Serum hepatitis B virus DNA levels differentiating inactive carriers from patients with chronic hepatitis B

Seo, Yasushi; Yoon, Seitetsu; Truong, Bui Xuan; Kato, Hirotaka; Hamano, Kenichi; Kato, Miyuki; Yano, Yoshihiko; Katayama, Megumi; Ninomiya, Toshiaki; Hayashi, Yoshitake; Kasuga, Masato

doi:10.1097/01.meg.0000170926.83850.dd

Cited by 16 publications

(10 citation statements)

References 19 publications

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“…According to the American and European guidelines [34,35], the differentiation between the inactive and active phases of HBeAg-negative CHB is based on an HBV DNA cut-off set up at 2000 IU/ml. This cut-off has led to several controversial reports [30,[36][37][38].…”

Section: Current Evidencementioning

confidence: 99%

Hepatitis B surface antigen quantification: Why and how to use it in 2011 – A core group report

Chan

Thompson

Martinot–Peignoux

et al. 2011

Journal of Hepatology

299

272

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Quantitative HBsAg had been suggested to be helpful in management of HBV, but assays were cumbersome. The recent availability of commercial quantitative assays has restarted the interest in quantitative serum hepatitis B surface antigen (HBsAg) as a biomarker for prognosis and treatment response in chronic hepatitis B. HBsAg level reflects the transcriptional activity of cccDNA rather than the absolute amount of cccDNA copies. Serum HBsAg level tends to be higher in hepatitis B e antigen (HBeAg)-positive than HBeAg-negative patients. Among patients with a low HBV DNA (<2000IU/ml), HBsAg <1000IU/ml in genotype D HBV infection and HBsAg <100IU/ml in genotype B/C HBV infection is associated with inactive carrier state in HBeAg-negative patients. The HBsAg reduction by nucleos(t)ide analogues (NA) is not as pronounced as by interferon treatment. On peginterferon treatment, sustained responders tend to show greater HBsAg decline than the non-responders. The optimal on-treatment HBsAg cutoff to predict response needs further evaluation in HBeAg-positive patients, but an absence of HBsAg decline together with a <2 log reduction in HBV DNA at week 12 can serve as stopping rule in HBeAg-negative patients with genotype D HBV infection. A rapid serum HBsAg decline during NA therapy may identify patients who will clear HBsAg in the long-term. There are early reports among Asian patients that an HBsAg level of <100IU/ml might predict lower risk of relapse after stopping NA treatment. In clinical practice, serum HBsAg level should be used together with, but not as a substitute for, HBV DNA.

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Section: Current Evidencementioning

confidence: 99%

Hepatitis B surface antigen quantification: Why and how to use it in 2011 – A core group report

Chan

Thompson

Martinot–Peignoux

et al. 2011

Journal of Hepatology

299

272

View full text Add to dashboard Cite

show abstract

“…HBV DNA levels are not primary determinants of therapy, because viral loads are not necessarily reflective of disease severity. Median viral loads in inactive chronic hepatitis B are lower than in HBeAg-positive patients; however, there is some overlap in viral load between individuals in these phases (66,96,129). Cirrhosis has also been observed in patients with low viral loads (Ͻ2,000 IU/ml) (160).…”

Section: Quantitative Hbv Dna Assays: Utilitymentioning

confidence: 99%

Molecular Testing in the Diagnosis and Management of Chronic Hepatitis B

Valsamakis

2007

Clin Microbiol Rev

137

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SUMMARY Hepatitis B virus (HBV) is an enveloped virus with a small (3.2-kb) partially double-stranded DNA genome that causes acute and chronic infections. The impact of these infections on public health worldwide is enormous, with an estimated prevalence of 2 billion acute infections and 360 million chronic infections globally. This review focuses on chronic hepatitis B and the molecular assays used in its diagnosis and management. Background information, including that about features of the hepatitis B virion, viral replication, and epidemiology of infection, that is important for understanding chronic hepatitis B and molecular diagnostic tests for HBV is provided. To facilitate an understanding of the utility of molecular testing for chronic hepatitis B, the four stages of chronic hepatitis B infection that are currently recognized, as well as an additional entity, occult hepatitis B, that can be diagnosed only by sensitive nucleic acid amplification methods, are reviewed in detail, including available therapeutic agents. The molecular diagnostic content focuses on tests for HBV DNA quantification, genotyping, and mutation detection (including precore/core promoter and antiviral resistance mutations). The discussion of these tests encompasses their current utility and performance characteristics, drawing from current clinical guidelines and other studies from the literature. In recognition of the continual evolution of this field, the final section describes emerging molecular markers with future diagnostic potential.

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“…Differentiation between CHB and IC state is based on HBV DNA cutoff value of 2000 IU/mL. This cutoff value may be misleading in some instances (Feld et al, 2007;Seo et al, 2005). Recently, HBsAg quantification assay has been proposed to help the differentiation of these clinical scenarios (Martinot-Peignoux et al, 2010).…”

Section: Discussionmentioning

confidence: 98%

Can serum level of HBsAg differentiate HBeAg-negative chronic hepatitis B from inactive carrier state?

Sali

Sharafi

Alavian

et al. 2015

Diagnostic Microbiology and Infectious Disease

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Serum hepatitis B virus DNA levels differentiating inactive carriers from patients with chronic hepatitis B

Abstract: The measurement of serum HBV DNA more than twice is useful for assessing chronic hepatitis B surface antigen carriers and confirms that 10 copies/ml may be an appropriate level of HBV for characterizing the inactive carrier state.

Cited by 16 publications

References 19 publications

Hepatitis B surface antigen quantification: Why and how to use it in 2011 – A core group report

Hepatitis B surface antigen quantification: Why and how to use it in 2011 – A core group report

Molecular Testing in the Diagnosis and Management of Chronic Hepatitis B

Can serum level of HBsAg differentiate HBeAg-negative chronic hepatitis B from inactive carrier state?

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