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

Chronic forms of viral B,C and D hepatitis and fulminant hepatitis represent a serious healthcare problem. The study deals with the changes in the strategy in treating these diseases. During the chronic active hepatitis caused by the B hepatitis virus, the main aim of treatment is to cease multiplication of viruses, eliminate the clinical symptoms, prevent the development of cirrhosis, or the origin of hepatocellular carcinoma. The authors analyze the possibilities of the application of corticosteroids, viricidal drugs (vidarabin and interferons) and other medicaments (acyclovir, zidovudin, duramin, gancyclovir, chinacrin, and others) besides corticosteroids, interleukin 2 and tymozin from the group of immunomodulators were tested. The testing included the factor stimulating the colonies of granulocytes and myeloblasts and other substances. The therapy of acute protracted B hepatitis by means of interferon still requires controlled studies. Superinfection by D virus in chronic carriers of HBsAG causes chronic hepatitis which quickly leads to the development of cirrhosis. The therapy on basis of alpha interferon decreases the RNA virus D hepatitis serum level and leads to an improvement in the development of chronic hepatitis in half of the patients. Therapy of chronic C hepatitis on basis of corticosteroids is ineffective, and can be dangerous. Acyclovir is proved to be ineffective as well. The open study indicated certain positive results in application of interferon. The fulminant hepatitis can be defined as a development of encephalopathy and a decrease of the prothrombin time to less than 50% in the course of acute hepatitis. The break-point in the therapy of fulminant hepatitis took place in association with the performance of the transplantation of the liver. Impossibility to transplant the liver means that the effect of therapy of fulminant hepatitis is merely of supportive value. Majority of patients die due to neurologic complications, namely unmanageable oedema of the brain. But still, neither the antioedema therapy, e.g. on basis of manitol, as well as by means of corticosteroids, hemodialysis, hemofiltration, plasmapheresis and hemoperfusion, nor the treatment on basis of E1 prostaglandine improved the survival of patients. (Tab. 2, Ref. 82).
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PMID:[Treatment of viral hepatitis]. 855 59

The aetiological agents responsible for, and the outcome of, acute liver failure were investigated prospectively in 44 children (29 males, 15 females) attending a tertiary health care facility in India. The children were between the ages of 2 months and 13 years. Studies for viral infections and other etiologies could be carried out in 40 patients. Specific aetiological labels were possible in 35 (87.5%) patients. Thirty (75%) had evidence of acute viral hepatitis. Acute hepatitis E virus (HEV) infection was found in a total of 18 children, with hepatitis A (HAV) in 16, hepatitis B in 5, and C in 1. Seven had isolated infection with hepatitis E, five with A, and four with B. Nine had both E and A infection. Superinfection of HEV was observed in a child with Indian childhood cirrhosis (ICC). Acute HEV infection was confirmed by immunoblot assay in all the patients and in eight of these, HEV-RNA was also detected in the serum. HAV was involved in 37.5% of cases with isolated infection in 10% (4 of 40). The aetiological factors associated with acute liver failure, apart from HAV and HEV, were other hepatotropic viruses (22.5%), Wilson's disease (5%), ICC (5%), and hepatotoxic drugs (7.5%). In five patients, no serological evidence of acute viral hepatitis could be found, neither did the metabolic screen yield any result. It was observed that enterically transmitted hepatitis viruses (HAV and HEV) were associated with 60% of acute hepatic failure in children. Mixed infection of HAV and HEV formed the single largest aetiological subgroup. In developing countries, where hepatitis A and E infections are endemic, severe complications can arise in the case of mixed infection. This may contribute to most of the mortality from acute liver failure during childhood.
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PMID:Acute viral hepatitis types E, A, and B singly and in combination in acute liver failure in children in north India. 880 Dec 80

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

Superinfection with hepatitis C virus (HCV) in already chronically infected subjects has been documented. Whether a complete response to antiviral therapy is associated with protective immunity against reinfection with HCV remains unknown. We describe a patient who had a sustained biochemical and virologic response with loss of intrahepatic HCV RNA after a course of combination therapy using interferon plus ribavirin. Histopathologically, the chronic hepatitis was in remission on follow-up biopsy 6 months post-therapy. Unfortunately, 34 weeks post-therapy, a flare of hepatitis with reappearance of hepatitis C viremia was noted 2 months after he received injections from a non-licensed medical provider. Analysis of the core gene sequences showed a 95% homology between the HCV strains isolated before antiviral treatment and during the hepatitis flare. The data indicated that the hepatitis flare after a period of sustained response to combination therapy in this patient could have been caused by reinfection with homotypic HCV. Our observation indicates the lack of protective immunity against reinfection with HCV in patients with chronic hepatitis C, even after successful clearance of the virus. Therefore, reinforcing the education of these subjects to avoid HCV reinfection should be stressed.
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PMID:Probable reinfection with hepatitis C virus in a chronic hepatitis C patient with a sustained response to combination therapy. 1180 23

A total of 1,220 subjects from Equatorial Guinea living in Spain (median age = 41 years; 453 male and 767 female) was examined for antibodies to human immunodeficiency virus (HIV) and Hepatitis B (HBV), C (HCV), and D (HDV) viruses. Extracted RNA and DNA from the positive samples were used to quantify viral load. The prevalence of HIV antibodies, HCV RNA, and HBV surface antigen (HBsAg) was 10.8% (N = 132), 11.6% (N = 141), and 7.9% (N = 96), respectively. The most prevalent HIV variant was CRF02_AG (38.5%; N = 40). HCV genotype 4 (60%; N = 36) and HBV genotype A3 (32%; N = 8) were the hepatitis variants most frequently found. Superinfection with HDV was seen in 20.9% (N = 24) of HBsAg carriers. A control group of 276 immigrants from other sub-Saharan countries showed similar rates of HIV and HBsAg, although no HCV cases were found. Immigrants constitute a major source of HIV and hepatitis viruses in Spain; therefore, it is important that control measures are intensified.
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PMID:Hepatitis B, C, and D and HIV infections among immigrants from Equatorial Guinea living in Spain. 2333 1


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