Hepatitis D natural history: Difference between revisions
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===Viral Dominance=== | ===Viral Dominance=== | ||
The simultaneous presence of [[HBV]], [[HDV]] and sometimes [[HCV]], influences the [[serologic]] findings in each patient. Infection by [[HDV]] and [[HBV]] (either in [[coinfection]] or [[superinfection]]) suppresses the [[replication]] of HBV genome.<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> Patients coinfected with HDV often show:<ref name="pmid18098143">{{cite journal| author=Cross TJ, Rizzi P, Horner M, Jolly A, Hussain MJ, Smith HM et al.| title=The increasing prevalence of hepatitis delta virus (HDV) infection in South London. | journal=J Med Virol | year= 2008 | volume= 80 | issue= 2 | pages= 277-82 | pmid=18098143 | doi=10.1002/jmv.21078 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18098143 }} </ref><ref name="pmid11050062">{{cite journal| author=Sagnelli E, Coppola N, Scolastico C, Filippini P, Santantonio T, Stroffolini T et al.| title=Virologic and clinical expressions of reciprocal inhibitory effect of hepatitis B, C, and delta viruses in patients with chronic hepatitis. | journal=Hepatology | year= 2000 | volume= 32 | issue= 5 | pages= 1106-10 | pmid=11050062 | doi=10.1053/jhep.2000.19288 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11050062 }} </ref><ref name="pmid19566789">{{cite journal| author=Heidrich B, Deterding K, Tillmann HL, Raupach R, Manns MP, Wedemeyer H| title=Virological and clinical characteristics of delta hepatitis in Central Europe. | journal=J Viral Hepat | year= 2009 | volume= 16 | issue= 12 | pages= 883-94 | pmid=19566789 | doi=10.1111/j.1365-2893.2009.01144.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19566789 }} </ref> | The simultaneous presence of [[HBV]], [[HDV]] and sometimes [[HCV]], influences the [[serologic]] findings in each patient. Infection by [[HDV]] and [[HBV]] (either in [[coinfection]] or [[superinfection]]) suppresses the [[replication]] of HBV genome.<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> Patients coinfected with HDV often show:<ref name="pmid18098143">{{cite journal| author=Cross TJ, Rizzi P, Horner M, Jolly A, Hussain MJ, Smith HM et al.| title=The increasing prevalence of hepatitis delta virus (HDV) infection in South London. | journal=J Med Virol | year= 2008 | volume= 80 | issue= 2 | pages= 277-82 | pmid=18098143 | doi=10.1002/jmv.21078 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18098143 }} </ref><ref name="pmid11050062">{{cite journal| author=Sagnelli E, Coppola N, Scolastico C, Filippini P, Santantonio T, Stroffolini T et al.| title=Virologic and clinical expressions of reciprocal inhibitory effect of hepatitis B, C, and delta viruses in patients with chronic hepatitis. | journal=Hepatology | year= 2000 | volume= 32 | issue= 5 | pages= 1106-10 | pmid=11050062 | doi=10.1053/jhep.2000.19288 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11050062 }} </ref><ref name="pmid19566789">{{cite journal| author=Heidrich B, Deterding K, Tillmann HL, Raupach R, Manns MP, Wedemeyer H| title=Virological and clinical characteristics of delta hepatitis in Central Europe. | journal=J Viral Hepat | year= 2009 | volume= 16 | issue= 12 | pages= 883-94 | pmid=19566789 | doi=10.1111/j.1365-2893.2009.01144.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19566789 }} </ref> | ||
*Negative [[ | *Negative HBeAg | ||
*Low [[serum]] levels of [[HBV]] [[DNA]] | |||
Once [[infection]] with [[HDV]] is cleared, either by host's [[immune system]] or with [[interferon]] treatment, [[replication]] of [[HBV]] will then be reactivated.<ref name="pmid16941695">{{cite journal| author=Castelnau C, Le Gal F, Ripault MP, Gordien E, Martinot-Peignoux M, Boyer N et al.| title=Efficacy of peginterferon alpha-2b in chronic hepatitis delta: relevance of quantitative RT-PCR for follow-up. | journal=Hepatology | year= 2006 | volume= 44 | issue= 3 | pages= 728-35 | pmid=16941695 | doi=10.1002/hep.21325 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16941695 }} </ref> | |||
==Complications== | ==Complications== | ||
Revision as of 19:37, 17 August 2014
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Hepatitis D |
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Treatment |
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Hepatitis D natural history On the Web |
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American Roentgen Ray Society Images of Hepatitis D natural history |
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Risk calculators and risk factors for Hepatitis D natural history |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S. [2]; Jolanta Marszalek, M.D. [3]; João André Alves Silva, M.D. [4]
Overview
The clinical manifestations of HDV infection are similar to those of HBV infection, although infection with both may progress to more severe liver disease compared with HBV.
Natural History
HDV requires an associated HBV infection. After an initial incubation period of 3-7 weeks, the preicteric phase of acute HDV infection occurs with symptoms of fatigue, lethargy, anorexia and nausea lasting 3 to 7 days. ALT and AST levels elevate at this stage. Following the preicteric phase, the icteric phase is characterized by the manifestation of jaundice, acholic stools and dark urine. Serum bilirubin levels elevate. Fatigue and nausea continue to be present. In patients with acute, self-limiting infection, convalescence begins with the disappearance of clinical symptoms. [1]
Fulminant viral hepatitis is rare, however, its mortality rate may reach 80%, and it is about 10 times more common in hepatitis D than in other types of viral hepatitis. It is characterized by:[1][2]
- Hepatic encephalopathy showing changes in personality
- Sleep disturbances
- Confusion
- Concentration difficulties
- Abnormal behavior
- Somnolence
- Coma
About 60 to 70% of patients with chronic hepatitis D develop cirrhosis. Progression to cirrhosis usually takes 5 - 10 yrs, but it can appear 2 years after onset of infection. Many of these patients die of hepatic failure.[1][3]
Coinfection
Coinfection of HBV and HDV results in both acute type B and acute type D hepatitis. The incubation depends on the HBV titer of the infecting inoculum. One or two bouts of hepatitis may be seen depending on the relative titers of HBV and HDV. The host's response to HBV determines the fate of HDV. In more than 95% of adults, HDV is cleared, whereas the chronic form occurs in less than 5% of co-infected patients. Although the disease presentation may differ greatly among patients, acute coinfection of HBV and HDV can result in a more severe disease state than acute mono-infection with HBV.[4][5]
Superinfection
HBV and HDV superinfection (HDV infection of a chronically infected HBV carrier) frequently causes severe acute hepatitis within a short incubation time. The majority of cases lead to chronic hepatitis D.[4] This form of the disease often presents as acute hepatitis in a previously undiagnosed HBsAg carrier. Most times it is misdiagnosed as an acute form of HBV infection.[6]
Superinfection is associated with fulminant hepatitis and severe chronic active hepatitis, often progressing to cirrhosis. Less frequently, HDV replication stops and the natural history becomes that of the HBV infection. In cases where HDV replication stops, residual liver disease may still be more advanced. Superinfection can present as acute hepatitis in a previously undiagnosed carrier of HBsAg. It is sometimes misdiagnosed as acute HBV or as chronic HBV causing a worsening of the liver disease.[4]
Although it is associated with a higher rate of cirrhosis, a concomitant increase in the rate of HCC was not noted, possible due to the suppression of HBV replication, caused by HDV.[7]
Viral Dominance
The simultaneous presence of HBV, HDV and sometimes HCV, influences the serologic findings in each patient. Infection by HDV and HBV (either in coinfection or superinfection) suppresses the replication of HBV genome.[5] Patients coinfected with HDV often show:[7][8][9]
Once infection with HDV is cleared, either by host's immune system or with interferon treatment, replication of HBV will then be reactivated.[10]
Complications
Common complications of hepatitis D include:
- Chronic active hepatitis
- Fulminant hepatitis
- Hepatic cirrhosis
- Hepatic failure
- Hepatocellular carcinoma
Hepatocellular Carcinoma
- Hepatocellular carcinoma (HCC) occurs in chronically infected HDV patients with advanced liver disease, with the same frequency as in those with hepatitis B.[1]
- HCC may be considered more a secondary effect of the associated cirrhosis than a direct carcinogenic effect of the virus.[1]
Prognosis
The mortality rate for HDV infections lies between 2% and 20%. These values are ten times higher than those of hepatitis B.[1]
Exposure to hepatitis D may worsen the symptoms of hepatitis B. Patients with coinfection are more likely to have fulminant hepatitis than those with HBV infection alone.
When acute infection with HDV occurs in the face of an existing chronic HBV infection, especially in persons with progressive, symptomatic chronic disease, there is increased progression of hepatic cirrhosis and hepatic failure.[11]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 World Health Organization. Department of Communicable Disease Surveillance. Hepatitis Delta 2001. http://www.who.int/csr/disease/hepatitis/HepatitisD_whocdscsrncs2001_1.pdf
- ↑ Fields, Bernard (2013). Fields virology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 1451105630.
- ↑ Fields, Bernard (2013). Fields virology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 1451105630.
- ↑ 4.0 4.1 4.2 World Health Organization. Department of Communicable Disease Surveillance. Hepatitis Delta 2001. http://www.who.int/csr/disease/hepatitis/HepatitisD_whocdscsrncs2001_1.pdf
- ↑ 5.0 5.1 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.
- ↑ Farci P, Smedile A, Lavarini C, Piantino P, Crivelli O, Caporaso N; et al. (1983). "Delta hepatitis in inapparent carriers of hepatitis B surface antigen. A disease simulating acute hepatitis B progressive to chronicity". Gastroenterology. 85 (3): 669–73. PMID 6873613.
- ↑ 7.0 7.1 Cross TJ, Rizzi P, Horner M, Jolly A, Hussain MJ, Smith HM; et al. (2008). "The increasing prevalence of hepatitis delta virus (HDV) infection in South London". J Med Virol. 80 (2): 277–82. doi:10.1002/jmv.21078. PMID 18098143.
- ↑ Sagnelli E, Coppola N, Scolastico C, Filippini P, Santantonio T, Stroffolini T; et al. (2000). "Virologic and clinical expressions of reciprocal inhibitory effect of hepatitis B, C, and delta viruses in patients with chronic hepatitis". Hepatology. 32 (5): 1106–10. doi:10.1053/jhep.2000.19288. PMID 11050062.
- ↑ Heidrich B, Deterding K, Tillmann HL, Raupach R, Manns MP, Wedemeyer H (2009). "Virological and clinical characteristics of delta hepatitis in Central Europe". J Viral Hepat. 16 (12): 883–94. doi:10.1111/j.1365-2893.2009.01144.x. PMID 19566789.
- ↑ Castelnau C, Le Gal F, Ripault MP, Gordien E, Martinot-Peignoux M, Boyer N; et al. (2006). "Efficacy of peginterferon alpha-2b in chronic hepatitis delta: relevance of quantitative RT-PCR for follow-up". Hepatology. 44 (3): 728–35. doi:10.1002/hep.21325. PMID 16941695.
- ↑ Center for Substance Abuse Treatment. Screening for Infectious Diseases Among Substance Abusers. Rockville (MD): Substance Abuse and Mental Health Services Administration (US); 1993. (Treatment Improvement Protocol (TIP) Series, No. 6.) Chapter 15 - Viral Hepatitis D.