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)

146 patients (62 female, 84 male) with chronic hepatitis B and 80 patients (34 female, 46 male) with chronic hepatitis C were regularly examined in 1 to 2 year intervals with an average follow-up period of 12 years (mean). Each time patients were evaluated by physical examination, routine laboratory data, immunological and serological testing, ultrasonography, and laparoscopy and/or percutaneous liver biopsy. No patient of the study underwent immunosuppressive or antiviral treatment at any time.-The average time data in years are given as the median value (mean). Chronic hepatitis B: Histologic diagnoses and their long-term prognosis: Chronic persistent hepatitis (CPH) on first biopsy: 10% of cases complete recovery after 15 years, 70% progression to chronic active hepatitis (CAH) after 5 years; CAH: 30% advanced remission/complete recovery 8 years after the first diagnosis of CAH, 40% progression to liver cirrhosis after 5 years; liver cirrhosis: 50% advanced remission/recovery 4 years after the first diagnosis of cirrhosis, 5% developed a hepatocellular carcinoma (HCC) 11 years after the first diagnosis of cirrhosis. Natural history: In the 11 years following initial diagnosis of HBV-infection spontaneous recovery was observed in 49% of cases. In 3% of the patients the disease eventually caused death (1 x hemorrhage of oesophageal varices, 3x HCC after 14 to 20 years). Chronic hepatitis C: All patients were anti-HCV- and HCV-RNA-positive.-There was no spontaneous elimination of virus in any patient (maximal follow-up 27 years).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term prognosis of chronic B and C viral hepatitis]. 750 Aug 7

Hepatitis C virus (HCV) has been associated with acute and chronic posttransfusion and with sporadic non-A non-B (NANB) hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). Cloning of the sequence encoding an antigenic component of HCV in 1989 led to the development of tests to detect antibody to HCV in serum. Viral HCV RNA can be detected and estimated with polymerase chain reaction (PCR) and branched-chain DNA (bDNA) signal amplification tests. The entire viral genome has been sequenced. The HCV envelope region varies considerably, and infections with mutant HCV have been described. Approximately 0.5-1.5% of healthy blood donors test positive, and HCV infection can be acquired by blood transfusion or i.v. drug abuse. Vertical and sexual transmission of the virus is rare, and the transmission mode remains obscure in a large group of patients. Acute hepatitis C is mild and often asymptomatic. Chronic hepatitis C has an indolent course but may progress to cirrhosis and HCC. Recombinant alpha interferon (IF) is used to treat chronic HCV disease, but no consensus has been reached on patient selection, dose, and duration of treatment. Approximately 50% of treated patients respond, but 50-80% of responders relapse over time. Liver transplantation in patients with end-stage, HCV-related liver disease is often followed by allograft infection. Short-term survival with reinfection is good, but the long-term consequences remain to be defined.
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PMID:Hepatitis C: an overview. 759 67

Clinically, acute hepatitis C is an asymptomatic disease in up to 90% of cases. Transaminases fluctuate characteristically. Anti-HCV (RIBA-II) and HCV-RNA (PCR) are diagnostic early in the course of the disease. The risk of chronification is high, exceeding 50% of cases, irrespective of disease transmission (parenterally or sporadic). Alpha-interferon is applicated in pilot-studies to reduce the risk of chronification, with varying results. Chronic hepatitis C is an insidious disease. Again, most cases are asymptomatic. Bilirubin is normal. GPT-activity tends to fluctuate during the course. Anti-HCV and HCV-RNA can be detected in serum. About 20% of cases progress to cirrhosis (and HCC) after a long-lasting disease (20 to 30 years after infection). Alpha-Interferon therapy is successful in about 25% of patients.
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PMID:[Hepatitis C: clinical aspects, course and therapy]. 793 55

Chronic hepatitis C infection is associated with the rapid development of cirrhosis and hepatocellular carcinoma. A quantitative assay to determine the level of hepatitis C (HCV) viraemia during treatment would be useful in determining the effect of antiviral agents. Such an assay has been developed with the principle of the method being the co-amplification of the viral genome isolated from the patient with an RNA competitor molecule (CM) using the competitive reverse transcription-polymerase chain reaction (RT-PCR). Known amounts of the CM compete for amplification with HCV RNA from the patient. To quantify each sample, 5 amplification reactions with titrated amounts of CM were performed. The CM can be distinguished from the normal HCV PCR product since it has been genetically altered to be a smaller molecule by the process of restriction digestion, ligation and reamplification. This quantitative method was used to monitor the viral load in 10 patients undergoing antiviral therapy with lymphoblastoid interferon. The level of HCV viraemia in these patients ranged from 10(9) to 10(12) genomes/ml serum. Declines in the level of viraemia were seen in 8 of the 10 patients after therapy. Since patients with low HCV viraemia levels are more likely to respond to interferon therapy in a sustained fashion, this method may also be employed to quantitate the level of viraemia in patients prior to interferon treatment, and may be an indicator of the dose and schedule of treatment. These results show that this quantitative method is useful in the monitoring of HCV viral load in patients.
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PMID:Quantitation of hepatitis C viraemia by a competitive reverse transcription-polymerase chain reaction system. 877 56

Most haemophiliacs treated with non-virally-inactivated clotting factor concentrates have been infected with hepatitis C virus (HCV). We have studied the natural history of chronic HCV infection by following all 138 HCV-positive patients from our centre for periods of up to 28 years. As well as the clinical and biochemical characteristics, we studied 116 liver samples from 63 patients obtained at elective biopsy (n = 103) or autopsy (n = 13). 36 (26%) of the patients were HIV positive, and three were chronic carriers of hepatitis B. Evidence of previous exposure to hepatitis A and B was found in 37.2% and 48.1% respectively. Raised transaminase levels were found in 82.6% of patients. 11 of 15 patients with normal transaminases tested by PCR for HCV RNA were positive, indicating that most patients, even in this group, have chronic hepatitis C infection. Cirrhosis was diagnosed by liver histology in 19 patients, and nine patients developed liver failure. The incidence of cirrhosis rose rapidly 15 years after HCV infection to 15.6 per 1000 person-years. Multivariate analysis showed that HIV status, length of time since HCV infection and age at HCV infection were independently associated with both the development of cirrhosis and liver failure. Two patients developed hepatocellular carcinoma: one of these was exposed only to a single batch of FVIII concentrate 11 years earlier. Chronic hepatitis C is increasingly recognized as a major cause for morbidity and mortality in haemophiliacs, especially those who are HIV positive and who were infected at an older age.
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PMID:The natural history of chronic hepatitis C in haemophiliacs. 907 37

The natural history of hepatitis C is complex and still poorly known. Hepatitis C virus (HCV) replication can be detected very soon after exposure and, at least in the transfusional setting, it persists indefinitely in up to 90% of the cases. While liver damage during the acute phase of hepatitis is almost invariably mild (fulminant cases are exceptions), chronic sequelae of HCV infection may be severe in the long run. Chronic hepatitis C, in fact, is a long-lasting indolent process which leads to cirrhosis in approximately 20% of all infected patients. Hepatocellular carcinoma is a well-recognized complication of old infections, as are a number of extrahepatic manifestations, including type II cryoglobulinaemia. The determinants of the severity of the liver disease are still unclear. However, the risk of cirrhosis seems to be greater for patients with old infections, those infected with the genotype 1b and those with associated conditions. The latter are a heterogeneous and increasing group of 'problem' patients, including patients who are co-infected with the human immunodeficiency virus (HIV1), or who are being treated with cytotoxic or immunomodulating drugs. Data suggest that the natural history of hepatitis C is altered in patients with associated conditions, and this might have an impact on strategies of patient management and treatment.
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PMID:The natural history of hepatitis C. 886 34

Chronic hepatitis C is endemic among chronic haemodialysis patients. There have been a number of reports on hepatocellular carcinoma developing in such patients in Japan. The present study reports on the treatment of 15 patients who showed elevated ALT levels due to biopsy proven chronic hepatitis C with interferon alpha-2a (IFN). The dose schedule was 6 mega units (MU) daily for the first two weeks followed by 3 doses per week for 5.5 months. Side effects were so severe that IFN treatment was discontinued early in one patient, the dosage reduced in 11 and only tolerated in the original schedule by three patients. Excluding one patient who only recently completed the therapy, 13 were able to be evaluated for therapy efficacy by assessment of serum ALT and viral RNA. The overall results showed that IFN was effective in eight of 13 patients, a rate somewhat higher than the reported figures in this country. It is concluded that IFN therapy is indicated in haemodialysis patients with progressive chronic hepatitis C, but the dose administered should be lower and the dose schedule more flexible, perhaps 3 MU three times a week, in order to minimize untoward side effects.
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PMID:Interferon treatment for chronic hepatitis C in haemodialysis patients: suggestions based on a small series. 896 42

Chronic hepatitis C virus (HCV) infection has been clearly established as a major risk factor in the development of hepatocellular carcinoma. In the present study we have attempted to identify the HCV genotypes associated with hepatocellular carcinoma in patients from the USA and Japan. RNAs from tumorous and non-tumorous tissues from 11 HCV seropositive Japanese patients, and plasma from 4 American patients were analysed by reverse transcription-polymerase chain reaction (RT-PCR) methods employing primers specific for the 5'UTR, the NS5 and E2/NS1 regions. Amplified products were cloned and compared by nucleotide sequencing and phylogenetic analysis. The 5'UTR region could be successfully amplified and sequenced from all samples, and phylogenetic analysis of the nucleotide sequences demonstrated with the exception of two of Japanese viruses were closely related to HCV type 1. Type 2 was detected in these two cases. In addition, two of the Japanese patients who were found to have cholangiocarcinoma were also found to be infected with type 1. HCV amplification of the NS5 was successful in 7 of the Japanese and 1 USA sample and clearly demonstrated that genotype 1b was predominant. Amplification of the E2/NS1 regions proved to be extremely difficult and was unsuccessful in all HCC patients despite the fact that these regions could be consistently amplified in samples from patients with both acute and chronic HCV infection. These findings might suggest that with long term persistent HCV infection, there may be marked heterogeneity in both the structural and non-structural regions of the virus, and/or possibly that the viral genomes may be defective.
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PMID:[Analysis of hepatitis C virus (HCV) genotypes in hepatocellular carcinoma]. 899 37

Hepatitis C virus (HCV) is a major cause of chronic hepatitis worldwide, which finally leads to development of hepatocellular carcinoma. Chronic hepatitis C is characterized by several histological features in the liver which discriminate it from other forms of hepatitis: bile duct damage, lymphoid follicles and steatosis (fatty change). Little is known, however, about the role of HCV or its viral proteins in the pathogenesis of hepatitis. Recently, the core protein of HCV has been suggested to have a transcriptional regulatory function, and thereby to be involved in inducing phenotypic changes in hepatocytes. To clarify whether or not the HCV core protein has an effect on pathological phenotypes in the liver, two independent transgenic mouse lines carrying the HCV core gene were established. These mice developed progressive hepatic steatosis, indicating that the HCV core protein plays a direct role in the development of hepatic steatosis, which characterizes hepatitis C. This transgenic mouse system would be a good animal model for the study of pathogenesis in human HCV infection.
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PMID:Hepatitis C virus core protein induces hepatic steatosis in transgenic mice. 922 25

Hepatitis C virus has recently been identified as an important cause of morbidity and mortality worldwide. Acute hepatitis C infection is clinically indistinguishable from other types of viral hepatitis but is much more likely to become chronic. Chronic hepatitis C is a significant cause of cirrhosis and hepatocellular carcinoma. While modes of transmission, diagnosis, and treatment are currently controversial, Dr Brady discusses some approaches for dealing with this emerging problem.
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PMID:Controversies in diagnosis and treatment of hepatitis C. Which patients benefit most from therapy? 938 41


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