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 order to understand the impact of viral hepatitis on anti-oxidant defence system of the body, blood levels of superoxide dismutase (SOD), an enzymatic anti-oxidant, and total anti-oxidant (TAO) were evaluated and co-related to etiological viral hepatitis in various forms of liver diseases. A total number of 110 patients including 50 patients with acute viral hepatitis (AVH), 30 patients with chronic active hepatitis (CAH) and 30 patients with cirrhosis of liver were analysed for different hepatitis viral markers and the anti-oxidant levels in their blood. For comparison, blood from 100 healthy persons were also simultaneously tested for anti-oxidant levels. Analysis of results indicated that none of the patients belonging to these three liver diseases had hepatitis A viral (HAV) and hepatitis D viral (HDV) infections. AVH group had mainly hepatitis B viral (HBV), hepatitis C viral (HCV) and hepatitis E viral (HEV) infections, CAH group had B and C infections and cirrhosis group had B, C and E infections. A sizeable number of patients in each group had no markers and were labelled as non-BCE group. On co-relating anti-oxidant levels to viral etiology in these patients, it was observed that in comparison to healthy control group, SOD level was significantly reduced in all the patients irrespective of the viral etiology (P<0.05-0.001). The impact of different viruses on reduction in SOD level was recorded to be the same with no significant difference in SOD level between any two viral infections. On the contrary, TAO level in the majority of patients was found to be comparable with that observed in healthy persons. An appreciable change in SOD level but little impact on TAO level during viral hepatitis may be explained by the possible adaptive rise of some other anti-oxidant level in the blood of these patients.
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PMID:Superoxide dismutase and total anti-oxidant levels in various forms of liver diseases. 1207 13

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

A molecular epidemiological survey of various hepatitis viral infections, including hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus (HDV), was carried out in Ho Chi Minh City, Vietnam. This study included of 295 patients with liver disease (234 viral related and 61 non-viral related) and 100 healthy individuals. The infection rates of HBV and HCV in 234 liver disease patients with acute hepatitis, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma, were 31.2 and 19.2%, respectively. On the other hand, detection rates of these viruses in healthy populations were 10 and 2%, respectively (P<0.005 and <0.0001, respectively). None of cases tested was positive for HDV RNA. The most common viral genotypes were type B and C of HBV (43 and 57%) and type 2a of HCV (33.3%). Surprisingly, high prevalence of HBV pre-S2 deletion mutant was found in 22 of 87 (25.3%) patients with chronic liver disease. Moreover, antibody to hepatitis E virus (HEV) immunoglobulin G (IgG) was detected in 78 of 185 (42%) and IgM in 1 of 185 (0.5%) patients. The age prevalence of anti-HEV IgG was reached 61.9% in 21-40-year-olds. These results suggest that these hepatitis viruses, except for HDV, are spreading among liver disease patients in Ho Chi Minh city, Vietnam and HBV was the most important causative agent correlated with liver disease in this area.
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PMID:Prevalence of hepatitis virus types B through E and genotypic distribution of HBV and HCV in Ho Chi Minh City, Vietnam. 1296 26

Virus D hepatitis continues to represent a public health problem in the south-eastern European countries, but the spread of the D virus infection in Romania is not completely elucidated. The paper proposes to assess the prevalence of the hepatitis D virus infection in patients with HBsAg-positive chronic hepatitis and liver cirrhosis in Romania. A number of 219 patients with chronic hepatitis and 168 with liver cirrhosis, all testing positive for HBsAg were studied. Viral markers were determined by immunoenzymatic methods. In HBsAg-positive chronic hepatitis the prevalence of the D virus was 37.9 % and in liver cirrhosis 51.19%. The great majority of the cases infected with hepatitis B virus were HBeAg-negative. These findings situate Romania among countries with a high prevalence of the hepatitis D virus infection, but which is decreasing as compared to the data communicated by previous reports.
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PMID:What is the real prevalence of the D virus infection in chronic hepatitis and liver cirrhosis in Romania? 1450 16

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

Four subtypes (adw, adr, ayw, and ayr ) and eight genotypes (A to H) of the hepatitis B virus (HBV) have been identified. They appear to be associated with particular geographic distribution, ethnicity, and possibly clinical outcomes. In this study, hepatitis B surface antigen (HBsAg) subtyping and HBV genotyping were carried out on sera obtained from HBsAg-positive HBV carriers, including healthy blood donors; patients with acute hepatitis, chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma; and patients on hemodialysis all located in Surabaya, Indonesia. We report here that all HBV isolates tested in Surabaya belonged to genotype B, with more than 90% of them being classified into subtype adw. Our results also revealed that prevalence of hepatitis C virus (HCV) co-infection among HBV carriers in Surabaya was approximately 10% for healthy blood donors and patients with chronic liver disease, and approximately 60% for patients on maintenance hemodialysis. Interestingly, HBsAg titers were lower in HBV carriers with HCV co-infection than in those without HCV co-infection. We also found that prevalence of hepatitis D virus (HDV) co-infection was < 0.5% among HBV carriers in Surabaya.
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PMID:Genotype and subtype analyses of hepatitis B virus (HBV) and possible co-infection of HBV and hepatitis C virus (HCV) or hepatitis D virus (HDV) in blood donors, patients with chronic liver disease and patients on hemodialysis in Surabaya, Indonesia. 1469 47

The impact of human immunodeficiency virus (HIV) coinfection on the survival of patients with hepatitis C virus (HCV)-related end-stage liver disease (ESLD) is unknown. Because HIV infection is no longer considered an absolute contraindication for liver transplantation in some countries, it has become a priority to address this topic. The objective of this study was to compare the survival of HIV-infected and HIV-uninfected patients with decompensated cirrhosis due to HCV. In a retrospective cohort study, the survival of 1,037 HCV monoinfected and 180 HCV/HIV-coinfected patients with cirrhosis after the first hepatic decompensation was analyzed. Of the group, 386 (37%) HCV-monoinfected and 100 (56%) HCV/HIV-coinfected subjects died during the follow-up. The median survival time of HIV-infected and HIV-uninfected patients was 16 and 48 months, respectively (P < .001). The relative risk (95% CI) of death for HIV-infected patients was 2.26 (1.51-3.38). Other independent predictors of survival were age older than 63 years (2.25 [1.53-3.31]); Child-Turcotte-Pugh class B versus class A (1.95 [1.41-2.68]) and class C versus class A (2.78 [1.66-4.70]); hepatitis D virus infection (1.56 [1.12-4.77]); model for end-stage liver disease score, (1.05 [1.01-1-11]); more than one simultaneous decompensation (1.23 [1.12-3.33]); and the type of the first hepatic decompensation, with a poorer prognosis associated with encephalopathy compared with portal hypertensive gastrointestinal bleeding (2.03 [1.26-3.10]). In conclusion, HIV coinfection reduces considerably the survival of patients with HCV-related ESLD independently of other markers of poor prognosis. This fact must be taken into account to establish the adequate timing of liver transplantation in HIV-coinfected subjects.
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PMID:HIV coinfection shortens the survival of patients with hepatitis C virus-related decompensated cirrhosis. 1602 2

Significant progress in the understanding of the natural history of hepatitis B and C has been made in recent years due to molecular diagnosis techniques. The most important biologic feature of hepatitis B and C viruses (HBV, HCV) is their ability to cause chronic hepatitis. The natural course of HBV infection is variable, ranging from inactive HBsAg carrier state to progressive chronic hepatitis that can evolve into liver cirrhosis and hepatocellular carcinoma. HBeAg-negative chronic hepatitis is due to a naturally occurring HBV variant with mutations in the precore or basic core promoter regions. It accounts for the majority of cases in many European countries and is generally associated with a more severe liver disease. The morbidity and mortality in chronic hepatitis B are linked to the evolution to cirrhosis and hepatocellular carcinoma. The progression of fibrosis is strongly associated with persistent active viral replication When the diagnosis is made, the 5-year cumulative incidence of developing cirrhosis ranges from 8% to 20%. The 5-year cumulative incidence of hepatic decompensation is 20%. Hepatocellular carcinoma is one of the most common cancers worldwide, 75% of which are related to chronic HBV infection. Coinfection with hepatitis D virus can lead to a more progressive liver disease in a shorter period of time. Hepatitis C virus infection becomes chronic in 80% of infected persons resulting in different stages of chronic hepatitis, with 20%-30% progressing to cirrhosis within 20 years period. The progression of fibrosis determines the ultimate prognosis. The major factors known to be associated with fibrosis progression are older age, male gender and alcohol consumption. Viral load and genotype do not play a role in the disease progression. Progression to fibrosis is more rapid in immunocompromised patients.
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PMID:[Hepatitis B and C: natural course of disease]. 1638 Dec 32

Hepatitis B virus (HBV) is transmitted by parenteral, sexual and perinatal routes. While fulminant hepatitis may occur in 1% of cases of symptomatic acute hepatitis, the principal problem of HBV infection is that it may become chronic, classically defined by carriage of HB surface antigens (HBsAg) for more than 6 months. This occurs in only 0.5 to 3% of immunocompetent adults but more frequently in children (up to 90%) and in immune-compromised patients (30 to 100%). The course of chronic HBV infection is characterized by variations in viral replication with spontaneous reactivation or discontinuation, and potential exacerbations observed clinically or by laboratory testing. The pathogenesis of HBV infection is mainly immune-mediated, resulting from host-virus interactions but also from the complexity of the virus itself (integration, mutation, occult replication). These factors explain the variety of presentations of chronic HBV infection, which range from immune tolerance to inactive carriage of HBsAg, passing through a stage of immune clearance, where chronic active hepatitis which may lead to cirrhosis (yearly incidence of 1.3 to 5.9%). Cirrhosis may be complicated by portal hypertension, liver failure, or hepatocellular carcinoma, which together explain 80% of the morbidity and mortality associated with HBV. The 5-year survival rate for HBV-related cirrhosis ranges from 52 to 82%. Immunosuppression, hepatitis D virus superinfection, and chronic alcohol consumption are the principal factors that modify this natural history. Chronic HBV infection is a major public health problem, particularly in developing countries, and it requires that efforts to make HBV vaccination universal be intensified.
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PMID:[Natural history of hepatitis B infection]. 1649 35

Hepatitis D virus (HDV) infection is one of the important etiologies of fulminant hepatitis and may aggravate the clinical course of chronic HBV infection to cirrhosis and liver failure. HDV was classified into three genotypes. Recent molecular phylogenetic analysis of HDV suggests at least seven major clades. The genotype I HDV is widely spread, genotype II is found in East Asia and genotype III HDV is prevalent in South America. The genomic size is 1682-1685 nucleotides (nt) for genotype II, and 1676 nt for genotype IV (IIb). The divergence in HDV nucleic acid sequences between genotype II and other genotypes varies from 13.8% to 35.3%. The divergences in the HDAg-coding region may range from 17.8% to 29.8% between genotype II and other genotypes. There is no genotypic or size restriction on the interactions of either the small or the large hepatitis delta antigens (HDAgs) between genotypes I and II, and there is also no genotypic incompatibility during co-package of HDAgs of different genotypes into virus like particles. There appears no apparent universal genotypic restriction of the transactivation of genotype I HDV RNA replication by small HDAg of genotype II. In contrast, there appears more genotypic restriction for genotype I small HDAgs to transactivate genotype II HDV RNA replication. Of the functional domains of HDAg, the 19 amino acids at the carboxyl-end of the large HDAg show the greatest divergences (70%-80%) between genotypes I and II. The viral packaging efficiencies of genotype I HDV isolates are usually higher than those of genotype II. The 19 amino acids at the carboxyl-end seem to be the most important determinant for viral packaging efficiencies. The editing efficiencies of the genotype I HDV are also higher than those of the genotype II. Genotype II HDV infection is relatively less frequently associated with fulminant hepatitis at the acute stage and less unfavorable outcomes [cirrhosis or hepatocellular carcinoma (HCC)] at the chronic stage as compared to genotype I. It appears that the clinical manifestations and outcomes of patients with genotype IV (IIb) HDV infection are more like those of patients with genotype II HDV infection. Persistent replication of HBV or HDV was associated with higher adverse outcomes (cirrhosis, HCC or mortality) compared to those who cleared both viruses from the sera. HBV of the genotype C is also a significant factor associated with adverse outcomes (cirrhosis, HCC or mortality) in patients with chronic hepatitis D in addition to genotype I HDV and age. However, most patients with chronic HDV infection have low or undetectable hepatitis B virus DNA levels. During longitudinal follow-up, genotype I HDV is the most important determinant associated with survival.
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PMID:Functional and clinical significance of hepatitis D virus genotype II infection. 1690 26


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