Hepatitis D medical therapy: Difference between revisions

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===Nucleotide and Nucleoside Analogues===
===Nucleotide and Nucleoside Analogues===
Studies have not demonstrated NUC's to produce a short-term antiviral effect on HDV, althought treatment with NUCs for several years may cause HBsAg decline in some patients. Because suppression of HBV DNA replication correlates with a decreased risk of developing progressive liver disease, NUC therapy is recommended in patients with HDV infection and a high HBV viral load.





Revision as of 23:27, 6 August 2014

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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 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.

Farci et all. showed that patients treated with higher doses of interferon-α had 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 NUC's to produce a short-term antiviral effect on HDV, althought treatment with NUCs for several years may cause HBsAg decline in some patients. Because suppression of HBV DNA replication correlates with a decreased risk of developing progressive liver disease, NUC therapy is recommended in patients with HDV infection and a high HBV viral load.




References

  1. Fields, Bernard (2013). Fields virology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 9781451105636.
  2. 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.
  3. 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.
  4. 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.

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