Hepatitis D pathophysiology: Difference between revisions
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==Pathogenesis== | ==Pathogenesis== | ||
There has been much progress in the understanding of the pathogenesis of [[hepatitis delta virus]]([[HDV]]), but the mechanisms determining whether a person will spontaneously clear HDV, become chronically infected, or rapidly progress to [[hepatic fibrosis]] are not yet fully understood.<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> | There has been much progress in the understanding of the pathogenesis of [[hepatitis delta virus]]([[HDV]]), but the mechanisms determining whether a person will spontaneously clear HDV, become chronically infected, or rapidly progress to [[hepatic fibrosis]] are not yet fully understood.<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> Hepatitis delta angtigen(HDAg) is not directly cytotoxic to human hepatocytes, nor is viral load associated with severity of liver injury.<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> | ||
===Transmission=== | ===Transmission=== |
Revision as of 16:28, 4 August 2014
Hepatitis D |
Diagnosis |
Treatment |
Hepatitis D pathophysiology On the Web |
American Roentgen Ray Society Images of Hepatitis D pathophysiology |
Risk calculators and risk factors for Hepatitis D pathophysiology |
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
Pathogenesis
There has been much progress in the understanding of the pathogenesis of hepatitis delta virus(HDV), but the mechanisms determining whether a person will spontaneously clear HDV, become chronically infected, or rapidly progress to hepatic fibrosis are not yet fully understood.[1] Hepatitis delta angtigen(HDAg) is not directly cytotoxic to human hepatocytes, nor is viral load associated with severity of liver injury.[1]
Transmission
The routes of transmission of hepatitis D are similar to those for hepatitis B. Infection is largely restricted to persons at high risk of hepatitis B infection, particularly injecting drug users and persons receiving clotting factor concentrates.
Transmission is similar to that of HBV:
- Bloodborne and sexual
- Percutaneous (IV drug use, haemophiliacs)
- Permucosal (sexual)
- Perinatal (rare)
HDV is transmitted percutaneously or sexually through contact with infected blood or blood products.
Blood is potentially infectious during all phases of active hepatitis D infection. Peak infectivity probably occurs just before the onset of acute disease.
Associated Conditions
Macroscopic Pathology
Microscopic Pathology
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References
- ↑ 1.0 1.1 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.