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At least 19 recordsLinked to original sources
PubMed2002

Interaction of alcohol and hepatitis viral proteins: implication in synergistic effect of alcohol drinking and viral hepatitis on liver injury.

Alcohol drinking and viral hepatitis are both recognized as major causes of liver disease worldwide, and they frequently coexist and synergistically cause liver injury in patients with chronic liver disease. Several mechanisms have been implicated in exacerbation of liver injury in patients with alcohol drinking and viral hepatitis. These include impairment of host defense and liver regeneration by alcohol consumption. The findings obtained from my laboratory have demonstrated that alcohol potentiates cooperatively several signals activated by hepatitis B virus X protein (HBX) or hepatitis C virus core protein, and HBX sensitizes hepatocytes to tumor necrosis factor-alpha (TNF-alpha)- and ethanol-induced apoptosis by a caspase-3-dependent mechanism, which may also contribute to the synergistic effect of alcohol drinking and viral hepatitis on liver injury.

Alcohol Drinking↗
PubMed1989

Differential diagnosis of viral hepatitis based on hepatitis viral markers.

192 patients of acute viral hepatitis (AVH) from three different hospitals of Madras metropolitan area during November 1985 to January 1986 were investigated for serologic markers of hepatitis A virus (anti HAVIgM) and hepatitis B virus (HBsAg, HBeAg, anti HBcIgM and anti HBs) by Enzyme linked immunosorbent assay (ELISA). While the overall pattern of AVH in Madras as revealed from the study showed Hepatitis A to be 36.4%, Hepatitis B 34.4% and Non-A Non-B 29.1%, the pattern differed significantly when areawise categorisation was done. The major AVH type in Government General Hospital was Hepatitis B (48.9%). While it was hepatitis A (46.9%) in Government Stanley Hospital and Non-A Non-B (40.0%) in Military Hospital. Using anti HBcIgM marker of Hepatitis B Virus and anti HAVIgM it was possible to make out that 13.5% of the cases, currently suffering from hepatitis A were either HBV carriers (8.3%) or cases convalescing from a previous Hepatitis B attack (5.3%). Various combinations of HBV markers positivity were observed and their diagnostic significance inferred.

Biomarkers↗
PubMed2000

Acute and chronic viral hepatitis.

Viral hepatitis is the most common cause of acute and chronic hepatitis. The term viral hepatitis generally refers to infections resulting from one of the hepatotrophic viruses: hepatitis A, B, C, D, and E. The last 10 years have brought many important advances in understanding the epidemiology, pathogenesis, molecular biology, and immunoprophylaxis of infections caused by hepatotrophic viruses. Development of sensitive and specific immunoassays has enabled detection of specific agents. This has allowed for identification of infected patients and monitoring response to therapy. Additionally, serologic markers have allowed for isolation of contaminated blood products and a reduction in the spread of disease. The remaining challenge is the application of this knowledge to the treatment and prevention of viral hepatitis. This article explores the risk factors, epidemiology, microbiology, clinical and laboratory diagnosis, treatment, and prevention of the hepatotrophic viral infections.

Acute Disease↗
PubMed1994

Therapy of acute and chronic viral hepatitis.

Viral hepatitis comprises five different diseases caused by five different viral agents: hepatitis A, B, C, D, and E virus. All five forms can cause acute hepatitis, only hepatitis B, C and D can cause chronic hepatitis. Alpha interferon has been shown to be effective in inducing sustained remissions in all three forms of chronic viral hepatitis. Its efficacy in acute viral hepatitis has not been documented, although preliminary results suggest that interferon may decrease the chronicity rate of acute hepatitis C. In chronic hepatitis B, alpha interferon therapy with 5 mu daily or 10 mu three time weekly for 16 weeks will induce a long-term remission in disease with loss of HBV DNA and HBeAg from serum in 25% to 40% of patients and ultimately, a loss of HBsAg in approximately half of the responders. Patients likely to respond are those with high initial serum aminotransferases and low levels of HBV DNA. In chronic hepatitis C, therapy with 3 to 5 mu of alpha interferon 3 times weekly for 24 to 48 weeks will induce a temporary remission in disease with loss of HCV RNA from serum, fall of aminotransferases into the normal range and improvement in liver histology in 50% of patients and a sustained remission persisting after therapy is stopped in 25% of patients. Patients with a short duration of disease and without cirrhosis are the most likely to respond. Unfortunately, there are no completely reliable means of predicting which patients are likely to respond to interferon and which of these will have a lasting response. In chronic hepatitis D, a prolonged course of alpha interferon given in doses of 3 to 5 mu daily or 9 to 10 mu three times weekly results in remission in disease as marked by loss of HDV RNA from blood and fall of aminotransferases into the normal range in up to 50% of patients. Unfortunately, this response is rarely sustained after treatment unless HBsAg becomes negative, which occurs in only a small number of patients. Despite the benefits of alpha interferon therapy in many patients with chronic viral hepatitis, several shortcomings of this therapy are evident: less than 50% of patients respond, side effects can be problematical, and some patients are not appropriate for therapy. Thus, interferon is not indicated for patients with advanced cirrhosis or for those who are severely immunosuppressed. Alpha interferon is an important first step in therapy for chronic viral hepatitis, but further approaches are needed to increase its efficacy and safety.

Acute Disease↗
PubMed1991

[The role of staphylococcal superinfection in viral hepatitis].

Viral hepatitis A was diagnosed in 69.35 percent of the 124 patients with viral hepatitides aged 15 to 62, 54.1 percent of these females and 45.9 percent males, and viral hepatitis B in 30.65 percent. The disease course varied in severity, was typical in all cases; the icteric form was observed in all the patients. An unfavorable pyoinflammatory premorbid background was present in 1/3 of the examinees. The studies have revealed that a staphylococcal superinfection with the icteric syndrome contributed to the pathogenesis of viral hepatitis. Antistaphylococcal agglutinins were detected in 65.6 percent of hepatitis A and in 73.7 percent of hepatitis B patients, and alpha antitoxins in 81.1 and 71.0 percent of patients, respectively. The disease severity correlated with high antitoxin titers, high antitoxin titers with a delayed convalescence of viral hepatitis A patients. Changes in the titers of antistaphylococcal agglutinins in hepatitis B patients were not rapid and their time course correlated with the terms of liver function recovery. The author comes to a conclusion that bacterial superinfection contributes to the pathogenesis of viral hepatitides, staphylococcal infection among other ones, that essentially influences the disease course.

Adolescent↗
PubMed1978

Viral hepatitis.

Viral hepatitis may be classified into three or more forms including type A hepatitis, type B hepatitis, and a group denoted as non-A non-B hepatitis which may represent viral hepatitis of one or more causes. The differentiation of these forms of hepatitis is primarily serologic. The development of antibody to hepatitis A virus can be detected by radioimmunoassay as well as by other test systems. The serologic diagnosis of type B hepatitis rests on the detection of hepatitis B surface antigen or on the development of antibody to hepatitis B core antigen or hepatitis B surface antigen. The serologic diagnosis of non-A non-B hepatitis is a diagnosis of exclusion for assay systems for this form of disease are not yet available.A prototype hepatitis B vaccine has been prepared and is currently undergoing clinical trials. Gamma globulin is now available that contains high titered antibody against hepatitis B virus. Normal immune globulin contains high titers directed against hepatitis A virus. Therefore, for documented exposure, effective prophylaxis is available for both of these forms of acute liver disease. The past decade has resulted in rapid advances in our understanding of the pathogenesis of acute hepatitis and its extrahepatic manifestations. However, it is clear that specific treatment for acute hepatitis and the accurate description of the etiologic agents of non-A non-B hepatitis require exploration.

Hepatitis B Antigens↗
PubMed1978

Developments in viral hepatitis.

Viral hepatitis is a major public health problem occurring endemically in all parts of the world. The general term viral hepatitis refers to infections caused by hepatitis virus type A, type B and a more recently identified infection referred to as "non-A: non-B" hepatitis. These clinically and pathologically similar forms of hepatitis have been studied intensively following the discovery of a specific antigen, Australia antigen, one of the markers of infection with hepatitis B virus.

Animals↗
PubMed2006

[Epidemiology and clinical manifestations of viral hepatitis].

Viral hepatitis is an infectious disease affecting the liver. At this time, five different human hepatitis viruses are recognized and characterized in detail: Hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV). The hepatitis viruses differ widely in their modes of transmission and clinical features. Whereas all of them can cause acute hepatitis, only HBV, HDV, and HCV cause chronic hepatitis. This article reviews the epidemiology and clinical manifestations of the different types of viral hepatitis.

Adolescent↗
PubMed2000

[Epidemiology, diagnosis and prevention of viral hepatitis].

Viral hepatitis is one of the most important infectious diseases worldwide. It is frequent in tropical and subtropical areas, but also plays still a significant role in the industrialized countries of Northern and Western Europe and the USA. In Germany more than 100,000 people are infected by viral hepatitis each year. Whereas hepatitis A and E are transmitted fecal-orally, hepatitis B, C and D are transmitted by the parenteral route. Most hepatitis A infections seen in Germany are acquired abroad. Hepatitis B is still a nosocomial disease; the majority of infections in Germany, however, seems to be transmitted sexually. For the serological diagnosis of viral hepatitis a battery of sensitive tests for specific antibodies and antigens is available; usually testing of one serum sample allows an unambiguous diagnosis. Prophylaxis of hepatitis A and B is possible using safe and efficient vaccines.

Cross-Cultural Comparison↗
PubMed2002

The cutaneous manifestations of viral hepatitis.

Viral hepatitis is a common disease with significant morbidity and mortality that is found throughout the world. It is a known cause of acute and chronic liver disease. Because the disease can be asymptomatic in its acute stages, the diagnosis is often missed. This article reviews the extrahepatic manifestations of the disease, in particular the visible cutaneous lesions, which offer clues to the diagnosis of viral hepatitis. Familiarity with the most common skin lesions associated with each type of hepatitis virus will be useful in identifying previously undiagnosed individuals. This article serves as a review of the most widely published associations between skin diseases and specific subtypes of viral hepatitis.

Hepatitis, Viral, Human↗
PubMed1997

[New viral hepatitis].

Viral hepatitis are essentially caused by 5 types of viruses which differ in way of transmission and their evolution to chronicity or not. Like the virus causing hepatitis A, the E-virus-discovered en 1983-is a virus with oral-fecal transmission, responsible only for acute hepatitis which may be fulminant, notably in pregnant woman. Responsible for epidemics in Asia and Africa, the E-virus is nearly non-existent in our regions. Just like the B, C and D viruses, the G-virus is a RNA-virus with intravenous transmission. Notwithstanding a high prevalence, its pathogenic role remains hypothetical so that some hesitate to consider it as a virus causing clinical hepatitis. Etiological viral or non-viral agents for the cryptogenic hepatitis which can appear as acute, fulminant, post-transfusional or chronic illness, remain to be discovered.

Acute Disease↗
PubMed2005

Liver transplantation for viral hepatitis.

Viral hepatitis is associated with two forms of liver failure that may require liver transplantation: fulminant hepatic failure associated with all forms of acute viral hepatitis and chronic liver failure as a result of chronic hepatitis B and C infection (or both). This review briefly discusses liver transplantation for fulminant hepatitis but focuses on transplantation for hepatitis B- and hepatitis C-associated cirrhosis.

Antiviral Agents↗
PubMed1978

[Viral hepatitis].

Viral hepatitis is one of the most frequent infectious diseases of our time. It is of great concern to the epidemiological risk groups such as research laboratories, dialysis units and other public health agencies. The result of epidemiological, immunological, morphological and biochemical studies have demonstrated, that this disease is caused by at least two different viruses. The hepatitis A virus (HAV) induces the type A hepatitis and the hepatitis B virus (HBV) the type B hepatitis. Two antigen-antibody systems are associated with viral hepatitis type B: the hepatitis B-surface antigen (HBsAg) and antibody (anti-HBs) and the hepatitis B-core Antigen (HBcAg) and antibody (anti-HBc). In the last years great progress has been made in the characterization of these distinct viruses. Both can be transmitted to monkeys. Advances in biophysical and biochemical procedures of treatment of hepatitis B sera have already resulted in first vaccination trials.

Hepatitis B Antigens↗
PubMed1981

Nosocomial viral hepatitis.

Viral hepatitis has long been recognized as a hazard in the health care environment. Nosocomial hepatitis B initially emerged in the setting of transfusion-associated infection and later in patients in dialysis units and on oncology wards. Health care workers are also at risk of acquiring nosocomial hepatitis B and more likely to acquire the infection from their patients than vice versa. Rare instances of nosocomially-transmitted hepatitis A have been documented, but hepatitis A virus excretion patterns in relation to onset of disease generally preclude significant transmission in the hospital setting. With virtual elimination of transfusion-transmitted hepatitis B, non A/non B hepatitis is the most significant cause of post-transfusion hepatitis and may occur in as high as 15 percent of the patients given multiple transfusions. Control of nosocomial viral hepatitis is based on the creation of environmental barriers specific for each viral agent. For hepatitis B, serologic surveillance of staff and patients in high risk areas, together with use of immunoglobulins for post-exposure prophylaxis and hepatitis B vaccine in susceptible persons, promises to significantly reduce nosocomial infection. Isolation procedures for patients admitted with hepatitis A or B are based on use of blood precautions for hepatitis B, modified enteric precautions for hepatitis A and a combination of both for non A/non B or etiologically unspecified hepatitis.

Cross Infection↗