Monday, February 19, 2024

Hepatitis B Core Antibody Positive

Hbc Antibody Positive/hbs Antigen Negative/hbs Antibody Positive

Hepatitis B Serology: Surface Antigen (HBsAg), Surface Antibody (anti-HBs), Core Antibody (anti-HBc)

There are reports of HBV reactivation in HBc-ab negative/HBs-ag positive/HBs-ab positive cases, and reactivation occurred in 6.9% of them. HBV reactivation in HBc antibody negative/HBs antigen negative/HBs antibody positive cases has also been reported , and reactivation was reported in 3.4% of them.

Particular attention must be paid to patients with < 300 mIU/mL of HBs antibody during maintenance treatment with rituximab since the HBs antibody status might become negative .

Since HBV reactivation was reported even in patients with a high HBs antibody titer, HBs antibody follow-up is not sufficient for detecting the occurrence of reactivation. Monthly follow-up for the presence of HBV-DNA is necessary during treatment.

Administration Of Nucleoside Analogs Upon Hbv Reactivation

We must evaluate whether to discontinue nucleoside analog administration in patients receiving those drugs that promote HBV reactivation. Since HBs antibody might become negative during rituximab treatment, discontinuation should be considered after the treatments completion. An additional problem exists with regard to determining the duration of the discontinuation period. Cases of HBV reactivation even after long periods of discontinuation have been documented. For example, even after HBs antibody became temporarily positive, it disappeared later and HBV reactivation was induced. If nucleoside analog treatment is given to HBs antibody negative patients who later become antibody positive, such treatment can be discontinued. On the other hand, HBV vaccination is unable to suppress HBV reactivation. If rituximab is administered continuously, HBs antibody may not be induced even after HBV vaccination. It is necessary to evaluate not only the induction of HBs antibody after HBV vaccination but also diseases that are appropriate for the discontinuation of nucleoside analog treatment. Based on the above discussion, Figure shows the modified guidelines from the Ministry of Health, Labour and Welfare.

The review is summarized as schematics. The treatment direction described here is based on the assumption that all patients are screened in advance. HBsAg: Hepatitis B surface antigen HBV: Hepatitis B virus.

Implications Of All The Available Evidence

We found that cancer patients who receive intravenous immunoglobulin may be at risk for passive transfer of hepatitis B core antibody . Our study supports that anti-HBc testing should be done before IVIG infusion to avoid false-positive results due to passive transfer. Hepatitis B testing with hepatitis B surface antigen and anti-HBc should be performed in all patients before IVIG is initiated to identify the viral status of patients receiving anti-cancer therapies and clarify the risk of hepatitis B reactivation. In patients known to have hypogammaglobulinemia and prior hepatitis B infection, anti-HBc may be negative. HBV DNA testing may be considered however, HBV DNA would be undetectable in the serum of most patients with past hepatitis B infection.

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Hepatitis B Serologic Markers And Definition Of The Isolated Anti

As hepatitis B infection progresses or resolves, clinical states of infection are reflected in HBV serologies. The presence of hepatitis B surface antigen marks active acute or chronic HBV infection. Suboptimal immune responses due to host factors such as age at time of exposure, or advanced immunosuppression, increase the risk for chronic HBV and subsequent complications. Due to mechanisms of immune control, and the presence of covalently closed circular DNA that persists lifelong after HBV exposure, HBV reactivation is always possible even following immunologic recovery and clearance of HBsAg. During chronic infection, markers for HBeAg and anti-HBe may be helpful in delineating phases of chronic HBV infection. Hepatitis B core antibody may be seen in acute or chronic infection, and also may persist for life after immunity is developed . As infection resolves hepatitis B surface antibody develops . Anti-HBs, in the absence of HBsAg or anti-HBc, denotes immunity from hepatitis B vaccination. The isolated anti-HBc profile is defined as the presence of anti-HBc in the absence of HBsAg and anti-HBs. Interpretations of hepatitis B serologies are listed below .

Can Hepatitis B Antibodies Disappear

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With the passage of time, the body hepatitis protective antibodies continuously decreased or disappeared, Therefore, in order to maintain the hepatitis protective antibodies capable of continuous, effective presence needed every three to four booster vaccination once hepatitis b vaccine, hepatitis B core antibody can

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The Fourth Or Reactivation Phase

The previous phase of HBeAg-negative/anti-HBe-positive inactive HBsAg carrier state is not synonymous with permanent termination of HBV replication and of HBV-induced chronic liver damage. Although the majority of patients may remain for life in an inactive HBsAg carrier state, and a number of them may also lose HBsAg and enjoy a complete recovery, others retain or redevelop over time significant HBV replication and progressive liver damage .

This state of HBV-induced liver damage has been first referred to as HBeAg-negative/anti-HBe-positive CHB, and similarly to HBeAg-positive CHB, it also represents an immune active phase in the natural course of chronic HBV infection. It is generally viewed as a fourth phase in the natural history of chronic HBV infection usually developing because of reactivation of HBV replication, though in some patients, it may immediately follow the second phase of HBeAg-positive CHB despite clearance and even seroconversion of HBeAg .

Stephen N.J. Korsman MMed FCPath, … Wolfgang Preiser MRCPath, in, 2012

Mechanisms Of The Isolated Anti

Hepatitis B virus persists as cccDNA following exposure. Persistent HBV infection with low or undetectable levels of HBV viremia in the setting of an isolated anti-HBc potentially involves methylation of HBV cccDNA within the hepatocyte, thereby downregulating DNA and subsequent mRNA expression, with subsequent quiescence of HBsAg production . Other epigenetic factors such as downregulation of acetylation may also play important roles towards transcriptional suppression of cccDNA in hepatocytes to explain serological patterns noted in patients with the isolated anti-HBc profile.

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Blood Products And Intravenous Immunoglobulin

Transfusion of blood products or infusion of intravenous immunoglobulin can result in passive transmission of antibodies associated with HBV. This can lead to patients being falsely informed that there is evidence of past HBV or, more importantly, being considered for antiviral prophylaxis in the context of immunosuppression. Baseline anti-HBc should be measured early during the course of disease to avoid this scenario and, if negative, subsequent positive serology can be disregarded in the absence of ongoing risk of acquisition of HBV. Should liver function tests become deranged during the course of immune suppression, HBsAg should be retested, as in any other patient.

Chronic Hepatitis B Virus Infection

Part 6 – Hepatitis B Core antibody positivity – Prof John Fung

The aim of treating chronic HBV infection is primarily to prevent complications since cure is often not achievable.

Evaluation to decide if therapy is indicated includes HBeAg and anti-HBe serology, HBV load, transaminases and liver biopsy. Patients with evidence of significant viraemia and chronic inflammation without cirrhosis will benefit the most from therapy. Since HBV has a reverse transcriptase enzyme it is susceptible to a range of nucleoside reverse transcriptase inhibitors: lamivudine, emtricitabin, telbivudine, tenofovir entecavir and adefovir dipivoxil show response rates of between 20% and 40%. These drugs are well-tolerated, but resistance develops, especially to lamivudine and emtricitabine.

The other alternative for chronic HBV therapy is pegylated interferon therapy. Interferon has the advantage of a higher rate of permanent response but has more side effects and adverse effects than the nucleoside analogues .

Janice Main, Howard C. Thomas, in, 2010

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Risk Of Transfusion Transmission

In the US, with testing for HBsAg and anti-HBc, the estimated residual risk of HBV transmission before DNA testing was 1:280,000â1:357,000, significantly higher than that for HIV or HCV. Voluntary minipool testing for HBV DNA has been widely implemented in the US, and is now required by the FDA. Current residual risk estimates are 1:750,000 or less in an era of universal immunization. Minipool HBV DNA assays have similar sensitivity to current HBsAg tests, accounting for the clinically marginal decrease of the window period .

Gregory L. Armstrong, Susan T. Goldstein, in, 2007

Taking A Hepatitis B Test

Testing for hepatitis B is performed on a sample of blood. A doctor, nurse, or other health care provider can obtain a blood sample using a small needle to draw blood from a vein.

At-home hepatitis B testing requires that users carefully follow instructions provided in the test kit to collect a small sample of blood, package the sample, and mail it to a lab for testing.

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Risk Of Hbv Perinatal Transmission

The overall rate of transmission of HBV from an HBsAg-positive woman to her neonate during the perinatal period can be as high as 90% in the absence of immunoprophylaxis. The presence of HBeAg and the associated higher HBV DNA levels mediate this risk: mothers with a positive HBeAg test have a perinatal transmission rate of 70 to 90% whereas those with a negative HBeAg test have a rate of transmission less than 10%. Most perinatal transmission of HBV occurs during or shortly before delivery, but can take place less frequently in utero. The exact rate of perinatal HBV transmission among mothers with HIV-HBV coinfection is not well established. Most perinatal transmission of HBV occurs during or shortly before delivery, but can take place less frequently in utero.

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Hepatitis B And Pregnancy

Risk of hepatitis B virus (HBV) reactivation and hepatitis ...

If youâre pregnant, you might pass the virus to your baby at birth. Itâs less likely to happen during your pregnancy.

If your baby gets the virus and isnât treated, they could have long-term liver problems. All newborns with infected mothers should get hepatitis B immune globulin and the vaccine for hepatitis at birth and during their first year of life.

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What Is The Difference Between Hepatitis B Surface Antibody And Antigen

An antigen is a substance that induces antibody production. Hepatitis B surface antigen is a protein on the surface of hepatitis B virus.

Hepatitis B surface antibodies are produced by the bodys immune system in response to HBsAg. The presence of adequate hepatitis B surface antibodies in the blood indicates protection against hepatitis B virus infection.

Hepatitis B Virus Life

Hepatitis B virus establishes itself in chronic infection by way of dynamic processes involving viral and host immunity defenses. Attachment entry of the HBV virus requires interaction between HBsAg and hepatocyte surface proteins. HBV relaxed circular DNA is converted to covalently closed circular DNA , which serves as a transcriptional template for subsequent viral mRNA production and pregenomic RNA . This matures into nucleocapsid with viral polymerase, for viral propagation in the forms of virions outside the hepatocyte, or return to the nucleus as cccDNA . The persistence of cccDNA despite effective inhibition of HBV viral polymerase through nucleoside analogues is the key reason why cure of HBV remains elusive , as it provides a transcriptional reservoir for continued replication of virus . The presence of cccDNA also leads to production of the core antigen to which antibody is formed in the form of anti-HBc. This explains why anti-HBc is present in acute, chronic, and resolved infection.

Hepatitis B Virus Life Cycle

Figure 1 depicts the HBV lifecycle. Yellow arrows highlight cccDNA and the production of the core protein, demonstrating that the production of core protein occurs independent of HBV viral replication and as a direct result of the presence of the transcriptionally active reservoir of cccDNA

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Acute Hepatitis B Infection

High titers of immunoglobulin M anti-HBc, thought to be predominantly a thymus-independent response, appears early in the course of acute HBV infection, together with HBsAg and HBeAg . Anti-pre-S1 may also occur early in the course of infection. This is accompanied by a vigorous major histocompatibility complex class I restricted cytolytic T lymphocyte response against multiple epitopes throughout the structural and nonstructural proteins of the virus. The CTLs, by direct lysis of infected hepatocytes, are thought to be important in clearance of the virus. There is also some evidence for a role in viral elimination of the cytokines interferon γ and tumor necrosis factor α .

Figure 2. The natural history of acute HBV infection. HBsAg and HBeAg can be detected early in the serum, prior to the onset of clinical hepatitis. Antibody to pre-S1 can sometimes be detected during this early phase. AST (aspartate aminotransferaseis an indication of lysis of infected hepatocytes.

There is a strong MHC class II restricted T helper cell proliferative response to the nucelocapsid antigens, HBcAg and HBeAg, but not to the envelope proteins, during the early phase of acute hepatitis B. The association of recovery with the presence of the MHC class II locus DRB1*-1302 supports an important role for the CD4 response in recovery.

Louis M. Katz MD, Roger Y. Dodd PhD, in, 2013

What Is A Hepatitis B Surface Antibody Test

Medical School Hepatitis B Serology

Hepatitis B surface antibody test is part of a panel of blood tests to diagnose HBV infection. Hepatitis B surface antibody test determines the presence and quantity of anti-HBs in the blood serum, which can indicate protection from HBV infection.

Hepatitis B disease affects the liver and commonly spreads through body fluids such as blood, semen, and vaginal secretions.

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Hepatitis B Virus Reactivation Following Rituximab Treatment In Rheumatoid Arthritis

Baseline hepatitis B surface antigen positivity is a significant protective factor for reactivation of hepatitis B virus in patients with HBsAg-negative, HBV core antibody -positive rheumatoid arthritis receiving rituximab therapy, according to study results published in the International Journal of Rheumatic Diseases.1

Worldwide, approximately 2 billion people are infected by HBV, and 75% of them inhabit Southeast Asia and the Western Pacific regions.2,3 A considerable number of patients with RA have coexisting HBV infection, and RA is a risk factor for developing rHBV as a result of using immunosuppressive therapies.4-7 RTX is used for treating patients with RA with an inadequate response to anti-tumor necrosis factor -alpha therapy, and rHBV has recently been recognized as a complication of RTX therapy.8-18

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Susceptibility To Hbv Infection

In HIV infection, the presence of the isolated anti-HBc pattern does not necessarily indicate immunity to HBV infection. Indeed, varying anamnestic responses to a single dose of HBV vaccine have been reported, ranging from as low as 7% to 32% , with higher levels of response to multiple doses of HBV vaccine administered. A prospective study conducted by Piroth and colleagues demonstrated that in 54 HIV-infected patients with the isolated anti-HBc profile, a single dose of 20 μg HBV vaccine resulted in a 46% response rate, defined as anti-HBs > 10 mIU/ml in those who did not respond to a single dose, a 3-dose series of double-dose 40 μg HBV vaccine resulted in 89% of remaining patients developing anti-HBs titers of > 10 mIU/mL at 28 weeks following vaccination . Based on the results of this study, the current DHHS guidelines recommend that HIV infected patients with the isolated anti-HBc profile receive one standard dose of HBV vaccine followed by anti-HBs assessment 1-2 months post dose. If anti-HBs is < 100 IU/mL then the individual should receive the full series of either single or double-dose HBV vaccine, with subsequent anti-HBs testing 1-2 months after completion of the vaccine series .

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Hbcab Or The Hepatitis B Core Antibody Test

The hepatitis B core antibody is produced by your immune system after infection by the hepatitis B virus, and it can persist for life. It is a sign that you either have an new, active hepatitis B infection or that you acquired hepatitis B in the past.

HBcAb is an immune system response to a protein in the core of the virus, and it is only present if you have been infected, rather than immunized against the virus. It is part of a routine screening panel of tests for hepatitis B. If your rest results turn out to be positive, your healthcare provider will order further tests to determine the stage of the infection: acute or chronic .

Also Known As: anti-HBc, HBcAb

Hbc Antibody Positive/hbs Antigen Negative/hbs Antibody Negative

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The HBc antibody positive/HBs antigen negative serotype is further divided into naïve and occult types . However, since HBV reactivation is often observed in HBc antibody positive/HBs antigen negative cases, it may be preferable to divide HBc antibody positive/HBs antigen negative cases based on whether they are positive or negative for HBs antibodies. For HBc antibody positive patients, perhaps HBV reactivation is induced by rituximab. Although Hui et al reported a 3%-25% reactivation rate, prophylactic treatment may be desirable since the mortality is relatively high after reactivation occurs. In 2013, Huang et al conducted a randomized controlled trial to evaluate the effect of the prophylactic administration of entecavir on the frequency of HBV reactivation in HBc antibody positive patients. In their report, unlike in retrospective analyses, the prophylactic administration of entecavir was the most important factor, at least for HBc antibody positive patients. Furthermore, Seto et al recently reported frequent reactivation of HBV in patients with 10 mIU/mL HBs antibody prior to rituximab treatment. In HBc antibody positive patients, prophylactic treatment is necessary, at least for those who are antibody negative prior to rituximab treatment . We believe that the prophylactic administration of a nucleic acid analog is preferable in HBc antibody positive/HBs antigen negative/HBs antibody negative cases.

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How To Get Tested

Hepatitis B testing is typically prescribed by a doctor and performed in a hospital, lab, or other medical setting. Taking a hepatitis B test requires a blood sample, which can be collected by a health care professional.

For laboratory-based testing, blood is drawn from a patients vein. After blood is collected, the sample is sent to a laboratory for analysis.

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