viral hepatitis ( useful points for gps in w herts) dr alistair king consultant gastroenterologist...
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Viral Hepatitis(Useful Points for GPs in W
Herts)
Dr Alistair KingConsultant Gastroenterologist
Hemel Hempstead General Hospital
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New viral hepatitis service! West Herts Chronic hepatitis B and hepatitis C All referrals (Watford, Hemel, St
Albans) AK Local care, rather than referral to
Royal Free
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Hepatitis B Hepadnavirus Double strand
DNA virus Massively
overproduces envelope proteins (HBsAg, Australia antigen)
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Modes of transmission Sexual Blood products IVDU Vertical
High endemnicity Transmission occurs at birth
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Acute infection Incubation 60-180 days Self limiting jaundiced illness HBsAg, HBeAg, HBV DNA detectable IgM anti-HBc. Anti-HBs confirms
resolving infection Raised ALT (>AST) & Bilirubin Should resolve within 6 months
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Fulminant hepatic failure 1% of cases Encephalopathy within 8/52 of Sx Prolonged PT (>17s) or INR
(>=1.5)
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Management (acute) Rest/supportive Avoid EtOH Counsel re contacts Watch for FHF Check Hep B serology in 6/12-
Should be HBsAg-ve, HBsAb+ve
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Immunity HBsAb = immune
Reassure ++ no further action
HBsAb+ve, HBcAb+ve = immune 2o to past infection
HBsAb+ve, HBcAb-ve = immune 2o to vaccination
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Serological course
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Chronic hepatitis B 350 million worldwide UK prevalence < 1% risk cirrhosis, decompensation,
HCC 15-40% develop serious sequellae
3 potentially successive phases:
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1. Immunotolerant phase HBV-DNA levels high HBsAg+ve, HBeAg+ve,
normal/mildly deranged LFT Patient asymptomatic Often perinatally acquired
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2. Immunoactive phase HBsAg+ve HBV-DNA levels decrease Transaminases increase Patient may develop symptoms HBeAgHBeAb seroconversion
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‘Inactive carrier state’ HBV DNA<105
HBsAg+ve, HBeAg-ve, normal LFTs Low infectivity, little inflammation Low risk of complications BUT- DNA levels may fluctuate
(15%)
RARELY HBsAgHBsAb seroconversion (1-2% per year)
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Inactive carrier stateDo they need follow-up?
Normal LFT Antenatal screening, occupational
health Benign course 20-30% of patients may reactivate Cirrhosis HCC (+/- cirrhosis)
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Precore mutants 1-5% of patients with
HBeAgHBeAb seroconversion HBV-DNA levels >105
HBsAg+ve, HBeAg-ve, elevated transaminases
Due to mutation in viral precore region which prevents production of HBeAg
Otherwise behave like ‘immunoactive’ chronic hep B
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Cirrhosis 2-5.5% per year – HBeAg+ve 8-10% per year– HBeAg-ve chronic
hep Diagnosed 41-52yrs 3.3% decompensate (ascites,
jaundice, variceal bleed) HCC
Without cirrhosis 0.2-0.6% per year With cirrhosis 2% per year
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Mortallity
5-year mortallity: Without cirrhosis 0-2% Compensated cirrhosis 14-20% Decompensated 70-86%
HCC and complications of cirrhosis
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Hepatitis D ‘Incomplete’ virus Coinfection/superinfection Superinfection acute flare Suppresses hep B chronic hep D Drug users Mediterranean
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What do we do? (HBsAg+ve) Monitor LFT Lifestyle advice ‘Screen’ for development of HCC
AFP +/- U/S 6 monthly Treatment:
Interferon Lamivudine Adefovir
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Lifestyle advice Alcohol Drug users Hep A vaccination Screening/vaccination of close
contacts Barrier contraception, toothbrushes,
razors etc Occupations
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Treatment Not for:
Acute hep B (FHF liver transplant) Inactive carrier state/mild disease Decompensated cirrhosis
May be considered HBV-DNA>105, persistently elevated
transaminases 2xULN (>6 months)
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Antenatal screening All mothers offered Hep B, HIV,
Rubella, Syphillis screening in antenatal clinic
95-98% uptake HBsAg+ves
Vaccinate babies at birth HBIG
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Interferon (IFN) Previously ‘first line’Cons: Sc injection 5mU daily for 6mths-
2yrs Poorly tolerated Suppress viral replication but
rarely induce seroconversion
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Lamivudine
Pros: Well tolerated/non-toxic Suppresses viral replication/DNA
levels Rarely may induce seroconversionCons: Viral resistance develops (YMDD) May also provoke HIV resistance in
co-infected patients
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Adefovir dipivoxil
Pros: Well tolerated and effective Little resistanceCons: Expensive Can induce renal failure
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Hepatitis C Flavivirus (RNA) NANB Discovered 1989 200,000 people in
UK 38,000 diagnosed No vaccine
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Who gets it?
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‘The silent epidemic’ Only 10% report jaundiced illness 80% go chronic Nonspecific Sx (lethargy, myalgia,
RUQ pain) Routine screening Cirrhosis/HCC
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Clinical courseHCV infection
20% PCR-ve 80% chronic
7 years 30% cirrhotic
20 yrs 50% cirrhotic5% HCC
30yrs 15% death
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What do we do? (HCV Ab+ve) Exclude other causes of CLD HCV-RNA PCR Lifestyle advice If RNA+ve and for treatment liver
biopsy Treatment: PEG-IFN + Ribavirin
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Lifestyle advice Avoid EtOH Avoid blood donation, needle
sharing ?Barrier methods:
Monogamous relationships- No (<5%) Multiple sexual partners- Yes (?11.7%)
Vertical transmission rare Breast feeding OK
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Who do we treat?
No: HCV-RNA PCR-ve Mild hepatitis on Bx Decompensated cirrhosis Current EtOH++, IVDUYes: HCV-RNA PCR+ve, deranged LFT Moderate/severe hepatitis on Bx Fibrosis
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Treatment PEG interferon weekly + ribavirin
bd Genotype 1 (+4): 48weeks (recheck
PCR 12 weeks) Genotype 2,3: 24 weeks
Monitor FBC Ribavirin haemolysis IFN WCC, plt
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Response rates Sustained viral response:
Genotype 1: 50% Genotype 2,3: 80%
May be worse if: Male Older Infected a long time Cirrhotic HIV coinfection
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Cost PEG-IFN: £120-150/wk Ribavirin: £15-20/day
24 weeks therapy: £5,500-£7,000 48 weeks therapy: £11,000-£14,000
BUT: Probably cost effective
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Other follow up PCR negatives and responders
Yearly LFT and PCR Non-responders
Regular LFT, PCR, monitoring Re-biopsy after 3 years Other treatments may become
available HCV/HIV co-infection
Aggressive course cirrhosis
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CMO’s infectious diseases strategy
Identified as needing ‘intensified action’ Prevention Diagnosis Treatment
Emphasis on local services
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Summary Chronic HBV relatively rare and
need for treatment rarer Most are ‘inactive carrier state’ HCV common – IVDU – Rx makes
pharmaco-economic sense Cirrhosis/HCC
transplantation/death New W Herts clinic for viral
hepatitis
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Questions?