Quantification of serum hepatitis B surface antigen: is it useful for the management of chronic hepatitis B?

Janssen, Harry L.A.; Sonneveld, Milan J.; Brunetto, Maurizia Rossana

doi:10.1136/gutjnl-2011-301096

Cited by 66 publications

(60 citation statements)

References 46 publications

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“…Comparing the kinetics of the different HBV-markers according to response to Peg-IFN we found (Fig 3) that the decline of total-anti-HBc during therapy parallels that of HBV-DNA and this may be useful in clinical practice to confirm the effectiveness of Peg-IFN antiviral activity. However, during Peg-IFN-treatment total-anti-HBc is unable to distinguish REL from SVR who are instead identified better by HBsAg-kinetics as reported previously [17][18][19][20]. During NUC therapy the kinetics of total anti-HBc differ from those of the other HBV markers and the total-anti-HBc decline provides an added value to HBV-DNA and HBsAg monitoring beckoning the remission of HBV-induced liver damage under effective antiviral therapy.…”

Section: Discussionmentioning

confidence: 74%

“…HBV genotyping was performed by direct sequencing of small-HBs-region (17). Anti-HBc was measured using the newly developed double-antigen sandwich immune-assay (Wantai, Beijing, China) calibrated using WHO standards (NIBSC, UK) as previously reported [17][18][19]. Total anti-HBc levels were reported in IU/mL.…”

Section: Serological Testsmentioning

confidence: 99%

“…Thus, a satisfactory non-invasive marker of HBV-induced liver disease in chronic HBV infection remains an unmet need. In clinical practice the combined quantification of serum HBV-DNA and HBsAg is currently used to discriminate HBeAg-negative-CHB from inactive infection and to monitor the switch from CHB to inactive-carrier during antiviral therapy [17][18][19][20]. However, in HBeAgnegative CHB patients undergoing antiviral treatment HBsAg kinetics vary according to HBV genotype and genotype-specific monitoring timeframes and end-of-treatment thresholds have yet to be standardized for a proper response-guided treatment 19].…”

Section: Introductionmentioning

confidence: 99%

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Total hepatitis B core antigen antibody, a quantitative non-invasive marker of hepatitis B virus induced liver disease

Moriconi

Yuan

Song

et al. 2015

Digestive and Liver Disease

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Non invasive immunologic markers of virus-induced liver disease are unmet needs. We tested the clinical significance of quantitative total and IgM-anti-HBc in well characterized chronic-HBsAg-carriers. Sera (212) were obtained from 111 HBsAg-carriers followed-up for 52 months (28-216) during different phases of chronic-HBV-genotype-D-infection: 10 HBeAg-positive, 25 inactive-carriers (HBV-DNA2000IU/ml, ALT<30U/L), 66 HBeAg-negative-CHB-patients and 10 with HDV-super-infection. In 35 patients treated with Peg-IFN ±nucleos(t)ide-analogues (NUCs) sera were obtained at baseline, end-of-therapy and week-24-off-therapy and in 22 treated with NUCs (for 60 months, 42-134m) at baseline and end-of-follow-up. HBsAg and IgM-anti-HBc were measured by Architect-assays (Abbott, USA); total-anti-HBc by double-antigen-sandwich-immune-assay (Wantai, China); HBV-DNA by COBAS-TaqMan (Roche, Germany). Total-anti-HBc were detectable in all sera with lower levels in HBsAg-carriers without CHB (immune-tolerant, inactive and HDV-superinfected, median 3.26, range 2.26-4.49 Log 10 IU/ml) versus untreated-CHB (median 4.68, range 2.76-5.54 Log 10 IU/ml), p<0.0001. IgM-anti-HBc positive using the chronic-hepatitis-cut-off" (0.130-S/CO) were positive in 102 of 212 sera (48.1%). Overall total-anti-HBc and IgM-anti-HBc correlated significantly (p<0.001, r=0.417). Total-anti-HBc declined significantly in CHB patients with response to Peg-IFN (p<0.001) and in NUCtreated patients (p<0.001); the lowest levels (median 2.68, range 2.12-3.08 Log 10 IU/ml) were found in long-term responders who cleared HBsAg subsequently. During spontaneous and therapy-induced fluctuations of CHB (remissions and reactivations) total-and IgM-anti-HBc correlated with ALT (p<0.001, r=0.351 and p=0.008, r=0.185 respectively). Total-anti-HBc qualifies as a useful marker of HBV-induced-liver-disease that might help to PLOS ONE |

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Section: Discussionmentioning

confidence: 74%

Section: Serological Testsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Total hepatitis B core antigen antibody, a quantitative non-invasive marker of hepatitis B virus induced liver disease

Moriconi

Yuan

Song

et al. 2015

Digestive and Liver Disease

View full text Add to dashboard Cite

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“…Serum HBsAg can not only reflect the activity of virus replication indirectly, but also evaluate the damage of hepatocytes in CHB [19,20] . Owing to the fact that a rapid on-treatment decline of serum HBsAg levels predicts the effects of anti-HBV therapy [21] , such as HBeAg serological conversion and HBsAg clearance, the dynamic monitoring of HBsAg is absolutely an indispensible indicator during the process of individualized therapy and follow-up [22] . HBeAg-negative CHB patients are older and have more advanced liver disease since these patients represent a later stage in the natural course of chronic HBV infection [11,12] .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of changes of serum hepatitis B surface antigen from a different perspective

Tan

Liu

et al. 2015

WJG

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AIM:To investigate the dynamic changes of serum hepatitis B surface antigen (HBsAg) levels apportioned by the same hepatic parenchyma cell volume (HPCV), namely, hepatic cell quantities. METHODS:Serum HBsAg levels were detected by electrochemiluminescence and serum HBsAg levels apportioned by the same HPCV were figured out according to the theory of sphere geometry. HBsAg levels were compared among different liver inflammation grades, as well as different hepatic fibrosis stages. RESULTS:In hepatitis B e antigen-negative chronic hepatitis B, serum HBsAg levels in liver histological inflammation grades 1-4 were 3.66 ± 0.40, 3.74 ± 0.35, 3.74 ± 0.26 and 3.71 ± 0.34 log10 COI (cut off index), respectively, and there were no differences before apportion (P = 0.640). Serum HBsAg levels apportioned by the same HPCV were 5.57 ± 0.62, 5.98 ± 0.65, 6.59 ± 0.50 and 6.81 ± 0.84 log10 COI, respectively, and there were significant differences after apportion (P < 0.001). Serum HBsAg levels in hepatic fibrosis stages Ⅰ-Ⅳ were 3.66 ± 0.43, 3.75 ± 0.33, 3.71 ± 0.28 and 3.75 ± 0.26 log10 COI, respectively, and there were no differences before apportion (P = 0.513). Serum HBsAg levels apportioned by the same HPCV were 5.53 ± 0.66, 5.98 ± 0.53, 6.29 ± 0.46 and 7.06 ± 0.48 log10 COI, respectively, and there were significant differences after apportion (P < 0.001).CONCLUSION: Serum HBsAg levels apportioned by the same HPCV (hepatic cell quantities), rather than serum HBsAg levels, increase with liver inflammation grades and hepatic fibrosis stages. Core tip: Hepatitis B surface antigen (HBsAg)-negative chronic hepatitis B patients always feature increasing liver fibrosis and decreasing hepatic parenchyma cells. Does it influence the circulating HBsAg released into the serum? It requires research on the condition that the impact of fibrous volume on hepatic cell quantities should be deducted. It turns out that there were significant differences in serum HBsAg levels apportioned by the same hepatic cell quantities among different liver histological inflammation grades, as well as different hepatic fibrosis stages. In conclusion, although hepatitis B virus replication place -hepatic cell quantities -were shrinking while fibrosis progresses, its replication and expression became more active rather than declined or silenced.Wu ZQ, Tan L, Liu T, Gao ZL, Ke WM. Evaluation of changes of serum hepatitis B surface antigen from a different perspective.

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“…Increasing evidence suggests that HBsAg levels at weeks 12 and 24 of treatment with Peg-IFN-␣ are important in predicting treatment response (23,24). The results of a large multicenter study in treatment-naive HBeAg-positive patients suggest that week 12 stopping rules should be based on the HBV genotype and that all patients with HBsAg levels of Ͼ20,000 IU/ml at 24 weeks should stop Peg-IFN-␣ therapy (25).…”

Section: Discussionmentioning

confidence: 99%

Sequential Combination Therapy with Pegylated Interferon Leads to Loss of Hepatitis B Surface Antigen and Hepatitis B e Antigen (HBeAg) Seroconversion in HBeAg-Positive Chronic Hepatitis B Patients Receiving Long-Term Entecavir Treatment

Chen

et al. 2015

Antimicrob Agents Chemother

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e Nucleos(t)ide analogues rarely result in a durable off-treatment response in chronic hepatitis B infection, whereas pegylated interferon (Peg-IFN) induces a long-lasting response only in a subset of patients. We assessed the effect of sequential combination therapy with Peg-IFN-␣2a and entecavir in hepatitis B e antigen (HBeAg)-positive patients with prior long-term entecavir therapy and investigated the predictors of response to treatment. HBeAg-positive individuals who did not achieve HBeAg seroconversion during previous long-term entecavir therapy, receiving Peg-IFN-␣2a added to ongoing entecavir therapy (sequential combination [S-C] therapy; n ‫؍‬ 81) for 48 weeks or remaining on entecavir monotherapy (n ‫؍‬ 116), were retrospectively included. A matched pair was created at a 1:1 ratio from each treatment group. The primary endpoint was HBeAg seroconversion at week 48. Subgroup analysis of response prediction was conducted for 81 patients with S-C therapy. More patients in the S-C therapy group achieved HBeAg seroconversion than those in the entecavir group (44% versus 6%; P < 0.0001). An HBeAg level of <200 signal-to-cutoff ratio (S/CO) at baseline was a strong predictor for higher HBeAg seroconversion than that achieved when HBeAg was >200 S/CO (64.2% versus 17.9%; P < 0.0001). Hepatitis B surface antigen (HBsAg) levels at baseline and the decrease in HBsAg levels predicted HBsAg loss in the S-C therapy group. The combination of baseline HBeAg of <200 S/CO and HBsAg of <1,000 IU/ml and an HBsAg decline at week 12 of >0.5 log 10 IU/ml provided the highest rate of HBeAg seroconversion (92.31%) and HBsAg loss (83.3%) at week 48. Patients receiving sequential combination therapy have a higher rate of HBeAg seroconversion and are more likely to experience HBsAg clearance than do those continuing entecavir monotherapy. Sequential combination therapy can be guided by baseline HBsAg/HBeAg levels and on-treatment HBsAg dynamics. Hepatitis B virus (HBV) infection is endemic in Asia, the Pacific islands, Africa, Southern Europe, and Latin America, and chronic hepatitis B (CHB) is a global health threat. There are approximately 350 million chronic HBV surface antigen (HBsAg) carriers worldwide (1). Patients with CHB have an increased risk of developing cirrhosis, hepatic decompensation, and hepatocellular carcinoma (HCC), which results in about 1 million deaths per year (2). Antiviral treatment is effective in halting progression of CHB in many patients. Two classes of antiviral agents are available: nucleos(t)ide analogues (NUCs), such as entecavir (ETV), which inhibit the viral polymerase and interfere with viral replication, and interferon alpha (IFN-␣), including conventional and pegylated forms, which has antiviral and immunomodulatory effects (3). NUCs are effective in most patients but must be continued indefinitely in the patients that do not achieve hepatitis B e antigen (HBeAg) seroconversion. In contrast, a finite course of pegylated IFN-␣ (Peg-IFN-␣) can induce a long-lasting therapeutic response, but on...

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Quantification of serum hepatitis B surface antigen: is it useful for the management of chronic hepatitis B?

Cited by 66 publications

References 46 publications

Total hepatitis B core antigen antibody, a quantitative non-invasive marker of hepatitis B virus induced liver disease

Total hepatitis B core antigen antibody, a quantitative non-invasive marker of hepatitis B virus induced liver disease

Evaluation of changes of serum hepatitis B surface antigen from a different perspective

Sequential Combination Therapy with Pegylated Interferon Leads to Loss of Hepatitis B Surface Antigen and Hepatitis B e Antigen (HBeAg) Seroconversion in HBeAg-Positive Chronic Hepatitis B Patients Receiving Long-Term Entecavir Treatment

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