chronic hepatitis.
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PMID:Nutritional guidelines for persons infected with the hepatitis C virus: a review of the literature. 1151 51

To this day, viral hepatitis remains a major public health problem in Thailand. Chronic infection with hepatitis B and C viruses are the leading causes of chronic liver diseases, including cirrhosis and hepatocellular carcinoma (HCC). Outbreaks of hepatitis A virus continue to occur in Thailand, even after several years of consistently declining prevalence rates. Also, the reduction in prevalence of hepatitis D virus infection has been observed among intravenous drug users over the past decade. Hepatitis E virus constitutes a rather unusual cause of sporadic acute hepatitis in Thailand. Highly effective vaccines are currently available for prevention of hepatitis A and B, however, as yet no effective vaccine for hepatitis C is imminent. Following rapid progress in the development of molecular techniques, several new hepatitis viruses have been identified. Among these, Hepatitis G, TT and SEN viruses have recently been described but their significance as to causation of human liver disease has yet to be established. This article reviews the current epidemiology, molecular biology, and strategies aimed at prevention and control of hepatitis virus infection in Thailand emphasizing new developments and recent data obtained from our research studies.
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PMID:Problems and prevention of viral hepatitis in Thailand. 1152 32

Hepatitis C was first recognized as a form of viral hepatitis that was distinct from disease caused by hepatitis A virus and hepatitis B virus. The etiologic agent of hepatitis C was proposed to be a small, enveloped virus based on demonstrations of its transmissibility to chimpanzees, electron microscopic studies, and sensitive to chloroform. Successful molecular cloning of viral genome in the late 1980's led to the development of assay for serological diagnosis of HCV and it is currently estimated that at least 170 million people are chronically infected with the hepatitis C virus. HCV evades host antiviral defenses by mechanisms that remain to be identified and establishes a persistent infection in a majority of patients. Persistent infection of HCV is a leading cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. Therefore development of antiviral treatment for HCV is an urgent worldwide health problem. Although much has been learned about HCV genome organization, polyprotein processing, protein function and structure, many key questions remain to be answered. Major efforts of Japanese investigators should now be directed at establishing cellular system and animal models appropriate for dissecting the various steps in HCV replication cycle and strategies for blocking them.
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PMID:[Overview of hepatitis C virus from its discovery to now]. 1157 79

Hepatitis C virus (HCV) is a widespread infectious disease in humans with the negative implication of becoming chronic in most persons. Patients infected with HCV are at risk of liver cirrhosis or hepatocellular carcinoma at later stages. In contrast to hepatitis A and hepatitis B, there is no immunization yet available, neither prophylactic nor therapeutic. Thus, there is an urgent need to develop a safe, protective vaccine against this fatal disease. Developing countries are even more at risk for HCV. There are currently a number of scientific approaches aimed towards solving this problem. Taking both risks and costs of immunization into consideration, a peptide-based vaccine may be a reasonable prophylactic protection. Also, it might be of therapeutic use in already infected patients by increasing a specific CTL response against HCV. In our lab, we are focusing on immunopotentiating reconstituted influenza virosomes (IRIVs) as carriers for immunogenic HLA-A2-restricted core epitopes to induce peptide-specific cytotoxic T lymphocytes (CTLs). The IRIVs are similar to liposomes, but in addition contain influenza-derived hemagglutinin and neuraminidase on their outer surface which makes them fusogenic, thus, permitting antigen delivery to host cells. So far, virosomes have been successfully used for vaccine development and as a result a virosomal vaccine against both influenza virus (Inflexal) BERNA) and hepatitis A virus (HAV) (Epaxal) BERNA) already exist on the market. This paper focuses on the importance of development of a successful vaccine against HCV and, more specifically, we discuss the use, advantages and disadvantages of a peptide-based vaccine. A brief report of our latest findings will be included.
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PMID:Perspectives: towards a peptide-based vaccine against hepatitis C virus. 1174 97

Replication of hepatitis A virus (HAV) in cultured cells is inefficient and difficult to study due to its protracted and generally noncytopathic cycle. To gain a better understanding of the mechanisms involved, we constructed a subgenomic HAV replicon by replacing most of the P1 capsid-coding sequence from an infectious cDNA copy of the cell culture-adapted HM175/18f virus genome with sequence encoding firefly luciferase. Replication of this RNA in transfected Huh-7 cells (derived from a human hepatocellular carcinoma) led to increased expression of luciferase relative to that in cells transfected with similar RNA transcripts containing a lethal premature termination mutation in 3D(pol) (RNA polymerase). However, replication could not be confirmed in either FrhK4 cells or BSC-1 cells, cells that are typically used for propagation of HAV. Replication was substantially slower than that observed with replicons derived from other picornaviruses, as the basal luciferase activity produced by translation of input RNA did not begin to increase until 24 to 48 h after transfection. Replication of the RNA was reversibly inhibited by guanidine. The inclusion of VP4 sequence downstream of the viral internal ribosomal entry site had no effect on the basal level of luciferase or subsequent increases in luciferase related to its amplification. Thus, in this system this sequence does not contribute to viral translation or replication, as suggested previously. Amplification of the replicon RNA was profoundly enhanced by the inclusion of P2 (but not 5' noncoding sequence or P3) segment mutations associated with adaptation of wild-type virus to growth in cell culture. These results provide a simple reporter system for monitoring the translation and replication of HAV RNA and show that critical mutations that enhance the growth of virus in cultured cells do so by promoting replication of viral RNA in the absence of encapsidation, packaging, and cellular export of the viral genome.
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PMID:Replication of subgenomic hepatitis A virus RNAs expressing firefly luciferase is enhanced by mutations associated with adaptation of virus to growth in cultured cells. 1177 93

Common viral agents known to cause inflammation of the liver (hepatitis) are hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV). Some other viral agents that can cause hepatitis are Epstein Barr virus, herpes simplex virus, and cytomegalovirus. Some patients infected with these viral agents progress to develop chronic viral hepatitis. Approximately 45% of chronic hepatitis cases are associated with hepatitis C and approximately 15% are associated with hepatitis B. In addition to being a leading cause of chronic hepatitis, HCV is most frequently associated with liver cirrhosis and hepatocellular carcinoma. Although much has been published about HAV and HBV, health professionals have learned about HCV only in recent years. For this reason, this article will emphasize the epidemiologic challenges and current treatments for hepatitis C; hepatitis A and B will be discussed in brief.
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PMID:Current treatments for hepatitis. 1246 95

Identification of hepatitis viruses A-E has enabled researchers to investigate the epidemiology, pathogenesis, sequelae, and possible means of prevention of these infections. This knowledge also provides a basis for further study of the pathological significance of candidate hepatitis viruses. With improvements in hygiene in many parts of the world, hepatitis A virus infection has decreased markedly. However, this success has the unintended consequence of rendering a large percentage of the younger population susceptible to hepatitis A virus infection. Fortunately, effective active immunization for hepatitis A virus is now available. Hepatitis B remains a common condition, especially in Asia and Africa which have high prevalences of chronic infection. Chronic hepatitis B carriers serve as reservoirs of infection for the community and are at risk of chronic liver disease and hepatocellular carcinoma. A mass immunization program in Taiwan has been remarkably successful in reducing the prevalence of chronic hepatitis B infection. Genotypes of the hepatitis B viruses may be associated with the severity of liver disease and the responses to therapies. Hepatitis C is another important cause of death worldwide. The infection easily becomes refractory and the chronicity contributes to the development of cirrhosis and hepatocellular carcinoma. Although no effective immunization is currently available for hepatitis C, it can be controlled by preventative measures and recently developed interferon-based treatments, especially in combination with ribavirin. The prevalence of hepatitis D has markedly decreased in the last decade and new cases are now rarely encountered. Hepatitis E is endemic in limited areas and travel to these areas appears to be the main risk factor for contracting the infection. Several new candidate hepatitis viruses have been identified, including GB virus-C, TT virus, and SEN virus, but none of these has been shown to cause hepatitis, and they may be passenger viruses.
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PMID:Viral hepatitis: from A to E, and beyond? 1469 91

HIV caregivers face many challenges following initiation of ART. The development of jaundice is uncommon but worrisome. In this case, two distinct and contrasting episodes of jaundice were observed. In the first instance, isolated elevation of the indirect bilirubin without elevation of the alkaline phosphatase was noted. The normal PT and serum aminotransferase levels indicate the absence of intrinsic liver dysfunction. Elevations in the indirect bilirubin may result from either impaired uptake/conjugation or excess production. The latter, usually from acquired hemolysis, may be a complication of an occult NHL. A work-up for this AIDS-related malignancy was not initiated since the caregivers recognized jaundice as a complication of IDV, which inhibits UDP-glucuronyl transferase and produces a Gilbert's-like syndrome. Physicians can expect to encounter this syndrome even more frequently with ATV. Experienced patients given RTV-boosted ATV have experienced elevations of unconjugated hyper-bilirubinemia in up to 45 percent of cases in clinical trials. However, such elevations do not reflect liver dysfunction and symptomatic jaundice requiring dosage reduction that occurred infrequently (7 to 8 percent of study patients). Counseling patients about this syndrome may promote adherence and prevent self-directed interruptions of ATV that compromise efficacy. The second case of jaundice provides a more formidable diagnostic challenge. The triad of LFT abnormalities (mild elevation of aminotransferases, normal PT, and marked cholestatic jaundice) implies an acute process that is mildly toxic to hepatocytes without affecting their synthetic function. The subacute nature of the patient's cholestatic jaundice suggests either intrahepatic infiltrative disease of the liver or extrahepatic obstruction of the biliary tree, most likely due to the patient's relatively modest level of pain and lack of fever. Despite LFT abnormalities occurring 17 months after a switch in his ART, cumulative drug-related toxicities must still be considered. Ritonavir can produce significant elevations in the AST/ALT, especially with pre-existing chronic liver disease as with hepatitis C virus coinfection. The NRTIs can produce hepatic steatosis, a result of mitochondrial toxicity and impaired fatty acid oxidation. However, jaundice and cholestasis are not typical of the latter syndrome. With a negative contrast CT that excludes parenchymal liver disease, investigation of the biliary tree to assess the presence of AIDS-related cholangitis was the next step. Performing a sphincterotomy or stent placement, and obtaining brushings or biopsy specimens to determine the extent of extrahepatic obstruction may help define a pathogen and be life-saving. The negative results of the ERCP justify the final diagnostic step, a liver biopsy to evaluate microscopic infiltrative disease that might not have been detected on contrast abdominal CT. Examples might include granulomatous disease (MAC), fungal etiologies (histoplasmosis), carcinomatosis (lymphoma, hepatoma, cholangiocarcinoma), and microvascular disease (bacillary angiomatosis). The failure to observe granulomatous inflammation in the liver does not exclude MAC infection, as MAC may involve other peri-aortic or mesenteric lymph nodes. This form of IRIS is unlikely given the abdominal CT findings, lack of systemic complaints, and extended persistence of liver aminotransferases. The nonspecific results of the liver biopsy are a common outcome in advanced AIDS patients with elevated alkaline phosphatase levels. Despite not having identified a pathogen, the biopsy establishes chronic liver disease and prompts re-evaluation and change of treatment to NFV. The subsequent normalization of the patient's aminotransferase levels suggests a prior adverse effect of LPV/r in the setting of unexplained, chronic liver disease. Most importantly, this case highlights the importance of HIV caregivers to review ART for safety when noting chronic liver dysfunction. Patients need to be counseled to minimize acetaminophen use, to consume alcohol in moderation, and to avoid behavior with risk for hepatitis C. Finally, all HIV patients should receive appropriate vaccination against hepatitis A and B if serology shows lack of protective immunity.
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PMID:Clinical vignette in antiretroviral therapy: jaundice. 1498 14


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