World Health Organization. Hepatitis A. https://www.who.int/news-room/fact-sheets/detail/hepatitis-a. Published July 9, 2019. Accessed July 9, 2019.
World Health Organization. Hepatitis D. https://www.who.int/news-room/fact-sheets/detail/hepatitis-d. Published July 8, 2019. Accessed July 9, 2019.
Ontario, Ministry of Health and Long-Term Care. Infectious Diseases Protocol. Appendix A: Disease-Specific Chapters. Hepatitis A. http://www.health.gov.on.ca/en/pro/programs/publichealth/oph_standards/docs/hep_a_chapter.pdf. Published March 2017. Updated February 2019. Accessed July 9, 2019.
Ontario, Ministry of Health and Long-Term Care. Infectious Diseases Protocol. Appendix A: Disease-Specific Chapters. Hepatitis C. http://www.health.gov.on.ca/en/pro/programs/publichealth/oph_standards/docs/hep_c_chapter.pdf. Published January 2018. Updated February 2019. Accessed July 9, 2019.
Coffin CS, Fung SK, Alvarez F, et al. Management of Hepatitis B Virus Infection: 2018 Guidelines from the Canadian Association for the Study of Liver Disease and Association of Medical Microbiology and Infectious Disease Canada. Can Liv J. 2018:1(4):156-217. doi: 10.3138/canlivj.2018-0008. Published December 1, 2018.
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Etiology and PathogenesisTop
1. Etiologic factor: Hepatitis D (delta) virus (HDV), a defective RNA virus (viroid) with a capsule consisting of hepatitis B surface antigen (HBsAg) that is capable of replication only in the presence of hepatitis B virus (HBV). It probably has cytopathic effects on hepatocytes. Acute hepatitis D may be a result of coinfection (simultaneous infection with HBV and HDV) or HDV superinfection in an HBV carrier. The virus is present worldwide, affecting about 5% of all HBV patients. The reservoir, route of transmission, and risk factors are as in hepatitis B.
2. Incubation: 21 to 140 days (average, 35 days).
3. Clinical features and natural history: The course of HBV/HDV coinfection is similar to that of hepatitis B. HDV superinfection in a patient with chronic HBV infection leads to exacerbation of the disease, resulting in progression to fulminant hepatitis and acute liver failure (particularly in asymptomatic HBV carriers). Chronic HDV infection develops in 70% to 90% of patients with superinfection.
The protein encoded by the HDV genome (hepatitis delta antigen [HDAg]) is present in the blood only in the first few days of disease and can be detected using specialized techniques. The diagnosis of HBV/HDV coinfection is made in patients with high serum anti-HBc and anti-HDV IgM levels (detected using enzyme-linked immunosorbent assay [ELISA]). Anti-HDV IgM persist for ~6 weeks (in exceptional cases for 12 weeks) and are then replaced by anti-HDV IgG. Levels of HBsAg are low or undetectable (due to suppression by HDV; often this also affects anti-HBc IgM). In the case of HDV superinfection in an HBV-infected patient, anti-HDV IgM are detected, which are subsequently replaced by anti-HDV IgG; for some time both antibody classes can be detected in serum. Anti-HBc IgM are not detected. In patients with chronic HDV infection associated with active hepatitis, anti-HDV IgM persist in the blood. In HDV infection convalescents, anti-HDV IgG continue to be detectable.
Differential diagnosis is as in hepatitis A.
There are no guidelines for the treatment of acute HDV infection. In patients with chronic HDV infection, the recommended treatment is pegylated interferon alpha-2a administered for 48 weeks. In those with HBV DNA, nucleoside analogue (NA) therapy may be of benefit. The prognosis is worse in individuals with HBV-HDV coinfection compared with HBV infection alone in terms of rapid progression to cirrhosis and development of hepatocellular carcinoma.
As in hepatitis B.