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home - Liver - Various Viruses - Hepatitis D Written by Dr Sebastian Zeki
Knowledge


Understands the serological interpretation categorisation and
investigation of patients with chronic hepatitis B and/or C with
particular emphasis on the need for treatment and surveillance

Recognises the particular populations at risk
Aware of national and international agreed guidelines on viral
hepatitis management and use of interferon and antiviral drugs

Aware of hepatitis B reactivation in the context of immunosuppression
Skills
Uses appropriate diagnostic modalities including serology
genotyping viral load measurements liver biopsy and related
investigations

Monitors anti-viral and immunomodulatory therapies with appropriate
investigations

Behaviours
Communicates effectively with patients and relatives in the context of
viral liver disease and underlying social and psychological risk factors

Marshals multi-disciplinary support networks and in particular
recognise the crucial role of nurse practitioners in disease
management

Hepatitis D

Treatment and PreventionPatients with chronic hepatitis D and active liver disease should be treated early.Asymptomatic HDV carriers with normal ALT levels do not require therapy but should be monitored for signs of active disease.The optimal treatment of HDV is uncertain.The only treatment approved for chronic HDV is interferon alfa.Treat with pegylated IFNa for one year.Nucleos/tide analogues do not seem to have an advantage. Diagnosis Natural history of chronic hepatitis DComplications include anything from fulminant liver failure to the asymptomatic carrier state.It is associated with annual rates of development of cirrhosis and HCC of 4 and 2.8 %, respectively.Outcomes may be related to genotype. EpidemiologyTrue incidence of acute hepatitis D is underestimated as epidemiological assays detect total anti-HDV which appears late or absent (esp if immunodef).Anti-HDV may disappear with time so detection of past infection is impossible.5 % of the HBV carriers have HDV.Genotype I more common in the Western world.Genotype II is more common in the Far East and is less likely to progress to chronicity.Genotype III is more common in South America and can lead to fulminant liver failure.5 other genotypes exist in process of being characterized. 1- The HDV genomic RNA serves as template for synthesis of both multimeric antigenomic molecules and mRNA; 2- RNA antigenomic multimers are self-cleaved at monomeric intervals and circularize; 3- the antigenomes serve as template for synthesis of multimeric genomic RNA molecules; 4- RNA genomic multimers are self-cleaved at monomeric intervals and circularize; 5- HDV RNPs assemble and are exported to the cytoplasm where they meet HBsAgs; 10- mature HDV virions are produced and secreted; 7- translation of mRNA results in the synthesis of delta antigens which are imported to the nucleus. HDV genome —Small RNA molecule Single-stranded circleHigh G+C content causing the circle to collapse as a rod-like structure.8 HDV genotypes exist Virion StructureThe HD virion comprises an RNA genome, a single HDV encoded antigen, and a lipoprotein envelope provided by HBV. Hepatitis D antigen —Is a structural component of the virion.Consists of a phosphoprotein encoded by an open reading frame present on the RNA strand complementary to the RNA genome (antigenomic strand). 70 molecules of HDAg are complexed with each molecule of HDV RNA to form a ribonucleic core-like structure.2 forms of HDAg coexpressed in infected individual Lipoprotein envelope of HDV —From HBV with same proteins (large, middle and small S); relative proportion depends upon the level of HBV replication. Coinfection —Usually transient and self-limited.High incidence of liver failure has been reported among drug addictsPresents similarly to acute Hep B.Rate of progression to chronicity same as Hep B. Pathogenesis of HDV-induced hepatitis HDV causes directly cytopathic damage during acute infection, and immune-mediated damage during chronic infection. Hepatitis D The Mediterranean basin —EndemicAffects mainly children and young adults.Transmission is inapparent, permucosal, or percutaneous spread.Social class VPrevalence has declined (now in 8% Hep B) The Far East —HDV in HBV carriers from 90 % (Pacific islands) to 5 % (Japan). Western countries —UncommonMainly in IVDU and transfused Acute hepatitis of undetermined origin in a chronic HBV carrier —Difficult to distinguish but HBsAg is present in both situations, but IgM anti-HBc should be -ve in acute HDV superinfection.The diagnosis is made more difficult since HDV superinfection may cause transient suppression of HBV replication, resulting in very low and, rarely, undetectable levels of HBsAg.As in patients with acute HBV/HDV coinfection, patients with acute HDV superinfec-tion are usually +ve for HDAg and/or HDV RNA in serum at the time of presentation.However, in contrast to acute coinfection, acute HDV superinfection is characterized by persistent detection of HDV RNA in serum and rapidly increasing titres of anti-HDV (total and IgM). Increased risk of a fulminant course when compared to acute hepatitis B.Worsens HBV related liver disease with rapid pogression to cirrhosis but can be indolent Unknown whether more likely to cause HCC with coinfection Acute hepatitis B virus infection —Test if have hep B and at risk (IVDU/ endemic population) or who present with unusually severe or protracted hepatitis.Criteria: positive for HBsAg and have high titer IgM anti-HBc.However, markers of HBV replication may precede or follow those of HDV.In addition, occasional patients have already seroconverted to anti-HBs if they present during the second phase of a biphasic hepatitis.These patients should still be positive for high-titer IgM anti-HBc.Serum HDAg and/or HDV RNA are usually positive at presentation.If assays for serum HDAg or HDV RNA are not available, repeated testing for anti-HDV (total or IgM) should be performed to document anti-HDV seroconversion. HBsAg-positive chronic liver disease —Screen for total anti-HDV antibody to rule out coexistent chronic HDV infection.Confirm HDV by staining for HDAg in liver tissues.Measurement of serum HDV RNA should be limited to patients who are anti-HDV positive but have no detectable HDAg in the liver or to evaluate the effects of antiviral therapy.In chronic HDV infection, markers of HBV replication are usually absent, and the patient is typically HBeAg negative and anti-HBe-positive.HDV RNA and HBV DNA may occasionally coexist. Helper-independent latent infection —This is only present in transplants.Intranuclear HDAg can be detected in the grafted liver as early as a few hours after transplantation in the absence of both productive HDV infection.Patients dont get hapatitis or viraemia unless hep B is introduced. Superinfection —This usually presents as exacerbation of known chronic Hep B.Progression to chronic HDV infection occurs in almost all patients.HBV replication is usually suppressed by HDV. Cytoplasm Nucleus Antigenomic RNA mRNA 5 4 3 2 1 6 RNPs Genomic RNA RNPs Nuclear membrane 10. 7. 9. 8. HDV RNPs HDAg R.E. HBsAg Plasma membrane Symtpoms ALT elevated HDV DNA HBsAg Written by Dr Sebastian Zeki HDV components HDV RNA S-HDAg L-HDAg HDV virion36nm RNP 19nm Envelope HBV components Made of S,M and L-HBsAg HBV-HDV Coinfection Titre Time after exposure Total anti-HDV IgM anti-HDV anti-HBs

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