Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 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

Chronic hepatitis C is common in Saudi Arabia and most often presents in an advanced stage. To assess the response of patients to interferon, a randomized placebo-controlled double-blind study was undertaken. All but 1 patient had cirrhosis or fibrosis before interferon. After a 24-week observation period patients received alpha 2a interferon, 3 mega units sc tiw or placebo for 24 weeks, then the opposite treatment for another 24 weeks followed by 24 weeks of observation. Liver biopsies were performed before and after each of the treatment phases. Twenty-two out of 24 patients completed the study. The mean alanine aminotransferase (ALT) levels fell from 150.7 +/- 118.7 units/l to 91.0 +/- 42.6 units/l after 6 months interferon treatment (P = 0.03) but only 3 patients (14%) had complete normalization of mean ALT levels and 4 (18%) had > 50% reduction. The mean hepatitis activity index fell from 12.2 +/- 2.6 immediately before to 11.6 +/- 2.5 just after interferon (P = 0.4). After interferon there was an insignificant raise in 6-month mean ALT. Hepatitis C virus-RNA was positive in all 17 patients tested and remained so after treatment. Side-effects were mild and well tolerated. Alpha interferon 3 mega units tiw for 24 weeks is not an effective treatment of histologically advanced chronic hepatitis C.
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PMID:Histologically advanced chronic hepatitis C treated with recombinant alpha-interferon: a randomized placebo-controlled double-blind cross-over study. 751 10

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

Chronic hepatitis C is a major health issue, affecting up to 1.4% of the US population. A high proportion of hepatitis C virus (HCV) infections are chronic. Significant liver disease (chronic hepatitis that is moderate to severe, fibrosis, or cirrhosis) develops in up to 50% of patients chronically infected with HCV. Progression of the disease is unpredictable but is typically slow and evolves over decades. Viral genotype, level of viremia, severity of liver disease, and hepatic iron content influence the response of chronic hepatitis C to therapy. Standard therapy is with interferon alfa-2b (Intron A), 3 million U given subcutaneously three times a week for 6 months. Forty percent of patients have an initial response to interferon therapy, but only half (or fewer) of these patients maintain a long-term sustained response. New treatment strategies are currently being evaluated; however, none, as yet, has emerged as a significant improvement over standard interferon therapy.
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PMID:Hepatitis C. Recent advances in understanding and management. 760 49

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 is one of the major causes of liver cirrhosis and seems to play a role in the pathogenesis of primary liver cancer. So far, no effective therapy--with the exception of some antiviral agents--was available for this disease. Interferon-alpha (IFN-alpha) therapy results in about half of patients in a normalisation of liver transaminases within 4 weeks. Placebo-controlled studies confirm that in about 40% of patients IFN therapy achieves complete remissions. Frequently termination of IFN therapy is followed by a relapse. Therefore higher IFN doses and longer and/or repeated therapy cycles are currently investigated in order to improve treatment results. Furthermore, IFN-alpha is combined with other therapeutic principles. The possible usefulness of IFN-alpha for treatment of acute hepatitis C is under investigation.
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PMID:[Interferon therapy in hepatitis C]. 827 73

Autoimmune hepatitis is an inflammatory disease of the liver of unknown etiology that progresses toward cirrhosis and liver failure and is generally responsive to immunosuppressive treatment. The presence of anti-smooth muscle antibodies with anti-actin specificity and of anti-liver kidney microsomal antibodies defines two distinct subgroups of the disease. An autoantibody against liver cytosolic antigens has recently been described. Management of autoimmune hepatitis relies on immunosuppressive therapy with steroids alone or combined with azathioprine. When the disease is poorly controlled, despite good patient compliance to therapy, cyclosporin should be recommended. Progressive liver disease in chronic hepatitis B in adults has been associated with the presence of precore mutants of hepatitis B virus. In children, the presence of precore mutants seems not to affect the rate of seroconversion to anti-hepatitis B e antigen. However, high viremic levels of precore mutants are associated with persistent viral replication and liver disease. Interferon alfa seems to be less effective in children than in adults in the treatment of chronic hepatitis B; however, it hastens the seroconversion rate to anti-hepatitis B e antigen, accelerating the spontaneous clearance of the virus in children with already low levels of viral replication. Blood transfusions, especially those received in the perinatal period, are the single most important source of infection with hepatitis C in childhood. HIV coinfection is a major risk factor for vertical transmission of hepatitis C virus in pregnant women. Chronic hepatitis C in children is usually an asymptomatic disease associated with mild to moderate fluctuation of aminotransferase activities and histologic features of mildly active hepatitis. Severe active hepatitis and cirrhosis are infrequent during childhood and adolescence. Interferon may have a place in the treatment of chronic hepatitis C in children.
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PMID:Chronic hepatitis in children. 854 54

Chronic hepatitis C virus infection can be associated with mixed cryoglobulinemia and systemic vasculitis. The pathogenesis remains poorly understood. 55 consecutive patients with chronic HCI infection (anti-HCV- and serum HCV RNA-positive) were studies prospectively. Cryoglobulinemia was detected in 28 patients (51%) with a mean cryocrit level of 2.2%. Clinical symptoms of vasculitis were encountered in six patients. Compared to those HCV-infected patients without cryoglobulinemia the following distinctive features were observed in the presence of cryoglobulinemia: increased age (p<0.02), female preponderance (p<0.002), longer-lasting HCV infection (mean of 10.7 vs. 4.7 yrs), higher prevalence of cirrhosis (42.8 vs. 0%), increased serum concentration of IgM and increased rheumatoid factor activity, decreased concentration of serum C4 (each p<0.05). The response to interferon treatment was similar in patients with and without cryoglobulinemia. When cryoprecipitates were analyzed by immunofixation, type II cryoglobulinemia was present in 1/3 and type III in 2/3 of patients. By SDS-PAGE four different proteins were demonstrable in cryoprecipitates each identified by immunoblotting as IgG and IgM heavy or light chains respectively. Cryoprecipitate IgGs were shown to react with HCV structural as well a non-structural proteins in a recombinant immunoblotting assay (RIBA). In contrast, cryoprecipitate IgMs reacted only to the HCV core protein c22-3. HCV RNA was detected in cryoprecipitates without a significant enrichment when compared to the corresponding serum or supernatant HCV RNA content. Given the monoclonality of some cryoprecipitate IgM and their reactivity to HCV core, a cross-reactivity to IgG was postulated. In fact, when performing a computer-assisted search for sequence homology, a motif within the core protein (EGLGWAGWL, conserved in HCV genotypes) was identified homologous to a sequence of IgG heavy chains. Thus, temperature-dependent affinity changes of IgM anti-HCV core (nonapeptide) and ensuing complex formation with IgG via binding to the homologous IgG sequence could be a mechanism of cryoprecipitate formation.
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PMID:Cryoglobulinemia in chronic hepatitis C virus infection: prevalence, clinical manifestations, response to interferon treatment and analysis of cryoprecipitates. 860 Jun 60

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


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