Chronic Hepatitis in Carriers of Hepatitis B Surface Antigen, with Intrahepatic Expression of the Delta Antigen

Rizzetto, M.; Verme, G; Recchia, S.; Bonino, Ferruccio; Farci, Patrizia; Aricò, S; Calzia, R; Picciotto, A.; Colombo, Massimo; Pópper, Hans

doi:10.7326/0003-4819-98-4-437

Cited by 349 publications

(133 citation statements)

References 12 publications

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“…Infection with HDV causes the most severe form of acute and chronic viral hepatitis. The disease can be rapidly progressive, with cirrhosis developing within 1-2 years following acute hepatitis in 15% of cases [16][17][18]. Although over the past decade there has been a decline in the incidence of HDV infection in the world [15], most likely as a result of HBV vaccination programs and improved socioeconomic conditions, chronic hepatitis D still remains a major cause of liver transplantation and death.…”

Section: Hbv and Hdvmentioning

confidence: 99%

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

Chien

2008

Hepatol Int

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Concurrent hepatitis C virus (HCV), hepatitis delta virus (HDV), or human immunodeficiency virus (HIV) infection with chronic hepatitis B virus (HBV) appears to increase the risk of progressive liver disease including liver cirrhosis and hepatocellular carcinoma. There is a 10% prevalence of HCV infection in chronic HBV or HDV infection. Serological evidence of previous exposure to HBV is found in more than 80% of HIVpositive patients in the high risk group. Notably, the most recently acquired virus tends to suppress the pre-existing virus. In chronic HBV infection acquired perinatally or in early childhood, usually HCV is dominant and may suppress or even displace HBV and HDV. Less frequently, HBV or HDV suppresses HCV. It is generally agreed that the dominant virus should be identified in order to make appropriate treatment decisions. Studies with standard interferon (IFN) to treat patients with HCV dominantly dual HBV/HCV infection have showed only limited virological response. But high dose of IFN has been demonstrated with better response rate. Combined ribavirin with standard or pegylated IFN therapy could achieve a sustained HCV clearance rate comparable with those infected with HCV alone. On the contrary, patients with HBV dominantly dual viral infection might indicate more appropriate addition of lamivudine to IFN than ribavirin. Additionally, patients with concurrent infection of HBV and HDV, IFN seems to be the only effective agent. However, the efficacy of IFN is related to the dose. High dose of IFN [9 MU tiw (thrice per week)] and longer treatment duration (at least 2 years) have been shown to achieve adequate virological response. In patients with concurrently infected HBV and HIV, anti-HBV therapy should be considered for all patients with evidence of liver disease, irrespective of the CD4 cell count. In patients not requiring antiretroviral therapy, HBV therapy should be preferentially based on IFN, adefovir, or telbivudine. In contrast, in patients with CD4 cell counts \350 cells/ll or those already on antiretroviral therapy, agents with double anti-HBV and anti-HIV activity are preferred. At present, the evidence of therapeutic efficacy is not sufficient to make a recommendation in treating patients with dual HBV/HCV or HBV/HDV or HBV/HIV infection. Further studies of the well-designed, larger scale are needed to elucidate the role of different regimens or combination in the treatment of dual viral infection.

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Section: Hbv and Hdvmentioning

confidence: 99%

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

Chien

2008

Hepatol Int

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“…From the 1 Liver Diseases Section, Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, 2 Department of Nursing, The Warren E. Magnuson Clinical Center, 3 Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD; 4 National Genetics Institute, Los Angeles, CA; and 5 Abbott Laboratories, Abbott Park, IL.…”

mentioning

confidence: 99%

“…1,2 Chronic HDV infection often results in severe liver disease that progresses to cirrhosis in as many as 70% of patients. 3 All patients with delta hepatitis have HBsAg in serum, but most lack markers of active hepatitis B virus (HBV) replication such as hepatitis B e antigen (HBeAg) and HBV DNA. Diagnosis is suggested by the finding of anti-HDV in an HBsAg-positive patient and is confirmed by the finding of HDV RNA in serum or HDV antigen in liver.…”

mentioning

confidence: 99%

Lamivudine for chronic delta hepatitis

et al. 1999

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Chronic delta hepatitis is a severe form of chronic liver disease caused by hepatitis delta virus (HDV) infection superimposed on chronic hepatitis B or the hepatitis B surface antigen (HBsAg) carrier state. Therapy of delta hepatitis is currently unsatisfactory. We have evaluated lamivudine (3-thiacytidine), an oral nucleoside analogue with marked effects against hepatitis B, as therapy in 5 patients with chronic hepatitis D. Five men, ages 38 to 65 years, were treated. All had HBsAg, antibody to HDV, and HDV RNA in serum, as well as persistent elevations in alanine aminotransferase (ALT) levels and liver histology showing severe chronic hepatitis with fibrosis or cirrhosis. Lamivudine was given in a dose of 100 mg orally daily for 12 months. Patients were monitored carefully and tested for HBsAg, HBV-DNA and HDV-RNA levels serially during the year of treatment and for 6 months thereafter. Liver biopsies were performed before therapy and repeated after 1 year. Serum levels of HBV DNA fell rapidly in all 5 patients, becoming undetectable even by polymerase chain reaction (PCR) in 4. However, all 5 patients remained HBsAg-and HDV-RNA-positive, and serum ALT levels and liver histology did not improve. All patients tolerated therapy well. When lamivudine was stopped, HBV-DNA levels returned to pretreatment values without a change in disease activity. Lamivudine is a potent inhibitor of HBV-DNA replication, but does not improve disease activity or lower HDV-RNA levels in patients with chronic delta hepatitis. (HEPATOLOGY 1999;30:546-549.)The hepatitis delta virus (HDV) is a small defective RNA virus that replicates only in the presence of hepatitis B surface antigen (HBsAg). 1,2 Chronic HDV infection often results in severe liver disease that progresses to cirrhosis in as many as 70% of patients. 3 All patients with delta hepatitis have HBsAg in serum, but most lack markers of active hepatitis B virus (HBV) replication such as hepatitis B e antigen (HBeAg) and HBV DNA. Diagnosis is suggested by the finding of anti-HDV in an HBsAg-positive patient and is confirmed by the finding of HDV RNA in serum or HDV antigen in liver. 4 Therapy of chronic delta hepatitis is problematic. Pilot studies suggested that interferon alfa was effective in reducing serum aminotransferase elevations and improving hepatic histology. 5,6 Subsequent randomized, controlled trials showed that interferon was effective in only a proportion of patients and had to be administered in high doses for prolonged periods. [7][8][9][10][11][12] Relapses were common after therapy unless HBsAg was cleared, which occurred uncommonly. 13 Interferon alfa therapy is also expensive, difficult to administer, and often poorly tolerated. Thus, current options for therapy of chronic delta hepatitis are limited.Other antiviral agents have been used in chronic delta hepatitis, but results have been limited. Both ribavirin and levamisole appear ineffective. 14,15 Recently, lamivudine (3-thiacytidine), an oral nucleoside analogue, has been shown to have inhibitory effe...

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“…15 Histopathologically, a chronic active hepatitis or active cirrhosis is demonstrated in 90% of all superinfected cases of all ages. 16 At the present time, it is believed that hepatocellular carcinoma is rare in patients with chronic hepatitis delta virus infection. This may relate to the fact that these patients have a more rapidly progressive form of liver disease and therefore do not live long enough to produce hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Anti-Delta-Virus Antibody in Sera Positive for Hepatitis B Surface Antigen in Male Saudi Blood Donors

1989

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Anti-delta-virus antibody was determined by radioimmunoassay technique in 490 healthy male Saudi blood donors with serum positive for hepatitis B surface antigen. The presence of anti-delta-virus antibody was demonstrated in 11.2% (55/490) of donor sera. This is considerably higher than the reported incidence of 3.8%, 0.5%, and 5% from the United States, Canada, and Italy, and 8%, 6.7%, and 5.4% from Saudi Arabia in healthy HBsAg-positive blood donor sera.

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Chronic Hepatitis in Carriers of Hepatitis B Surface Antigen, with Intrahepatic Expression of the Delta Antigen

Cited by 349 publications

References 12 publications

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

Lamivudine for chronic delta hepatitis

Anti-Delta-Virus Antibody in Sera Positive for Hepatitis B Surface Antigen in Male Saudi Blood Donors

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