the little brother of hepatitis b min li andie lee
TRANSCRIPT
Case Study – Mr SG
35 year-old male Chronic HBV infection HIV
Diagnosed 2006, probably acquired 2001 Homosexual male, partner HIV positive On antiretroviral treatment since diagnosis HIV viral load undetectable, CD4 count 620
Major depression
Case Study – Mr SG
Presented in September 2008 with 3 weeks of: Malaise, fatigue Nausea, vomiting and diarrhoea Jaundice Dark urine and pale stool No fever or abdominal swelling
Case Study – Mr SG
Medications Atripla (tenofovir/ emtricitabine/ efavirenz)
1 tablet po daily Sildenafil 50mg po prn
Previously worked as a graphic designer, now on disability pension
Smoker Crystal methamphetamine
Case Study – Mr SG
Physical examination Afebrile Jaundiced Spider naevi and palmar erythema No abdominal tenderness,
hepatosplenomegaly or ascites
Case Study – Mr SG
Test 21.08.2008 24.09.2008 30.09.2008
Bilirubin (<18) μmol/L 6 62 334
ALP (30-130) U/L 71 123 135
GGT (<60) U/L 29 742 596
ALT (5-55) U/L 25 1245 3781
AST (5-55) U/L 24 470 3158
Albumin (38-48) g/L 46 39 39
INR (0.9-1.2) - 1.0 1.6
Platelet count (150-400) 178 170 116
Case Study – Mr SG
Hepatitis serology: Hepatitis A IgM –ve, IgG +ve Hepatitis B cAb +ve, B sAg +ve, B eAg –ve
HBV concentration 8954 copies/mL (1210 IU/mL) Hepatitis C Ab –ve, HCV PCR –ve Hepatitis D total Ab +ve Hepatitis E IgM –ve, IgG –ve
HDV superinfection Superinfection can lead to fulminant hepatitis Mortality rate for HDV infection is 2-20%
Case Study – Mr SG
Symptoms and liver function tests improved but ongoing fatigue
June 2010 - Liver function tests remained elevated probably due to chronic Hepatitis D (HBV DNA negative)
Case Study – Mr SG
Test result 21.08.2008 24.09.2008 30.09.2008 16.06.2010
Bilirubin (<18) μmol/L 6 62 334 10
ALP (30-130) U/L 71 123 135 109
GGT (<60) U/L 29 742 596 185
ALT (5-55) U/L 25 1245 3781 372
AST (5-55) U/L 24 470 3158 218
Albumin (38-48) g/L 46 39 39 46
INR (0.9-1.2) - 1.0 1.6 1.0
Platelet count (150-400) 178 170 116 121
Case Study – Mr SG
Consideration for liver biopsy and treatment with interferon therapy
Treatment deferred
Introduction
Hepatitis is serious inflammation of the liver caused by hepatitis viruses
Most common – Hepatitis A, B, C Less common – Hepatitis D, E Liver – Inflammation - cirrhosis - cancer
Hepatitis Delta
Hepatitis D or Hepatitis Delta: Discovered by Dr Rizzetto in 1977 Is a defective single stranded RNA virus It requires Hepatitis B virus for its own
replication It is the least common but most severe form
of viral hepatitis
What is HepD virus?
36-43 nanometres in diameter
The genome of the virus is very small and consists of single-stranded RNA and HD Ag
HDV does not synthesize its own coat, it is enveloped by Hepatitis B surface antigen
Its replication requires helper functions provided by HBsAg
HDV viral replication
inserts its genetic
material into liver cells
uses liver cell resources to
replicate itself
genetic material is assembled in the
host liver cell
outer coating synthesizes its
own outer protein coat
release from host cell as Hep D virus
HBsAg
Geographic distribution of HDV Infection
• Generally corresponds to prevalence of chronic HBV infection world wide. However, distinct features have been documented
• For those countries in which the prevalence of chronic HBV is low, distribution of HDV is low among chronic HBV carriers
• In these countries (like Australia) HDV infection commonly occurs among intravenous drug users
Route of transmission
Similar to those for HBV (except vertical transmission is rare)
Percutaneous Contaminated drug use equipment Transfusion of infected blood and blood products Permucosal Sexually transmitted, although less efficient than HBV
Who is at Risk of HDV infection?
Chronic HepB carrier Anyone at risk for HBV Injecting drug users Haemophiliacs/haemodialysis patients Homosexuals and heterosexuals with multiple sex
partners It has been estimated that 15 million people with
Hepatitis B are infected with Hepatitis D In Australia, over the last 6 years, 20-30 cases reported
each year
HDV infection clinical features Coinfection Superinfection
HDV HBV HDV
Healthy individual HBV Carrier
3-4% 90% Rare 7-10% 10-15% 80%
Fulminant Recovery Chronic Fulminant Acute, severe Chronic
Hepatitis with immunity HBV/HDV Hepatitis disease HBV/HDV
Death Cirrhosis Death Recovery Death
Symptoms of HDV infection
Similar to Hepatitis B loss of appetite nausea and vomiting tiredness pain in the liver (upper, right side of abdomen) muscle and joint pain jaundice (yellowish eyes and skin, dark urine
and pale-coloured faeces)
Diagnosis of Hepatitis D
Detection of HDV RNA by PCR : sensitive method can detect 10-100 copies of HDV genome in infected serum
HD Ag detection by EIA The finding of HD Ag in the serum indicating
acute HDV infection and early stage of infection
Anti –HD IgM, IgG detection by EIA The serological response to HDV infection.
Provides supplemental evidence for HDV infection.
RPAH Serology Section
Testing algorithm Normally would not test for HDV unless HBV
surface antigen present Sometimes patient history is not provided when a
request for HDV is received Testing requests for HDV are almost
exclusively by specialists HDV RNA requests uncommon, though requests
received are from experienced specialists Crucial window between RNA presence and HDV-Ab
presence These requests are forwarded to VIDRL
RPAH Serology Section
Qualitative HDV detection conducted by detecting total antibodies to HDV antigen (anti-HD) Dia Sorin ETI-AB-DELTAK-2 (P2808)
1. Well coated with recombinant HD Ag.
2. Anti-HD from sample or control.
3. Enzyme tracer: anti-HD antibodies (human) conjugated to horseradish peroxidase (H R P).
RPAH Serology Section
Dia Sorin EIA Performed fortnightly Manual test Samples tested in duplicate One blank, positive and negative controls / run
External controls periodically tested and monitored Results are calculated manually
Interpreted via cut-off values derived from positive and negative controls
All initial positives are repeated before reporting
Anti-HDV total anti-bodies (RPA)
0
20
40
60
80
100
120
2005 2006 2007 2008 2009 2010
Total samples
Pos
Treating Hepatitis D
There is no antiviral therapy specifically for chronic hepatitis D
Individuals with chronic HDV and HBV infection should follow HBV therapy
Research indicates using Pegylated interferon demonstrates some benefit in people with hepatitis D
Liver transplantation may be considered for end-stage chronic hepatitis D
Prevention of Hepatitis D
No vaccine specific for HDV Since HDV is dependent on HBV for
replication, preventing HDV through HBV vaccination can be effective
In HDV superinfection, education to reduce risk behaviours and reduce exposure to infectious blood
Australian Society for MicrobiologyNSW-ACT Branch
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