Hepatitis D medical therapy: Difference between revisions
Joao Silva (talk | contribs) |
Joao Silva (talk | contribs) No edit summary |
||
Line 13: | Line 13: | ||
[[Interferon-α]] is the only drug that has shown antiviral activity against [[HDV]]. Both forms of the drug (conventional and pegylated) are able to inhibit HDV replication cycle.<ref name="HeidrichManns2012">{{cite journal|last1=Heidrich|first1=Benjamin|last2=Manns|first2=Michael P.|last3=Wedemeyer|first3=Heiner|title=Treatment Options for Hepatitis Delta Virus Infection|journal=Current Infectious Disease Reports|volume=15|issue=1|year=2012|pages=31–38|issn=1523-3847|doi=10.1007/s11908-012-0307-z}}</ref><ref name="FarciMandas1994">{{cite journal|last1=Farci|first1=Patrizia|last2=Mandas|first2=Antonella|last3=Coiana|first3=Alessandra|last4=Lai|first4=Maria Eliana|last5=Desmet|first5=Valeer|last6=Van Eyken|first6=Peter|last7=Gibo|first7=Yukio|last8=Caruso|first8=Luciano|last9=Scaccabarozzi|first9=Sergio|last10=Criscuolo|first10=Domenico|last11=Ryff|first11=Jean-Charles|last12=Balestrieri|first12=Angelo|title=Treatment of Chronic Hepatitis D with Interferon Alfa-2a|journal=New England Journal of Medicine|volume=330|issue=2|year=1994|pages=88–94|issn=0028-4793|doi=10.1056/NEJM199401133300202}}</ref> | [[Interferon-α]] is the only drug that has shown antiviral activity against [[HDV]]. Both forms of the drug (conventional and pegylated) are able to inhibit HDV replication cycle.<ref name="HeidrichManns2012">{{cite journal|last1=Heidrich|first1=Benjamin|last2=Manns|first2=Michael P.|last3=Wedemeyer|first3=Heiner|title=Treatment Options for Hepatitis Delta Virus Infection|journal=Current Infectious Disease Reports|volume=15|issue=1|year=2012|pages=31–38|issn=1523-3847|doi=10.1007/s11908-012-0307-z}}</ref><ref name="FarciMandas1994">{{cite journal|last1=Farci|first1=Patrizia|last2=Mandas|first2=Antonella|last3=Coiana|first3=Alessandra|last4=Lai|first4=Maria Eliana|last5=Desmet|first5=Valeer|last6=Van Eyken|first6=Peter|last7=Gibo|first7=Yukio|last8=Caruso|first8=Luciano|last9=Scaccabarozzi|first9=Sergio|last10=Criscuolo|first10=Domenico|last11=Ryff|first11=Jean-Charles|last12=Balestrieri|first12=Angelo|title=Treatment of Chronic Hepatitis D with Interferon Alfa-2a|journal=New England Journal of Medicine|volume=330|issue=2|year=1994|pages=88–94|issn=0028-4793|doi=10.1056/NEJM199401133300202}}</ref> | ||
Despite some discrepancies among studies, relating to doses, forms and treatment durations of [[interferon-α]], 25-40% of patients showed sustained response to treatment | Despite some discrepancies among studies, relating to doses, forms and treatment durations of [[interferon-α]], 25-40% of patients showed sustained response to treatment 1 to 2 years after therapy. | ||
According to HIDIT I trial, about 28% of the patients who were treated with 180 μg of pegylated interpheron-α/week, for 48 weeks, were cured. When combined with adefovir, treatment caused a greater decline in the HBsAg levels. | According to the HIDIT I trial, about 28% of the patients who were treated with 180 μg of pegylated interpheron-α/week, for 48 weeks, were cured. When combined with adefovir, treatment caused a greater decline in the HBsAg levels. | ||
Patients treated with higher doses of interferon-α showed better survival outcomes than those treated with lower doses of [[interferon]].<ref name="FarciRoskams2004">{{cite journal|last1=Farci|first1=Patrizia|last2=Roskams|first2=Tania|last3=Chessa|first3=Luchino|last4=Peddis|first4=Giovanna|last5=Mazzoleni|first5=Anna Paola|last6=Scioscia|first6=Rosetta|last7=Serra|first7=Giancarlo|last8=Lai|first8=Maria Eliana|last9=Loy|first9=Maurizio|last10=Caruso|first10=Luciano|title=Long-term benefit of interferon α therapy of chronic hepatitis D: regression of advanced hepatic fibrosis|journal=Gastroenterology|volume=126|issue=7|year=2004|pages=1740–1749|issn=00165085|doi=10.1053/j.gastro.2004.03.017}}</ref> Prolonged therapies have shown better response rates, however, it is not clear which patients should stop and which should continue the treatment after the first year. | |||
Treatment is dependent on disease severity: | Treatment is dependent on disease severity: | ||
Line 24: | Line 24: | ||
===Nucleotide and Nucleoside Analogues=== | ===Nucleotide and Nucleoside Analogues=== | ||
Studies have not demonstrated | Studies have not demonstrated short-term antiviral effect of nucleotide and nucleoside analogues (NUCs) on [[HDV]]. | ||
However, long-term treatment with these drugs was shown to cause a decline in the [[HBsAg]] levels in some patients. Because the suppression of [[HBV]] DNA replication is related to a decrease in the risk of developing progressive [[liver disease]], NUC therapy is recommended for patients with [[HDV infection]] and a high [[HBV]] viral load. | |||
Some studies concluded that prolonged therapy with [[tenofovir]] of patients [[coinfection|coinfected]] with [[HDV]]-[[HBV]]-[[HIV]], lead to a significant decline in [[HBsAg]], [[HDV]] DNA, with some patients becoming HDV RNA negative. <ref name="pmid18389903">{{cite journal| author=Sheldon J, Ramos B, Toro C, Ríos P, Martínez-Alarcón J, Bottecchia M et al.| title=Does treatment of hepatitis B virus (HBV) infection reduce hepatitis delta virus (HDV) replication in HIV-HBV-HDV-coinfected patients? | journal=Antivir Ther | year= 2008 | volume= 13 | issue= 1 | pages= 97-102 | pmid=18389903 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18389903 }} </ref> <ref name="pmid21076274">{{cite journal| author=Martín-Carbonero L, Teixeira T, Poveda E, Plaza Z, Vispo E, González-Lahoz J et al.| title=Clinical and virological outcomes in HIV-infected patients with chronic hepatitis B on long-term nucleos(t)ide analogues. | journal=AIDS | year= 2011 | volume= 25 | issue= 1 | pages= 73-9 | pmid=21076274 | doi=10.1097/QAD.0b013e328340fde2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21076274 }} </ref> NUC therapy is recommended in HIV patients with high viral load. <ref name="pmid20334947">{{cite journal| author=Wedemeyer H| title=Re-emerging interest in hepatitis delta: new insights into the dynamic interplay between HBV and HDV. | journal=J Hepatol | year= 2010 | volume= 52 | issue= 5 | pages= 627-9 | pmid=20334947 | doi=10.1016/j.jhep.2010.02.001 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20334947 }} </ref> <ref name="pmid21511329">{{cite journal| author=Hughes SA, Wedemeyer H, Harrison PM| title=Hepatitis delta virus. | journal=Lancet | year= 2011 | volume= 378 | issue= 9785 | pages= 73-85 | pmid=21511329 | doi=10.1016/S0140-6736(10)61931-9 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21511329 }} </ref> <ref name="pmid22760651">{{cite journal| author=Calle Serrano B, Manns MP, Wedemeyer H| title=Hepatitis delta and HIV infection. | journal=Semin Liver Dis | year= 2012 | volume= 32 | issue= 2 | pages= 120-9 | pmid=22760651 | doi=10.1055/s-0032-1316467 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22760651 }} </ref> | |||
Line 35: | Line 37: | ||
--> | --> | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} |
Revision as of 22:23, 12 August 2014
Hepatitis D |
Diagnosis |
Treatment |
Hepatitis D medical therapy On the Web |
American Roentgen Ray Society Images of Hepatitis D medical therapy |
Risk calculators and risk factors for Hepatitis D medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. [2]; João André Alves Silva, M.D. [3] Jolanta Marszalek, M.D. [4]
Overview
Medical Therapy
Currently there is no effective antiviral therapy available for treatment of acute or chronic hepatitis D.[1] The goal of treatment in hepatitis D is the clearance of HDV and HBV helper virus. The complexity of the treatment resides in the need to address both viruses, and in the simplicity of the HDV. The fact that HDV uses the host cell's enzymes for replication limits the number of targets for therapeutic agents.[2]
Interferon-α
Interferon-α is the only drug that has shown antiviral activity against HDV. Both forms of the drug (conventional and pegylated) are able to inhibit HDV replication cycle.[2][3]
Despite some discrepancies among studies, relating to doses, forms and treatment durations of interferon-α, 25-40% of patients showed sustained response to treatment 1 to 2 years after therapy.
According to the HIDIT I trial, about 28% of the patients who were treated with 180 μg of pegylated interpheron-α/week, for 48 weeks, were cured. When combined with adefovir, treatment caused a greater decline in the HBsAg levels.
Patients treated with higher doses of interferon-α showed better survival outcomes than those treated with lower doses of interferon.[4] Prolonged therapies have shown better response rates, however, it is not clear which patients should stop and which should continue the treatment after the first year.
Treatment is dependent on disease severity:
- Patients with decompensated cirrhosis should not be treated with interferon-α
- Mild disease may not require immediate antiviral treatment
Nucleotide and Nucleoside Analogues
Studies have not demonstrated short-term antiviral effect of nucleotide and nucleoside analogues (NUCs) on HDV.
However, long-term treatment with these drugs was shown to cause a decline in the HBsAg levels in some patients. Because the suppression of HBV DNA replication is related to a decrease in the risk of developing progressive liver disease, NUC therapy is recommended for patients with HDV infection and a high HBV viral load.
Some studies concluded that prolonged therapy with tenofovir of patients coinfected with HDV-HBV-HIV, lead to a significant decline in HBsAg, HDV DNA, with some patients becoming HDV RNA negative. [5] [6] NUC therapy is recommended in HIV patients with high viral load. [7] [8] [9]
References
- ↑ Fields, Bernard (2013). Fields virology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 9781451105636.
- ↑ 2.0 2.1 Heidrich, Benjamin; Manns, Michael P.; Wedemeyer, Heiner (2012). "Treatment Options for Hepatitis Delta Virus Infection". Current Infectious Disease Reports. 15 (1): 31–38. doi:10.1007/s11908-012-0307-z. ISSN 1523-3847.
- ↑ Farci, Patrizia; Mandas, Antonella; Coiana, Alessandra; Lai, Maria Eliana; Desmet, Valeer; Van Eyken, Peter; Gibo, Yukio; Caruso, Luciano; Scaccabarozzi, Sergio; Criscuolo, Domenico; Ryff, Jean-Charles; Balestrieri, Angelo (1994). "Treatment of Chronic Hepatitis D with Interferon Alfa-2a". New England Journal of Medicine. 330 (2): 88–94. doi:10.1056/NEJM199401133300202. ISSN 0028-4793.
- ↑ Farci, Patrizia; Roskams, Tania; Chessa, Luchino; Peddis, Giovanna; Mazzoleni, Anna Paola; Scioscia, Rosetta; Serra, Giancarlo; Lai, Maria Eliana; Loy, Maurizio; Caruso, Luciano (2004). "Long-term benefit of interferon α therapy of chronic hepatitis D: regression of advanced hepatic fibrosis". Gastroenterology. 126 (7): 1740–1749. doi:10.1053/j.gastro.2004.03.017. ISSN 0016-5085.
- ↑ Sheldon J, Ramos B, Toro C, Ríos P, Martínez-Alarcón J, Bottecchia M; et al. (2008). "Does treatment of hepatitis B virus (HBV) infection reduce hepatitis delta virus (HDV) replication in HIV-HBV-HDV-coinfected patients?". Antivir Ther. 13 (1): 97–102. PMID 18389903.
- ↑ Martín-Carbonero L, Teixeira T, Poveda E, Plaza Z, Vispo E, González-Lahoz J; et al. (2011). "Clinical and virological outcomes in HIV-infected patients with chronic hepatitis B on long-term nucleos(t)ide analogues". AIDS. 25 (1): 73–9. doi:10.1097/QAD.0b013e328340fde2. PMID 21076274.
- ↑ Wedemeyer H (2010). "Re-emerging interest in hepatitis delta: new insights into the dynamic interplay between HBV and HDV". J Hepatol. 52 (5): 627–9. doi:10.1016/j.jhep.2010.02.001. PMID 20334947.
- ↑ Hughes SA, Wedemeyer H, Harrison PM (2011). "Hepatitis delta virus". Lancet. 378 (9785): 73–85. doi:10.1016/S0140-6736(10)61931-9. PMID 21511329.
- ↑ Calle Serrano B, Manns MP, Wedemeyer H (2012). "Hepatitis delta and HIV infection". Semin Liver Dis. 32 (2): 120–9. doi:10.1055/s-0032-1316467. PMID 22760651.