Serum hepatitis B surface antigen and hepatitis B e antigen titers: Disease phase influences correlation with viral load and intrahepatic hepatitis B virus markers

Thompson, Alexander; Nguyen, Thang; Iser, David; Ayres, Anna; Jackson, Kathy Merlock; Littlejohn, Margaret; Slavin, John; Bowden, Scott; Gane, Edward; Abbott, William G.H.; Lau, George; Lewin, Sharon R.; Visvanathan, Kumar; Desmond, Paul; Locarnini, Stephen

doi:10.1002/hep.23571

Cited by 376 publications

(373 citation statements)

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“…17,[19][20][21] Most recently, a thorough investigation that included both qHBsAg and qHBeAg was conducted to identify their relationship with intrahepatic markers of HBV replication, and it suggested potential practical implications for these quantitative serological markers. 24 Our study is the first to report serial qHBeAg values in patients on ETV therapy. We have shown that a decline in qHBeAg is highly predictive for SR with sensitivity and specificity values as high as 75.0% and 89.8%, respectively.…”

Section: Discussionmentioning

confidence: 84%

“…First, the mechanism of action of oral nucleos(t)ide analogues is the suppression of viral replication through inhibition of HBV polymerase; because HBsAg production proceeds by a pathway distinct from that of HBV DNA, the effect of ETV on qHBsAg is possibly less prominent. 24 Second, the HBV genotype seems to play a major role in qHBsAg. In a large series of retrospective data by Gish et al, 16 less HBsAg loss was seen in patients with genotype C (0.5%, 1/201) versus patients with genotype A (7.7%, 15/194) or D (8.1%, 7/79).…”

Section: Discussionmentioning

confidence: 99%

“…Briefly, qHBeAg was measured with an automated microparticle chemiluminescent immunoassay based on a previously described method. 18,21,24 Although this commercial HBeAg kit is not marketed as a quantitative assay, it produces a signal-to-cutoff ratio that is linear within a restricted range. The HBeAg reference preparation, which had a defined HBeAg activity of 100 Paul Ehrlich (PE) IU/mL, was obtained from the Paul Ehrlich Institute (Langen, Germany).…”

Section: Methodsmentioning

confidence: 99%

“…22,23 These studies have demonstrated significant differences in qHBsAg across the different phases of HBV infection over a long time period. Moreover, Thompson et al 24 reported differences in the correlations between qHBsAg and HBV DNA in HBeAg(þ) patients and HBeAg(À) patients in conjunction with qHBeAg. Their results have provided new insights into viral pathogenesis.…”

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confidence: 99%

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Quantitative hepatitis B surface antigen and hepatitis B e antigen titers in prediction of treatment response to entecavir

et al. 2011

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Quantitative hepatitis B surface antigen (qHBsAg) and quantitative hepatitis B e antigen (qHBeAg) titers are emerging as useful tools for measuring viral loads and for predicting the virological response (VR) and serological response (SR) to pegylated interferon therapy. However, the clinical utility of these assays in patients taking entecavir (ETV) is largely unknown. Treatment-naive patients with chronic hepatitis B (CHB) who were taking ETV for 2 years were enrolled. The qHBsAg and qHBeAg levels were serially measured with the Architect assay. From 95 patients, 60.0% of whom were hepatitis B e antigen-positive [HBeAg(1)], 475 samples were analyzed. The median baseline log hepatitis B virus (HBV) DNA, log qHBsAg, and log qHBeAg values were 6.73 copies/mL (4.04-9.11 copies/mL), 3.58 IU/mL (1.17-5.10 IU/ mL), and 1.71 Paul Ehrlich (PE) IU/mL (20.64 to 2.63 PE IU/mL), respectively. For the prediction of VR (HBV DNA < 60 copies/mL at 24 months) in HBeAg(1) patients, baseline alanine aminotransferase (P 5 0.013), HBV DNA (P 5 0.040), and qHBsAg levels (P 5 0.033) were significant. For the prediction of VR, the area under the curve for the baseline log qHBsAg level was 0.823 (P < 0.001); a cutoff level of 3.98 IU/mL (9550 IU/mL on a nonlogarithmic scale) yielded the highest predictive value with a sensitivity of 86.8% and a specificity of 78.9%. As for SR (HBeAg loss at 24 months), the reduction of qHBeAg was significantly greater in the SR(1) group versus the SR(2) group. The sensitivity and specificity were 75.0% and 89.8%, respectively, with a decline of 1.00 PE IU/mL at 6 months. With ETV therapy, the correlation between HBV DNA and qHBsAg peaked at 6 months in HBeAg(1) patients. Conclusion: Both qHBsAg and qHBeAg decreased significantly with ETV therapy. The baseline qHBsAg levels and the on-treatment decline of qHBeAg in HBeAg(1) patients were proven to be highly useful in predicting VR and SR, respectively. The determination of qHBsAg and qHBeAg can help us to select the appropriate strategy for the management of patients with CHB. However, the dynamic interplay between qHBsAg, qHBeAg, and HBV DNA during antiviral therapy remains to be elucidated. (HEPATOLOGY 2011;53:1486-1493 C hronic infection with hepatitis B virus (HBV) is a worldwide health problem, with more than 400 million people thought to be infected.Moreover, these patients are at increased risk for disease progression to cirrhosis and hepatocellular carcinoma. 1 Large cohort studies have shown that elevated levels of Abbreviations: ALT, alanine aminotransferase; anti-HBs, antibody to hepatitis B surface antigen; AUC, area under the curve; AUROC, area under the receiver operating characteristic

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Quantitative hepatitis B surface antigen and hepatitis B e antigen titers in prediction of treatment response to entecavir

et al. 2011

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“…The level of serum HBsAg has been shown to reflect the level and transcriptional activity of covalently closed circular (ccc) DNA [6]. However, among HBeAg-negative patients, the relationship between serum HBsAg level and cccDNA is much weaker than that in HBeAg-positive patients [7]. The exact reason for this observation is uncertain, but could be related to the production of HBsAg by integrated HBV surface gene fragments in the host chromosome or the uncoupling on the regulation of HBsAg and HBV DNA production after HBeAg seroconversion.…”

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confidence: 99%

Are we ready to use the hepatitis B surface antigen level to guide peginterferon treatment in HBeAg-negative chronic hepatitis B?

Chan

2012

Hepatol Int

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In chronic hepatitis B virus (HBV) infection, hepatitis B e antigen (HBeAg) seroconversion often indicates host immune clearance. Approximately 30 % of patients, however, still have active viremia and fluctuating alanine aminotransferase (ALT) levels in the HBeAg-negative phase [1]. These patients with HBeAg-negative chronic hepatitis B probably have an immune escape by the virus; a further attempt of immune modulator therapy by interferon might be difficult and the post-treatment relapse rate is high. Early experience in Europe using 12-month interferon-alpha combined with lamivudine only yielded a sustained viral suppression (undetectable by nonpolymerase chain reaction assay) rate of approximately 15 % at 6-12 months post-treatment [2,3]. With 12-month peginterferon alfa-2a with/without lamivudine combination in the phase III international trial for HBeAg-negative chronic hepatitis B, approximately 22.6 % of patients could achieve sustained viral suppression to B10,000 copies/ml at 3-year post-treatment [4]. Owing to the inconvenient subcutaneous route of administration, potential adverse effects, and a high drug cost of peginterferon, one should select patients who have a higher chance of response to the peginterferon therapy. On the other hand, peginterferon is not preferred or should be stopped earlier if the chance of response is too low.On post hoc analysis of the phase III trial of peginterferon alfa-2a (with/without lamivudine combination), HBeAg-negative patients at a younger age and those who had lower HBV DNA at baseline had a higher chance of achieving a response, which was defined as HBV DNA B20,000 copies/ml at 24-week post-treatment [5]. Patients infected by genotype C HBV also have a better response than those infected by genotype D HBV. Nonetheless, the differences in response between patients with different baseline predictive factors were too small to guide patient selection for treatment. For example, the mean baseline HBV DNA was 7

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Associations Between Hepatitis B Virus Infection and Risk of All Cancer Types

et al. 2019

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Key Points Question Is chronic hepatitis B virus infection associated with a higher risk of any cancer type when compared with individuals without hepatitis B virus? Findings This population-based cohort study of 496 732 Chinese individuals found that hepatitis B surface antigen seropositivity was associated with the risk of hepatocellular carcinoma, stomach cancer, colorectal cancer, oral cancer, pancreatic cancer, and lymphoma. The associations were validated in an independent population and tissue-based studies. Meaning Chronic hepatitis B virus infection was associated with nonliver cancer, especially digestive system cancers.

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Serum hepatitis B surface antigen and hepatitis B e antigen titers: Disease phase influences correlation with viral load and intrahepatic hepatitis B virus markers

Cited by 376 publications

References 33 publications

Quantitative hepatitis B surface antigen and hepatitis B e antigen titers in prediction of treatment response to entecavir

Quantitative hepatitis B surface antigen and hepatitis B e antigen titers in prediction of treatment response to entecavir

Are we ready to use the hepatitis B surface antigen level to guide peginterferon treatment in HBeAg-negative chronic hepatitis B?

Associations Between Hepatitis B Virus Infection and Risk of All Cancer Types

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