The Natural History of Asymptomatic Hepatitis B Surface Antigen Carriers

Franchis, Roberto de; Meucci, Gianmichele; Vecchi, Maurizio; Tatarella, M.; Colombo, Massimo; Ninno, E. Del; Rumi, Maria Grazia; Donato, Maria Francesca; Ronchi, G.

doi:10.7326/0003-4819-118-3-199302010-00006

Cited by 257 publications

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“…Six subjects belonged to a previously well characterized study group of chronic healthy HBsAg carriers with normal liver histology and inhibited HBV replication. 3,4,6 All HBsAg-positive subjects were negative for hepatitis B e antigen (HBeAg) and positive for the corresponding antibody (anti-HBe), as usually observed in chronic HBsAg carriers in our geographic area. 21,22 In both HDV-infected patients and healthy HBsAg carriers circulating HBV genomes could be detected by polymerase chain reaction (PCR) amplification performed following previously described methods.…”

Section: Patientsmentioning

confidence: 99%

“…Consequently, HBsAg-positive patients with suppressed viral replication and undetectable levels of viremia have usually low grade or absence of hepatocellular injury. [2][3][4] Nevertheless, several observations suggest that an undefined amount of free viral genomes may persist into the hepatocytes of these subjects, 5,6 and such episomal HBV forms might be implicated in the reactivation of silent infections that may occur either spontaneously [7][8][9] or in conditions of immunosuppression, [10][11][12] or, in patients treated with antiviral drugs, after stopping therapy. [13][14][15][16][17] Thus, analysis and quantification of intrahepatic HBV genomes appear to be of biological interest and may provide useful clinical information.…”

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confidence: 99%

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Quantification of intrahepatic hepatitis B virus (HBV) DNA in patients with chronic HBV infection

et al. 2000

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No data are available about the amount of hepatitis B virus (HBV) genomes in liver of patients with chronic HBV infection. The aim of this study was to quantify the intrahepatic HBV DNA in hepatitis B surface antigen (HBsAg)-positive patients with either active or suppressed viral replication and in HBsAg-negative subjects with occult HBV infection. We optimized the Roche ''Amplicor HBV Monitor'' kit for quantifying liver HBV DNA and analyzed hepatic DNA extracts and serum samples from 19 HBs-Ag-positive and 43 HBsAg-negative individuals. Eight of the HBsAg carriers had active HBV replication, and for 3 of them we analyzed samples obtained before and at the end of 1 year of lamivudine treatment. Five hepatitis Delta virus (HDV) coinfected patients and 6 healthy HBsAg carriers had inhibited HBV activity. Among the HBsAg-negative subjects 21 had occult HBV infection and 22 had no evidence of HBV infection. The median of HBV genomes per microgram of liver DNA milliliter of serum was 34,500 to 2,620,000 in patients with active viral replication, 20,000 to 3,900,000 before and 10,000 to 2,800 at the end of therapy in lamivudine-treated individuals, 9,800 to 600 in HDVinfected individuals, and 7,450 to 17,400 in healthy HBsAg carriers. These data indicate that cases with suppressed HBV activity, despite the very low levels of viremia, maintain a relatively high amount of intrahepatic viral genomes. This virus reservoir is likely involved in HBV reactivation, which is usually observed after stopping lamivudine treatment. Finally, the analysis of cases with occult HBV infection showed that the assay we used was able to specifically detect and quantify as few as 100 copies of viral genomes per microgram of liver DNA. (HEPATOLOGY 2000;31: 507-512.)Hepatitis B virus (HBV) is a major health problem worldwide and it is estimated that 350 million individuals are chronically infected with this virus. 1 Chronic HBV infection may be associated with a large spectrum of clinical forms ranging from the status of healthy carrier of hepatitis B surface antigen (HBsAg) to a moderate or severe chronic hepatitis susceptible of evolution to cirrhosis and development of hepatocellular carcinoma (HCC). 1 HBV-induced liver damage is strictly related with virus active replication, which is usually investigated detecting serum viral DNA by direct hybridization techniques. Consequently, HBsAg-positive patients with suppressed viral replication and undetectable levels of viremia have usually low grade or absence of hepatocellular injury. 2-4 Nevertheless, several observations suggest that an undefined amount of free viral genomes may persist into the hepatocytes of these subjects, 5,6 and such episomal HBV forms might be implicated in the reactivation of silent infections that may occur either spontaneously 7-9 or in conditions of immunosuppression, [10][11][12] or, in patients treated with antiviral drugs, after stopping therapy. [13][14][15][16][17] Thus, analysis and quantification of intrahepatic HBV genomes appear to be of biological inter...

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Section: Patientsmentioning

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Quantification of intrahepatic hepatitis B virus (HBV) DNA in patients with chronic HBV infection

et al. 2000

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“…15,41 Very little longitudinal data is available on the latter patients, but liver disease is generally present in patients with high HBV DNA levels. 30,32,42 Among adults in Asia and the Oceania with elevated ALT levels and carriers of all ages with childhood or adult-acquired HBV infection, the rate of clearance of HBeAg averages between 8% and 12% per year. [29][30][31][32][33]43 The rate of clearance of HBeAg is much lower in Asian children (most of whom have normal ALT levels) 34,35 and in immunocompromised subjects.…”

Section: Terminology and Natural History Of Chronic Hbv Infectionmentioning

confidence: 99%

Chronic hepatitis B

2001

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PREAMBLEThese guidelines have been written to assist physicians and other health care providers in the recognition, diagnosis, and management of patients chronically infected with the hepatitis B virus (HBV). They are intended to suggest preferable approaches to the clinical management of chronic hepatitis B. The recommendations are flexible and are not intended as the only acceptable approach to management and treatment. As the appropriate course of treatment will vary in light of the relevant facts and circumstances surrounding each individual patient with chronic hepatitis B, guidelines are not intended to define the applicable standard of medical care and may be updated periodically as new information becomes available.These guidelines were developed under the auspices of, and approved by, the Practice Guidelines Committee of the American Association for the Study of Liver Diseases. They should be taken as guidelines and not "standards of care." Data used to support the recommendations made were obtained by a literature search of peer-reviewed articles concerning the natural history, diagnosis, and treatment of chronic hepatitis B. In addition, the proceedings of a recent National Institutes of Health workshop on the "Management of Hepatitis B" were considered in the development of these guidelines. 1 The strength of each recommendation is categorized based on the quality of evidence in the literature according to the rating system indicated in Table 1. 2

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“…53 Other European and US studies based upon HBV carriers have confirmed this results. [54][55][56][57][58] In our study, it is reasonable to expect a low number of subjects with liver disease at entry of the cohort, because all subjects were screened volunteer blood donors. In fact, the risk of death from liver disease in our cohort was higher in the second decade of follow-up than in the first, suggesting that most of the HBV carriers were healthy at the entry of the cohort.…”

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Cofactors associated with liver disease mortality in an HBsAg‐positive Mediterranean cohort: 20 years of follow‐up

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et al. 2006

Intl Journal of Cancer

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The risk of developing liver cancer in hepatitis B virus (HBV) carriers differs across geographical areas, suggesting that exposure to other risk factors may contribute to HBV‐linked cancer risk. Our study estimates the mortality due to liver disease and the role of other risk factors in a Spanish HBV cohort. 2,352 hepatitis B surface antigen (HBsAg)‐positive and 15,504 HBsAg‐negative subjects were identified among blood donors during 1972–1985 and were followed until December 2000 through the Mortality Registry. Clinical examination and an epidemiological questionnaire were performed on 1,000 HBsAg‐positive survivors during 1994–1996. In subjects deceased from liver disease, medical records were revised and relatives were interviewed. A nested case‐control analysis was conducted comparing both groups. In HBsAg‐positive men, an excess mortality from liver cancer [standardized mortality ratio (SMR): 14.1; 7.7–23.6], cirrhosis (SMR: 10.5; 7.0–15.1), haematological neoplasms (SMR: 3.2; 1.2–6.9) and AIDS was detected (SMR: 5.5; 2.2–11.4). In women, an excess was found for cirrhosis (SMR: 7.2; 1.4–21.1). Progression factors to liver disease were alcohol intake [odds ratio (OR): 6.3; 3.1–12.8], diabetes (OR: 3.6; 1.3–9.6), HBV replication (OR: 50.0; 14.9–167.3) and hepatitis C virus (HCV) infection (OR: 27.4; 7.1–107.7). In conclusion, in Spain after 20 years of follow‐up, chronic HBV exposure appears as a major risk factor for liver cancer among men and for cirrhosis in both sexes. The risk of death from liver disease among HBV carriers with the presence of HBV replication, HCV, alcohol consumption and diabetes was significantly increased and suggests synergism among these exposures and HBV. Mortality from haematological neoplasms was detected and could be associated to HIV coinfection. These results support screening and adequate follow‐up among HBsAg‐positive subjects at high risk to develop liver disease, particularly when these risk cofactors are present. © 2006 Wiley‐Liss, Inc.

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The Natural History of Asymptomatic Hepatitis B Surface Antigen Carriers

Abstract: Italian HBsAg carriers with initially normal liver function tests have an excellent prognosis: Delta superinfection is infrequent and the risk for developing hepatocellular carcinoma is low.

Cited by 257 publications

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Quantification of intrahepatic hepatitis B virus (HBV) DNA in patients with chronic HBV infection

Quantification of intrahepatic hepatitis B virus (HBV) DNA in patients with chronic HBV infection

Chronic hepatitis B

Cofactors associated with liver disease mortality in an HBsAg‐positive Mediterranean cohort: 20 years of follow‐up

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