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)

In a series of 49 patients transplanted for cirrhosis due to hepatitis D virus (HDV) infection and receiving anti-HBs immunoglobulins, the 2-year actuarial rate of hepatitis B virus (HBV) reinfection was only 13%, a prevalence much lower than the 29% rate in patients transplanted for HBV-DNA-negative cirrhosis and the 96% rate in patients transplanted for HBV-DNA-positive cirrhosis. HBV reinfection after transplantation in patients with cirrhosis due to HDV infection was invariably associated with HDV reinfection. In a few patients, in the absence of HBV reinfection, transient replication of HDV took place and was not associated with liver lesions of hepatitis. In conclusion, patients with cirrhosis due to HDV infection are good candidates for liver transplantation.
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PMID:Liver transplantation in cirrhosis due to hepatitis D virus infection. 850 33

To determine the most prevalent forms of hepatitis in intravenous heroin addicts, 389 addicts consecutively admitted to outpatient treatment clinics throughout California were tested for antibodies to hepatitis A (anti-HAV), B core (anti-HBc), B surface (anti-HBs), C (anti-HCV), D (anti-HDV), and B surface antigen (HBsAg). The majority were also tested for serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, lactic dehydrogenase, total bilirubin, globulins, albumin, and platelet count. The seroprevalence of each marker was: anti-HAV (40.7%); anti-Hbc (73.6%); anti-HBs (46.7%); anti-HCV (93.6%); anti-HDV (9.6%), and HBsAg (3.5%). No single case was positive for IgM, anti-HAV, or for both HBsAg and anti-HDV, indicating the presence of recent hepatitis A or hepatitis D infection. Abnormal liver enzymes, serum proteins, total bilirubin, and platelet count were found to be normal in 5.3 to 44.8% of anti-HCV cases indicating persistent infection. Among anti-HCV cases, elevated total bilirubin or a low platelet count was invariably associated with one or more liver enzyme and protein abnormalities. We conclude that while acute hepatitis may be frequent and caused by various viral types, hepatitis C is the primary form of chronic hepatitis found in intravenous heroin addicts. Almost half of hepatitis C cases demonstrate liver function abnormalities indicating persistent infection that has the potential to be contagious and progress to cirrhosis, liver failure, and hepatocellular carcinoma.
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PMID:Seroprevalence of hepatitis A, B, C, and D markers and liver function abnormalities in intravenous heroin addicts. 855 78

A 28-year-old drug addict who had injected intravenously died of hepatic failure and coma caused by fulminant hepatitis (simultaneously: hepatitis A, persistent hepatitis B, hepatitis C and superinfection by delta hepatitis). Liver histology disclosed cirrhosis with severe necrotizing hepatitis and extensive microvesicular steatosis, compatible with a delta virus infection. Moderate pulmonary fat embolism (grade I-II according to Falzi) was accompanied by fat deposits in alveolar macrophages. It is postulated that protracted fat mobilization from necrotizing hepatocytes may be the cause of pulmonary fat embolism; the extravasation of fat from the vessels into the alveoli results in phagocytosis by alveolar macrophages.
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PMID:[An unusual form of a pulmonary fat embolism in fulminant viral hepatitis]. 865 Jan 46

Eighty-six patients were followed for 6.5 years to study the epidemiological, virological, and histological course of chronic delta hepatitis and the relationship of this disease with HIV and HCV infection. Patients were classified into four groups according to simultaneous HCV and/or HIV infection: group 1, HDV infection (20 cases); group 2, HDV and HCV infection (11 cases); group 3, HDV and HIV infection (12 cases), and group 4, HDV, HCV, and HIV infection (43 cases). All but 14 patients were asymptomatic at presentation. Liver histology showed chronic active hepatitis in 53 cases and cirrhosis in 19 cases. During followup, 52 patients remained asymptomatic, 34 developed hepatic dysfunction, 28 died, and 1 received a liver transplant. Among the 28 patients who died, 4 had HDV infection; 3 HDV and HCV infection; 3 HDV and HIV infection; and 18 HDV, HCV, and HIV infection. Death was due to liver failure in 16 (57%), AIDS in 10 (36%), and was unrelated to liver disease in 2 (8%) cases. There results demonstrate that chronic delta hepatitis is a severe disease, especially among drug users with HIV and HCV infection. The high morbidity and mortality of chronic delta hepatitis justifies the use of antiviral therapy to modify the natural course of the disease.
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PMID:Chronic delta hepatitis: is the prognosis worse when associated with hepatitis C virus and human immunodeficiency virus infections? 873 62

In endemic areas infection with hepatitis B virus is a common cause of chronic liver disease in childhood. High levels of viral replication and mild ALT abnormalities are the rule in children infected perinatally and many of them are likely to maintain viral replication through their youth. Conversely about 90% of children infected later in life clear HBeAg and achieve sustained remission of liver disease before reaching adulthood. The eventual outcome of infection and disease in these patients remains unpredictable as reactivation of liver damage and viral replication may occur after several years of sustained remission. Cirrhosis is a rare and early complication of chronic HBV infection in children, and a risk factor for hepatocellular carcinoma. IFN therapy can accelerate HBV DNA clearance, improving the spontaneous anti-HBe seroconversion rate in Caucasian children by two to three times. Hepatitis delta is the most severe form of chronic viral hepatitis in childhood. Cirrhosis can be diagnosed in up to 26% of patients at presentation, and few cases respond to IFN therapy. Hepatitis C is relatively rare in children. Before the discovery of HCV, blood transfusions were the most common source of infection. Hepatitis C is usually a mild, asymptomatic disease in otherwise healthy children, but has a poor propensity to spontaneous remission over the years. For this reason, and based on the experience in adults, IFN treatment is now being evaluated.
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PMID:Chronic viral hepatitis in childhood. 886 29

Hepatitis B virus (HBV) plays a major role in liver carcinogenesis. HBV-DNA integration into cellular DNA provides some molecular basis for understanding the mechanisms of neoplastic transformation of the liver cell. Persistence of HBV-DNA episomic forms, necro-inflammation in the liver, and cirrhosis appear to be additional promoting factors. We studied the possible association between hepatocellular carcinoma (HCC) and the defective hepatitis D virus (HDV), a virus that requires the helper function of HBV. Patients infected with HDV and HBV develop HCC about 10 years earlier than those infected with HBV alone. Persistence of active HDV disease and low levels of "wild-type" HBV (i.e., secreting the hepatitis B surface antigen [HBsAg]) are associated with progressive liver disease and HCC. Therefore, HBV replication, in spite of being inhibited by HDV, appears to play a major role sustaining HDV pathogenicity. Detection of antibody to the hepatitis C virus (HCV) in many HCC patients raises the important question whether HCV has oncogenic potential. Clinico-epidemiological data show that the most severe forms of liver disease in patients with multifactorial liver damage occur in those infected with HCV. The prevalence of HBV markers in patients with cirrhosis, HCC, and HCV infection is higher than in individuals with comparable age and other diseases. HBV-DNA integration occurring early during HBV infection can persist in those with and without detectable HBsAg in their serum. Therefore, one can speculate that in patients with integrated HBV-DNA and concurrent HCV infection, cirrhosis and HCC may develop more easily than in patients without HBV-DNA integration. HCV hampering the immune system also might play a role in the genesis of HCC. The evidence that multiple hepatitis viruses are more frequently associated with HCC than infections of one virus alone has important practical consequences. It warrants the identification of high risk patients so that they can be monitored frequently for early diagnosis and treatment.
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PMID:Hepatocellular carcinoma and infections with multiple hepatitis viruses. 887 10

Hepatitis C and D are relative newcomers to the study of viral hepatitis. Their transmission is mainly parenteral. The 0.5 to 2.2% prevalence of hepatitis C in the United States does not vary by patient age. Often, hepatitis C is asymptomatic. In older patients, symptomatic infection has a cholesteatic appearance, and progress to chronic hepatitis and cirrhosis is more rapid than in younger adults. Hepatitis D virus is a defective single-stranded RNA that presents as a co-infection or superinfection of hepatitis B. Prevalence varies by geographic region. The rate of progression to chronic disease and cirrhosis is high in superinfection.
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PMID:Viral hepatitis: how to manage type C and D infections. 915 16

The causative agent of hepatitis delta virus (HDV) is the most unusual of all causative agents for all hepatitis viruses. Current knowledge of the molecular biology of HDV strengthens its proposed classification within the satellites, a family of subviral agents, some of which are pathogens of higher plants. Hepatitis delta virus is the only virus in the satellite family known to infect animal species, with hepatitis D having affected more than 10 million people worldwide who are also infected with its helper virus, HBV. Recently, the world map for hepatitis D appears somewhat modified, with decreasing HDV prevalence in certain areas and some new foci of HDV endemicity. Despite changing HDV prevalence, hepatitis. D, particularly the chronic form, is still an important health problem worldwide in terms of morbidity and mortality (mainly due to chronic liver disease, including hepatocellular carcinoma). Molecular studies have greatly advanced our understanding of the life cycle of HDV and of the function of its proteins. The new molecular information is of clinical relevance, with implications for the pathogenesis of liver damage, the diagnosis of HDV infection, for the natural course of the disease and, potentially, for therapy. Sensitive assays for HDV-RNA by polymerase chain reaction and sequencing techniques have clarified the patterns of HDV transmission and have confirmed the existence of unusual clinical forms of the virus and their relationship to replicative levels and genotypes of HDV. Prevention and treatment of hepatitis D are still in their infancy. However, liver transplantation for delta cirrhosis has proven far more successful than in any other viral form of cirrhosis, with few reinfections of the grafted liver, and has given important information on HDV biology and the pathogenesis of liver damage.
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PMID:Review: hepatitis delta. 919 69

Superinfection by hepatitis D virus (HDV) leads to acute hepatitis and causes progression to liver cirrhosis in a significant proportion of hepatitis B surface antigen (HBsAg) carriers. Current regimens (interferon) to treat hepatitis D patients has only transient but no lasting effects. New approaches are, therefore, warranted. Recently, several laboratory studies have discovered interesting properties of HDV that may become targets for antiviral chemicals. Viral replication requires the small hepatitis delta antigen (s-HDAg). The s-HDAg is a nuclear phosphoprotein. There is evidence indicating that phosphorylation is important for HDV replication. A second step of replication requires HDV-RNA self-cleavage and self-ligation. Interestingly, one group of antibiotics, the aminoglycosides, exerts strong suppression effects on HDV ribozyme activities. In the following stage of viral assembly, two post-translational modifications, namely isoprenylation of large HDAg and glycosylation of HBsAg are involved. Agents capable of blocking the two modifications should reduce viral production. These four possible targets are reviewed. For prevention, effective vaccines are not yet available. Two novel approaches are discussed. The first demonstrates the immunogenicity of a nucleic acid vaccine in mice. The second approach assembled an empty HDV particle in yeast. Advances on such laboratory investigations may provide new methods for the control of hepatitis D in the future.
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PMID:Molecular biology of hepatitis D virus: research and potential for application. 940 37

The kinetics of the immunoglobulin (Ig) M type antibody to the hepatitis D virus (IgM anti-HD) were investigated in hepatitis B surface antigen (HBsAg) carriers with chronic hepatitis D treated with interferon (IFN) and in patients with terminal hepatitis delta virus (HDV) cirrhosis who underwent liver transplantation. The IgM antibody disappeared in each of 8 patients who responded to IFN therapy with the persistent normalization of aminotransferases and with the clearance of serum HBsAg and HDV-RNA. The IgM reactivity did not decline in the 45 treated patients who did not respond to the cytokine or who experienced a relapse after responding while on therapy. The antibody rapidly disappeared from serum post-transplantation in each of 10 examined patients with HDV who underwent transplantation. In 5 patients who underwent transplantation and who became reinfected with HDV, the antibody remained undetectable during the early reinfection phase, as marked by HDV replication and by the absence of liver damage; however, it rapidly raised to pre-transplantation levels with the recurrence of hepatitis D (HD) in the liver graft. Monomeric 7S IgM anti-HD predominated over pentameric 19S antibody in each of the two patients examined for IgM anti-HD molecular species. The IgM antibody to HDV raises in response to HDV-induced damage and represents a valid surrogate marker of liver damage which is immunopathologically related to HDV infection. Besides providing diagnostic information, it provides the best predictor of impending resolution of chronic HDV disease, whether spontaneous or IFN-induced.
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PMID:Serum immunoglobulin M antibody to hepatitis D as a surrogate marker of hepatitis D in interferon-treated patients and in patients who underwent liver transplantation. 950 Jul 21


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