Post on 27-Dec-2015
Viral Hepatitis(Useful Points for GPs in W
Herts)
Dr Alistair KingConsultant Gastroenterologist
Hemel Hempstead General Hospital
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
Hepatitis B Hepadnavirus Double strand
DNA virus Massively
overproduces envelope proteins (HBsAg, Australia antigen)
Modes of transmission Sexual Blood products IVDU Vertical
High endemnicity Transmission occurs at birth
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
Fulminant hepatic failure 1% of cases Encephalopathy within 8/52 of Sx Prolonged PT (>17s) or INR
(>=1.5)
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
Immunity HBsAb = immune
Reassure ++ no further action
HBsAb+ve, HBcAb+ve = immune 2o to past infection
HBsAb+ve, HBcAb-ve = immune 2o to vaccination
Serological course
Chronic hepatitis B 350 million worldwide UK prevalence < 1% risk cirrhosis, decompensation,
HCC 15-40% develop serious sequellae
3 potentially successive phases:
1. Immunotolerant phase HBV-DNA levels high HBsAg+ve, HBeAg+ve,
normal/mildly deranged LFT Patient asymptomatic Often perinatally acquired
2. Immunoactive phase HBsAg+ve HBV-DNA levels decrease Transaminases increase Patient may develop symptoms HBeAgHBeAb seroconversion
‘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)
Inactive carrier stateDo they need follow-up?
Normal LFT Antenatal screening, occupational
health Benign course 20-30% of patients may reactivate Cirrhosis HCC (+/- cirrhosis)
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
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
Mortallity
5-year mortallity: Without cirrhosis 0-2% Compensated cirrhosis 14-20% Decompensated 70-86%
HCC and complications of cirrhosis
Hepatitis D ‘Incomplete’ virus Coinfection/superinfection Superinfection acute flare Suppresses hep B chronic hep D Drug users Mediterranean
What do we do? (HBsAg+ve) Monitor LFT Lifestyle advice ‘Screen’ for development of HCC
AFP +/- U/S 6 monthly Treatment:
Interferon Lamivudine Adefovir
Lifestyle advice Alcohol Drug users Hep A vaccination Screening/vaccination of close
contacts Barrier contraception, toothbrushes,
razors etc Occupations
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)
Antenatal screening All mothers offered Hep B, HIV,
Rubella, Syphillis screening in antenatal clinic
95-98% uptake HBsAg+ves
Vaccinate babies at birth HBIG
Interferon (IFN) Previously ‘first line’Cons: Sc injection 5mU daily for 6mths-
2yrs Poorly tolerated Suppress viral replication but
rarely induce seroconversion
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
Adefovir dipivoxil
Pros: Well tolerated and effective Little resistanceCons: Expensive Can induce renal failure
Hepatitis C Flavivirus (RNA) NANB Discovered 1989 200,000 people in
UK 38,000 diagnosed No vaccine
Who gets it?
‘The silent epidemic’ Only 10% report jaundiced illness 80% go chronic Nonspecific Sx (lethargy, myalgia,
RUQ pain) Routine screening Cirrhosis/HCC
Clinical courseHCV infection
20% PCR-ve 80% chronic
7 years 30% cirrhotic
20 yrs 50% cirrhotic5% HCC
30yrs 15% death
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
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
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
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
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
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
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
CMO’s infectious diseases strategy
Identified as needing ‘intensified action’ Prevention Diagnosis Treatment
Emphasis on local services
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
Questions?