Systemic diseases and biotherapies: understanding, evaluating, and preventing the risk of hepatitis B reactivation.
Identifieur interne : 001472 ( PubMed/Corpus ); précédent : 001471; suivant : 001473Systemic diseases and biotherapies: understanding, evaluating, and preventing the risk of hepatitis B reactivation.
Auteurs : Françoise Lunel-Fabiani ; Charles Masson ; Alexandra DucancelleSource :
- Joint bone spine [ 1778-7254 ] ; 2014.
English descriptors
- KwdEn :
- Antiviral Agents (therapeutic use), Biological Therapy, Hepatitis B Vaccines (therapeutic use), Hepatitis B, Chronic (immunology), Hepatitis B, Chronic (physiopathology), Hepatitis B, Chronic (prevention & control), Hepatitis B, Chronic (therapy), Humans, Risk, Tumor Necrosis Factor-alpha (immunology), Vaccination, Virus Activation (immunology).
- MESH :
- chemical , immunology : Tumor Necrosis Factor-alpha.
- chemical , therapeutic use : Antiviral Agents, Hepatitis B Vaccines.
- immunology : Hepatitis B, Chronic, Virus Activation.
- physiopathology : Hepatitis B, Chronic.
- prevention & control : Hepatitis B, Chronic.
- therapy : Hepatitis B, Chronic.
- Biological Therapy, Humans, Risk, Vaccination.
Abstract
Hepatitis B virus (HBV) reactivation can occur in chronic carriers of the HBV surface antigen (HBsAg) and constitutes a well-known complication of immunosuppressive therapy. HBV reactivation has also been reported after contact with the HBV. The increasing use of biological agents (TNFα antagonists, rituximab, abatacept, and tocilizumab) to treat systemic diseases has resulted in numerous publications about the risk of HBV reactivation. The relevant scientific societies have issued recommendations designed to prevent HBV reactivation. The main measures consist of screening for markers indicating chronic HBV infection (HBsAg) or HBV infection in the distant past (antibodies to the HBV core antigen) before initiating biological therapies, vaccinating marker-negative patients, and considering close follow-up or antiviral treatment before immunosuppressive treatment initiation or in the event of HBV reactivation. Here, we discuss the pathophysiological mechanisms underlying HBV reactivation during biological treatments, most notably in patients with occult HBV infection or markers for remote HBV infection, whose hepatocyte nuclei may contain a resistance form of HBV DNA known as covalently closed circular DNA (cccDNA). Assessment of the risk of reactivation relies on the HBV status, drugs used, and data from the literature. Finally, we discuss the various recommendations and modalities for HBV vaccination, preemptive treatment, and patient management, according to the level of risk and to the circumstances in which reactivation occurs.
DOI: 10.1016/j.jbspin.2014.01.015
PubMed: 24561021
Links to Exploration step
pubmed:24561021Le document en format XML
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Electronic address: ChMasson@chu-angers.fr.</nlm:affiliation></affiliation></author><author><name sortKey="Ducancelle, Alexandra" sort="Ducancelle, Alexandra" uniqKey="Ducancelle A" first="Alexandra" last="Ducancelle">Alexandra Ducancelle</name><affiliation><nlm:affiliation>Laboratoire de virologie et laboratoire HIFIH, UPRES EA 3859, CHU d'Angers, 4, rue Larrey, 49933 Angers cedex 9, France.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24561021</idno><idno type="pmid">24561021</idno><idno type="doi">10.1016/j.jbspin.2014.01.015</idno><idno type="wicri:Area/PubMed/Corpus">001472</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001472</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Systemic diseases and biotherapies: understanding, evaluating, and preventing the risk of hepatitis B reactivation.</title><author><name sortKey="Lunel Fabiani, Francoise" sort="Lunel Fabiani, Francoise" uniqKey="Lunel Fabiani F" first="Françoise" last="Lunel-Fabiani">Françoise Lunel-Fabiani</name><affiliation><nlm:affiliation>Laboratoire de virologie et laboratoire HIFIH, UPRES EA 3859, CHU d'Angers, 4, rue Larrey, 49933 Angers cedex 9, France.</nlm:affiliation></affiliation></author><author><name sortKey="Masson, Charles" sort="Masson, Charles" uniqKey="Masson C" first="Charles" last="Masson">Charles Masson</name><affiliation><nlm:affiliation>Service de rhumatologie, CHU d'Angers, 4, rue Larrey, 49933 Angers cedex 9, France. Electronic address: ChMasson@chu-angers.fr.</nlm:affiliation></affiliation></author><author><name sortKey="Ducancelle, Alexandra" sort="Ducancelle, Alexandra" uniqKey="Ducancelle A" first="Alexandra" last="Ducancelle">Alexandra Ducancelle</name><affiliation><nlm:affiliation>Laboratoire de virologie et laboratoire HIFIH, UPRES EA 3859, CHU d'Angers, 4, rue Larrey, 49933 Angers cedex 9, France.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Joint bone spine</title><idno type="eISSN">1778-7254</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiviral Agents (therapeutic use)</term><term>Biological Therapy</term><term>Hepatitis B Vaccines (therapeutic use)</term><term>Hepatitis B, Chronic (immunology)</term><term>Hepatitis B, Chronic (physiopathology)</term><term>Hepatitis B, Chronic (prevention & control)</term><term>Hepatitis B, Chronic (therapy)</term><term>Humans</term><term>Risk</term><term>Tumor Necrosis Factor-alpha (immunology)</term><term>Vaccination</term><term>Virus Activation (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiviral Agents</term><term>Hepatitis B Vaccines</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Hepatitis B, Chronic</term><term>Virus Activation</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hepatitis B, Chronic</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Hepatitis B, Chronic</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Hepatitis B, Chronic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Biological Therapy</term><term>Humans</term><term>Risk</term><term>Vaccination</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hepatitis B virus (HBV) reactivation can occur in chronic carriers of the HBV surface antigen (HBsAg) and constitutes a well-known complication of immunosuppressive therapy. HBV reactivation has also been reported after contact with the HBV. The increasing use of biological agents (TNFα antagonists, rituximab, abatacept, and tocilizumab) to treat systemic diseases has resulted in numerous publications about the risk of HBV reactivation. The relevant scientific societies have issued recommendations designed to prevent HBV reactivation. The main measures consist of screening for markers indicating chronic HBV infection (HBsAg) or HBV infection in the distant past (antibodies to the HBV core antigen) before initiating biological therapies, vaccinating marker-negative patients, and considering close follow-up or antiviral treatment before immunosuppressive treatment initiation or in the event of HBV reactivation. Here, we discuss the pathophysiological mechanisms underlying HBV reactivation during biological treatments, most notably in patients with occult HBV infection or markers for remote HBV infection, whose hepatocyte nuclei may contain a resistance form of HBV DNA known as covalently closed circular DNA (cccDNA). Assessment of the risk of reactivation relies on the HBV status, drugs used, and data from the literature. Finally, we discuss the various recommendations and modalities for HBV vaccination, preemptive treatment, and patient management, according to the level of risk and to the circumstances in which reactivation occurs. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24561021</PMID><DateCompleted><Year>2015</Year><Month>07</Month><Day>23</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1778-7254</ISSN><JournalIssue CitedMedium="Internet"><Volume>81</Volume><Issue>6</Issue><PubDate><Year>2014</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Joint bone spine</Title><ISOAbbreviation>Joint Bone Spine</ISOAbbreviation></Journal><ArticleTitle>Systemic diseases and biotherapies: understanding, evaluating, and preventing the risk of hepatitis B reactivation.</ArticleTitle><Pagination><MedlinePgn>478-84</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jbspin.2014.01.015</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1297-319X(14)00039-6</ELocationID><Abstract><AbstractText>Hepatitis B virus (HBV) reactivation can occur in chronic carriers of the HBV surface antigen (HBsAg) and constitutes a well-known complication of immunosuppressive therapy. HBV reactivation has also been reported after contact with the HBV. The increasing use of biological agents (TNFα antagonists, rituximab, abatacept, and tocilizumab) to treat systemic diseases has resulted in numerous publications about the risk of HBV reactivation. The relevant scientific societies have issued recommendations designed to prevent HBV reactivation. The main measures consist of screening for markers indicating chronic HBV infection (HBsAg) or HBV infection in the distant past (antibodies to the HBV core antigen) before initiating biological therapies, vaccinating marker-negative patients, and considering close follow-up or antiviral treatment before immunosuppressive treatment initiation or in the event of HBV reactivation. Here, we discuss the pathophysiological mechanisms underlying HBV reactivation during biological treatments, most notably in patients with occult HBV infection or markers for remote HBV infection, whose hepatocyte nuclei may contain a resistance form of HBV DNA known as covalently closed circular DNA (cccDNA). Assessment of the risk of reactivation relies on the HBV status, drugs used, and data from the literature. Finally, we discuss the various recommendations and modalities for HBV vaccination, preemptive treatment, and patient management, according to the level of risk and to the circumstances in which reactivation occurs. </AbstractText><CopyrightInformation>Copyright © 2014 Société française de rhumatologie. Published by Elsevier SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lunel-Fabiani</LastName><ForeName>Françoise</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Laboratoire de virologie et laboratoire HIFIH, UPRES EA 3859, CHU d'Angers, 4, rue Larrey, 49933 Angers cedex 9, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Masson</LastName><ForeName>Charles</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Service de rhumatologie, CHU d'Angers, 4, rue Larrey, 49933 Angers cedex 9, France. 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