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					www.backtomedicalschool.co.uk
Chris Curtis




 1941 - 2005
Chris Curtis




 1941 - 2005
www.backtomedicalschool.co.uk
A beginners guide to hepatitis.



       Dr Paul Southern
       Transplant Fellow, Leeds Liver Unit
• What is Hepatitis (What are LFT’s)
• How should we manage abnormal LFT’s
• Review of various causes of Hepatitis
  –   Hep A / B / C
  –   Autoimmune Hepatitis
  –   Haemachromatosis
  –   Acute Alcoholic Hepatitis
  –   Drug induced hepatitis
  –   NAFLD
                Hepatitis
hepatitis
/hepp titiss/
 • noun a disease in which the liver becomes
  inflamed and there is jaundice and other
  symptoms, mainly spread by a series of
  viruses (hepatitis A, B, and C) transmitted
  in blood or food.
      How does it present ?

• Asymptomatic patient

• BUPA Health screen

• Medicals
   What is Hepatitis (To us) ?
• Abnormality of the
  LFT’s
         Symptomatic Patient
•   TATT
•   ‘Drug’ monitoring
•   ‘At – risk’ populations
•   Itch
•   Other disorders
    – Vasculitis
    – Renal problems
                     LFT’s
•   Commonest misonmer in hospital
•   Static test
•   Do not reflect function
•   May be normal in severe liver disease
•   Abnormal in other conditions
•   Abnormal in normal patients
    – (0.5% of healthy USAF recruits)
                   LFT’s
•   ALT / AST
•   Bilirubin
•   Alkaline Phosphatase
•   Gamma GT
  Aminotransferase Enzymes
• Predominately intra-cellular enzymes
• AST – Liver, Heart, Kidney, Pancreas,
  muscles
• ALT – As AST, but predominately in the
  liver
• Sensitive indicators of hepatic cell
  inflammation
                     ALT
• Sensitive
  – Normal level <40
  – In injury up to 20,000



  Raised ALT = Liver cell damage = hepatitis
Gamma GT
                Gamma GT
• Very poor specificity

• Hugely sensitive

• ? Useful for tracking alcoholics

• (If you’ve checked it and it remains abnormal it
  requires investigation)
Alkaline Phosphatase & Bilirubin
• Alkaline Phosphatase
  – Liver, Bone, Intestine

• Liver Alk. P
  – Raised in cholestasis, biliary obstruction

• Bilirubin
  – Pre hepatic, hepatic or post-hepatic
 Commonest abnormal LFTs
• Asymptomatic patient with raised ALT –
  commonest referral to liver clinic

• Abnormality ranges from mild to severe
          Abnormal LFT’s
• What to do next ?



     REPEAT THEM
              What to do
• Patient with raised isolated ALT

• ALT 89 (0-40)

• ALT 190 (0-40)

• ALT 400 (0-40)
Management of persistant raised
     aminotransferases
• History
  –   General History
  –   Alcohol History – CAGE & DD
  –   Travel
  –   Sexual history
  –   Drug history
  –   Past medical history
              Examination
• Stigmata of chronic liver disease

There are lots !!
        Liver Aetiology Screen
•   Hepatitis A / B / C
•   Ferritin / Ceuroloplasmin /
•   alpha 1 anti-trypsin
•   Autoantibody screen
•   Immunoglobulins
•   Glucose
•   Ultrasound scan
                  Hepatitis
• What they are

• How & If we treat them

• Prognosis / Side effects

• ‘Nuggets’
                   Hepatitis A
• Commonest cause of hepatitis worldwide
• Faecal-oral transmission
• Outbreaks common
   – Schools, institutions
• Incubation is 28 days (15 – 50)
• Abrupt onset
   – fever, malaise, anorexia, nausea, abdominal discomfort,
     dark urine, and jaundice
• Symptoms – age related
  – <6yrs 70% asymptomatic
  – >15yrs 70% icteric


• Diagnosis
  – Blood test for Hep A IgM


• Prognosis
  – 0.1% <15 yr
  – 0.4% 15 – 39 yrs
  – 1.1% >40
               Hepatitis A
• Hepatitis A is not a chronic disorder
  – (But 10 % may have a relapsing course)

• Vaccination is effective
  – 2nd. Vaccination at 6/12 is mandatory

• The first sign in smokers is going off the
  fags !!
              Hepatitis B
• Vertical transmission from mother to baby
• Spread via blood
• Spead via sex

Contracted at birth – 90% develop chronic
 infection,
Contracted in adulthood, 95% clear the virus
        Hepatitis B Serology

• HBsAg – Hallmark of infection

• Anti HBs - Immunity

• Anti HBc (core) previous exposure
• HBeAg marker of viral replication

• (HBV DNA) – Direct marker
                 Hepatitis B
• Treatment
  – Interferon
     • As Hep C – unpleasant
  – Lamivudine
     • Mutation risk
• Prevention (Is better than cure)
  – Vaccinate household contacts
  – Vaccinate babies – (active +/- passive)
Hepatitis C
      • RNA Virus
      • 2/3 of ‘Transfusion
        Related Hepatitis
      • 1991 Blood Screening
        began
    Hepatitis C - Prevalence
• 30 – 40,000 diagnosed in UK
• 400,000 infected in UK
• 5 million infected USA

• 60% of drug users HCV +ve
• >40 % of prison population
              Hepatitis C
• ‘Hep C’ on blood request = antibody test

• 85% Hep C antibody reactive will have the
  virus (PCR positive)

• 15% Hep C antibody reactive will not have
  the virus – they haven’t got Hep C
            Hep C symptoms
• Nothing to everything

  –   ® UQ pain
  –   ‘Brain fog’
  –   Depression
  –   Alcohol intolerance
            Treatment of HCV
• PEGylated Interferon & Ribavirin
  – Variable response rates
     • As good as 85%
     • As bad as 40%
  – Significant side effects
     •   Arthralgia, myalgia, alopecia
     •   Neutropenia, thyroid and AI disorders
     •   Rashes
     •   Pregnancy (lack of)
          Hep C ‘nuggets’
• If they’re HCV Ab positive they might not
  ‘have’ Hepatitis C
• 6% vertical transmission rate
• 3% lifetime sexual transmission rate
• Natural history is 30 -40 years
• Loose weight and don’t drink
       Autoimmune Hepatitis
• = Chronic active hepatitis / Lupoid hepatitis /
  plasma cell hepatitis

• Often presents with lethargy / rash
   – Often sub-clinical & asymptomatic

• Women more commonly than men
   – (often young women / girls)

• Associated with other AI disorders
• Auto-antibody positive
  – ANA / ASMA /

• Aetiology screen + liver biopsy

• Treatment
  – Steroids initially (Calcium !!)
  – Steroid sparing agent

• Pregnancy is possible
        Haemachromatosis
• Autosomal recessive
  – Commoner than you might think
• 75% present with abnormal LFT’s
• Women present later than men
• High ferritin
  – But not only a high ferritin
• Multiple associations
                  Presentation
•   Liver function abnormalities — 75 %
•   Weakness and lethargy — 74 %
•   Skin hyperpigmentation — 70 %
•   Diabetes mellitus — 48 %
•   Arthralgia — 44 %
•   Impotence in males — 45 %
•   Electrocardiographic abnormalities — 31 %.
                 Treatment
• Venesection
  – Often twice weekly until ferritin falls
  – Eventually infrequent


• Arthralgia often improves

• Cirrhosis can reverse
                   Alcohol
• Broad spectrum
  – From asymptomatic fatty liver
  – To end stage alcohol related cirrhosis
• Not all alcoholics will develop liver disease
  – 30% develop cirrhosis
  – 2% per year over 40 units
• Blood tests may have raised ALT
          Alcoholic Hepatitis
• Excess alcohol for a long time –without ill
  effect 40 – 70 units / week
• Suddenly become ill
  –   Hepatomegaly
  –   Jaundice
  –   Pyrexia
  –   Anorexia
• 50% may die, 50% survivors get cirrhosis
               Fatty Liver
•   Asymptomatic to dull ® UQ pain
•   Mildly elevated ALT
•   ? Hepatomegaly
•   Resolves with abstinence ?
•   10 % develop cirrhosis
           Alcoholic Cirrhosis
• Micronodular cirrhosis
• Alcohol excess

• Other problems with alcohol
  –   Cardiovascular – Cardiomyopathy
  –   Neurological – central & peripheral
  –   Endocrine – Impotence
  –   GI – Oesphagitis & pancreatitis
     Drug induced Hepatitis
• Varies from ALF to mild hepatitis
• Often idiosyncratic – but some ‘repeat
  offenders’
  – Isoniazid – 1%
  – Augmentin .01%
• Hepatitic picture
  – Paracetamol, methotrexate, tetracyclines,
    isoniazid.
                   Statins
• Common reason for referral

  – 0.5 – 3.0 % incidence
  – Pravastatin trials – 112,000 patient years – no
  difference c/f placebo
  – Be guided by Sheffield tables, discuss &
    consider change in agent if 2-3X ULN ALT
                      NAFLD
•   Fatty liver
•   Bland steatosis
•   Steatohepatitis
•   NASH

• = NAFLD
• Spectrum –Bland steatosis to
  fibrosis/cirrhosis
• 40-60% of obese individuals have
  NAFLD
• 80% – steatosis
• 20% – steatohepatitis
• 25% progress to cirrhosis over 8 years!
• Risk of HCC is identical to HCV
• Liver biopsy
• Classical patient

• Mr X
  –   ALT 98
  –   Aetiology screen negative
  –   BMI 33
  –   +/- Hypertension / Diabetes
  –   USS = ‘Hyperechoic liver in keeping with fatty
      infiltration”
         NAFLD Treatment
• Previously thought to be benign

• Loose weight (but not too fast)
• Good DM control
  – Ideally a glitazone
• Control other risk factors
       Metabolic Disorders
• Alpha-1 antitrypsin

• Wilsons disease
                 Hepatitis C
• Exposure -
   – NO post exposure treatment available
   – Hep C Immunoglobulin - research stages

• Conversion
   – 3% ??

• Future
   – ? Early use of combination therapy
                 Hepatitis C
• 5 Instances of 15 transmissions of HCV
  from HCW to patient

• DOH Circular Aug 2002
  – No PCR positive person ….
     • Carry out exposure prone procedures
     • Begin training to carry out procedures
  – However …
     • After succesful treatment can carry out procedures
                  Hepatitis B
• > 90 % Efficacy
• Re-combinant vaccine
• Exposure in non-vaccinated
   – Urgent active & passive vaccination
• Vaccination
   – 5 yr follow up vaccination - then nil else
   – If exposed - booster vaccination

				
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