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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic hepatitis B infection is frequently diagnosed within the genitourinary clinic setting with sexual transmission the commonest route of acquisition in the United Kingdom. Only 3--5% of adults who contract acute hepatitis B will progress to chronic infection, and these individuals can be identified by the presence of hepatitis B surface antigen (HBsAg) in the bloodstream 6 months after infection. Individuals at highest risk of long-term complications such as cirrhosis and hepatocellular carcinoma, carry HBeAg and have high levels of circulating hepatitis B virus (HBV) deoxyribonucleic acid (DNA). Therapy should be targeted towards this group of patients. Two forms of therapy are now licensed for use in chronic hepatitis B infection: interferon-alpha and lamivudine. Seroconversion occurs in 30--40% of patients treated with interferon and treatment is often limited by toxicity. Lamivudine is well tolerated with seroconversion rates of 15--20% at one year, rising with increasing duration of therapy. Long-term monotherapy is limited however by the development of resistance mutations and combination nucleoside therapy is likely to become the treatment of choice in the future. Patients with chronic hepatitis B should be counselled regarding transmission, partner vaccination and alcohol intake and co-infection with other hepatitis viruses should be excluded.
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PMID:The management of chronic hepatitis B infection. 1180 40

Chronic hepatitis B virus (HBV) infections are frequently associated with exacerbations of hepatitis of which the majority are due to reactivation of viral activity. Variation in a viral genome during persistent infection has been shown to be a possible cause for reactivation. In this study, we have found another possible mechanism. HBV in a patient with repeated exacerbations was isolated at six different times during follow-up and was characterized by polymerase chain reaction and DNA sequencing. The first episode of exacerbation was accompanied with increased replication of an HBV strain. The second episode, however, was associated with the sudden appearance of an HBV strain that displayed enough sequence variations to warrant the designation as a separate strain. The results suggested a reinfection event by another independent HBV. Subsequent exacerbations were then related to coactivation of both viral strains. These observations provide significant information toward understanding the acute exacerbations of chronic type B hepatitis. Copyright 2001 S. Karger AG, Basel
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PMID:A Viral Mechanism in Acute Exacerbations of Chronic Type B Hepatitis: Hepatitis B Virus Reinfection and Subsequent Reactivation of Two Viral Strains. 1172 1

The term hepatitis virus is reserved for those viruses that are predominantly hepatotropic, although several new agents have been assigned to this category in the absence of hepatotropism and clinical disease. The hepatitis viruses can be broadly divided into those transmitted via the fecal-oral route, and those by blood, blood products and body fluids. Hepatitis A (picornaviridae), hepatitis B (hepadnaviridae) and hepatitis C (flaviviridae) represent the major public health problems. The epidemiology of hepatitis A virus (HAV) and hepatitis B virus (HBV) is changing in response to vaccination. In the case of HAV, older age groups are now deemed at risk, particularly of fulminant hepatitis if exposed over the age of 50. Chronic hepatitis B in some regions is now predominantly of the so-called precore mutant type where high levels of HBV replication persist in the presence of anti-hepatitis B virus (HBe) antibodies. The HBV vaccination is among the most cost-effective health care measures. The epidemiological significance of mutations found increasingly in the HBV S gene isolated from vaccinated children is unclear. Evidence that hepatitis G and TT virus are significant causes of hepatitis is lacking. Of interest, however, is the finding that the related GBV-B agent of monkeys may be a model for developing new antiviral agents against HCV. Animal models of hepatitis infections are providing new insights into the pathogenesis of hepatitis in humans. Indeed it is possible that hepatitis E is primarily an agent of pigs and other domesticated livestock. Intriguingly, the new TT virus shares many properties with the circoviruses, significant pathogens of chickens and pigs. The challenge in the next decade will be to assess the significance of these new agents in terms of public health and resources. Value judgements will have to be made in assessing the risks associated with blood containing trace amounts of these adventitious agents.
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PMID:Hepatitis viruses: a pandora's box? 1253 79

Chronic hepatitis B virus (HBV) infection can cause a broad spectrum diseases, including from asymptomatic HBV carriers or cryptic hepatitis, to acute hepatitis, chronic hepatitis, Liver cirrhosis and primary hepatocellular carcinoma. The variable pattern and clinical outcome of the infection were mainly determined by virological itself factors, host immunological factors and genetic factors as well as the experimental factors. Among the human genetic factors, major candidate or identified genes involved in the process of HBV infection fall into the following categories: (1) genes that mediate the processes of viral entry into hepatocytes, including genes involved in viral binding, fusion with cellular membrane and transportation in target cells; (2) genes that modulate or control the immune response to HBV infection; (3) genes that participate in the pathological alterations in liver tissue; (4) genes involved in the development of liver cirrhosis and hepatocellular carcinoma associated with chronic HBV infection, including genes related to mother-to-infant transmission of HBV infection; and (5) those that contribute to resistance to antiviral therapies. Most of the reports of human genes associated with HBV infection have currently focused on HLA associations. For example, some investigators reported the association of the HLA class II alleles such as DRB1*1302 or HLA-DR13 or DQA1*0501-DQB1*0301-DQB1*1102 haplotypes with acute and/or chronic hepatitis B virus infection, respectively. Several pro-inflammatory cytokines such as Th1 cytokines (including IL-2 and IFN-gamma) and TNF-alpha have been identified to participate the process of viral clearance and host immune response to HBV. In contrast, the Th2 cytokine IL-10 serves as a potent inhibitor of Th1 effector cells in HBV diseases. The MBP polymorphisms in its encoding region were found to be involved in chronic infection. Thus, reports from various laboratories have shown some inconsistencies with regard to the effects of host genetic factors on HBV clearance and persistence. Since genetic interactions are complex, it is unlikely that a single allelic variant is responsible for HBV resistance or susceptibility. However, the collective influence of several single nucleotide polymorphisms (SNPs) or haplotype (s) may underlie the natural combinational or synergistic protection against HBV. The future study including the multi-cohort collaboration will be needed to clarify these preliminary associations and identify other potential candidate genes. The ongoing study of the distributions and functions of the implicated allele polymorphisms will not only provide insight into the pathogenesis of HBV infection, but may also provide a novel rationale for new methods of diagnosis and therapeutic strategies.
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PMID:Current status and prospects of studies on human genetic alleles associated with hepatitis B virus infection. 1267 1

Although the histological features of various causes of chronic liver disease have been well described, usually the inflammatory activity of the disease is important after the cause has been established. Some patients have co-infection or concomitant liver disease and on occasion it is difficult to decide the treatment. In order to clarify the histological differences, we investigated the inflammatory activity among autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), chronic hepatitis C (CHC) and chronic hepatitis B (CHB) in a standardized way using the modified histological activity index (HAI). According to the modified HAI, inflammatory activity is divided into four categories; categories A/D explains portal/periportal inflammation and categories B/C explains lobular activity. The inflammatory score of AIH tended to be greater in all categories from the early stage of fibrosis, whereas scores of PBC were lower, except for portal inflammation. Chronic hepatitis C patients had portal or periportal inflammation, and their inflammatory scores were linked to the development of fibrosis. Chronic hepatitis B patients tended to have severe lobular injury, but did not have a relationship between the inflammatory score and their stage. To know the distribution of inflammation using the modified HAI scoring system may be helpful and convenient in evaluating patients with chronic inflammatory liver disease.
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PMID:Histological grading and staging in chronic hepatitis: its practical correlation. 1268 45

Hemodialysis patients are a high-risk group for hepatitis B and C virus infections. The aim of the study was to evaluate the prevalence of B and C viral hepatitis, level of its control among patients on hemodialysis. In December of 1997, 1998, 1999, 2000, 2001 we visited all hemodialysis centers of Lithuania and gathered information about these infections in patients on hemodialysis. Eleven percent (11.4%) of all hemodialysis patients were not examined for HB(s)Ag and 15.2% for anti-HCV, 67.3%--for anti-HB(s) and 57.7% for anti-HBc in 2001. The number of examined patients for the markers of hepatitis had increased in 2001 in comparison with 1997. The same number of hemodialysis patients with HB(s)Ag was found in each year of study (14% in 1997, 14.4% in 2001). We observed the decrease in percentage of anti-HCV positive patients from 23% in 1998 till 15.4% (p<0.01) in 2001. Only 10.6% hepatitis B virus vaccinated patients was registered in 2001 and this percentage increased if compared to 6.3% in 1999. About (1/4) of anti-HB(c) positive patients were HB(s)Ag positive in 2000-2001. Chronic hepatitis B could be diagnosed for them. The duration of hemodialysis of HB(s)Ag and anti-HCV positive patients was longer compared to HB(s)Ag and anti-HCV negative patients (p<0.001).
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PMID:[Control of viral hepatitis in Lithuanian hemodialysis centers in 1997-2001]. 1276 37

Chronic hepatitis B virus (HBV) infection, which can lead to cirrhosis and hepatocellular carcinoma, is a major health threat worldwide. Classic patients with chronic hepatitis B are positive for hepatitis Be-antigen (HBeAg) and HBV-DNA. In the Mediterranean basin, 30-80% of patients with chronic hepatitis B (CHB) are HBeAg-negative, in contrast to Northern European countries and the US, where only 10-40% of CHB patients are lacking HbeAg. HBeAg-negative CHB usually runs a progressive course. The greatest problem with the treatment of HBeAg-negative CHB is the high relapse rate. Their end treatment response rates are similar to those of classic CHB patients, but after discontinuation of treatment most of them relapse. All the data available in the literature show that more than 80% of patients with HBeAg-negative CHB do not respond to the current approved therapies. A literature review and our experience with thymosin indicate that the combination of IFN alpha2b and T-alpha1 is better tolerated and more likely to induce a sustained response in HbeAg-negative chronic hepatitis B patients when compared to other currently available therapies. As thymosin-alpha1 treatment is relatively free from adverse effects, future controlled trials are needed, with a longer follow-up, in order to fully evaluate the role of the combination therapy of thymosin-alpha1 with other emerging therapeutic agents.
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PMID:Thymosin in the treatment of HBeAg-negative chronic hepatitis B. 1294 46

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

Chronic hepatitis B virus (HBV) infection and dietary exposure to aflatoxin B1 (AFB1), two of the major risk factors in the multifactorial aetiology of hepatocellular carcinoma (HCC), co-exist in those countries with the highest incidences of and the youngest patients with this tumour, raising the possibility of a synergistic carcinogenic interaction between the two agents. Experimental studies in HBV-transgenic mice and woodchucks infected with woodchuck hepatitis virus were the first to show a synergistic hepatocarcinogenic effect between hepadnaviral infection and AFB1 exposure. With the availability of urinary and serum biomarkers that more accurately reflect dietary exposure to AFB1 than did the initially used food sampling and dietary questionnaires, cohort studies of patients with HCC in China and Taiwan have provided compelling evidence for a multiplicative or sub-multiplicative interaction between HBV and AFB1 in the genesis of human HCC. A number of possible mechanisms for the interaction have been suggested. Chronic HBV infection may induce the cytochrome P450s that metabolise inactive AFB1 to the mutagenic AFB1-8,9-epoxide. Hepatocyte necrosis and regeneration and the generation of oxygen and nitrogen reactive species resulting from chronic HBV infection increase the likelihood of the AFB1-induced p53 249ser and other mutations and the subsequent clonal expansion of cells containing these mutations. Nuclear excision repair, which is normally responsible for removing AFB1-DNA adducts, is inhibited by HBV x protein, favouring the persistence of existing mutations. This protein also increases the overall frequency of DNA mutations, including the p53 249ser mutation, and may contribute to uncontrolled cell cycling when p53 is non-functional.
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PMID:Synergistic interaction between aflatoxin B1 and hepatitis B virus in hepatocarcinogenesis. 1498 13

Chronic hepatitis B virus (HBV) infection is a well-recognized risk factor for the development of hepatocellular carcinoma (HCC), which is becoming a more prevalent clinical problem, especially in HBV-endemic areas. It is estimated that 1.25 million people in the United States and more than 300 million people worldwide are chronically infected with HBV. Despite the introduction of universal vaccination against hepatitis B in over 100 countries, persistent HBV infection is still a serious problem worldwide, causing an estimated annual death rate of one million. It may take several decades until the effect of vaccination will be translated into reduced transmission and morbidity. Meanwhile, patients with persistent HBV infection require better antiviral therapeutic modalities than are currently available. It is well accepted that antiviral therapy for chronic hepatitis B is effective to improve prognosis of patients with HBV by preventing development of hepatitis state and HCC. The therapeutic endpoints for hepatitis B treatment are: 1) sustained suppression of HBV replication, as indicated by HBsAg and HBeAg loss, 2) decrease of serum HBV DNA of an undetectable level by a non-PCR method, 3) remission of disease, as shown by normalization of ALT, 4) improvement in liver histology, and 5) reduction of the acute exacerbation, cirrhosis, and HCC. In the present, the antiviral treatment of hepatitis B consists of either interferon alpha or oral lamivudine alone or in combination with existing therapy. Each major antiviral drug of interferon alpha and lamivudine has pros and cons, and effect of combination therapy of both drugs is also still limited. More powerful and safe new antiviral therapies are required to achieve final goal of these therapeutic endpoints. Management of chronic hepatitis B requires significant knowledge of approved pharmacotherapeutic agents and their limitations. Therapeutic options for managing hepatitis infection after liver transplantation (LT) are also evolving.
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PMID:Antiviral therapy for chronic hepatitis B: a review. 1503 42


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