1. Asymptomatic abnormal LFTs…..again!
ignore, reassure, investigate or refer?
Alastair MacGilchrist
Laboratory/Primary care Meeting
7 November 2013

2. Why bother? (1)

3. Why bother? (2)
Liver disease is usually asymptomatic until irreversible…..the classic “silent killer”
Most liver disease is due to alcohol, NAFLD or viral hepatitis…..all preventable or reversible in early stages

5. Price  Consumption  Harm
Alcohol kills a Scot every 3 hours
1 in 20 of all deaths in Scotland
Twice that of England
Doubled in last 15 years
1 in 10 of deaths in Scots aged is due to alcoholic liver disease.
Enough alcohol is sold in Scotland to enable every adult to exceed safe drinking guidelines
almost double that of England
Britain’s consumption has doubled since 1960
Alcohol is 70% more affordable than in 1980
Price  Consumption  Harm

7. NAFLD is a big problem Very common Up to 30% of population
Up to 75% if obese
2-5% will develop cirrhosis over 20 years
Difficulty distinguishing progressive disease (i.e. fibrosis)

8. The future of hepatitis C therapy
e.g. sofosbuvir, daclatasvir, ledipasvir
interferon-free
single combi-pill
oral
short course
once-daily dosing
minimal side effects

9. hepatitis C therapy is changing
pre 2011
genotype 2 or 3
genotype 1
drugs
peg-interferon + ribavirin
duration
24 weeks
48 weeks
cure
up to 80%
up to 40%
now
genotype 2 or 3
genotype 1
drugs
peg-interferon + ribavirin
peg-interferon + ribavirin + bocepravir or telapravir
duration
24 weeks
up to 48 weeks
cure
up to 80%
up to 70%
2015 ?
genotype 2 or 3
genotype 1
drugs
DAAs
duration
12 weeks ?
cure
100% ?

10. What are abnormal liver function tests?
bilirubin
ALT
alkaline phosphatase
GGT
albumin
AST
prothrombin time
FBC
creatinine

11. routine LFTs in primary care: remove GGT and add AST?
GGT v AST
GGT
isolated GGT with raised MCV – consider alcohol
in female NAFLD, GGT predicts cirrhosis
GGT indicates liver source for ALP
ignore GGT alone <100
AST
in ALD, AST often > 2 x ALT
in NAFLD, suspect significant fibrosis if
AST > ALT (AST/ALT > 0.8)
APRI score (AST: platelet ratio) >1.5
routine LFTs in primary care: remove GGT and add AST?

12. The patient with asymptomatic abnormal LFTs
NAFLD is not the only diagnosis
Pattern and duration are important
Consider:
Alcohol history
Hepatitis risk factors
Drugs
metabolic syndrome clues
Autoimmune disease clues
Family history
Measure:
Viral hepatitis serology HBsAg, anti-HCV Ab HBV, HCV
Autoimmune markers ASMA, ANA, AMA AIH, PBC
Glucose NAFLD
Lipids NAFLD
Ferritin haemochromatosis
Caeruloplasmin (if <55y) Wilson’s disease
Alpha-1-antitrypsin phenotype α-1-Antitrypsin deficiency
Ultrasound

13. Have they got fibrosis/cirrhosis? 1. Primary care
Clinical exam
Hepatosplenomegaly
Spider naevi, etc.
LFTs
GGT
AST/ALT
Albumin
Platelets
Ultrasound

14. Have they got fibrosis/cirrhosis? 2. Secondary care
APRI score
Hyaluronic acid
Marker panels
ELF
Fibrotest
Elastography
Fibroscan
ARFI
Liver biopsy

15. “liver screen” Who? ↑ALT/GGT/AP > 2 x ULN
2 occasions > 4 weeks apart
What? USS
Aetiology HCV Ab, HBsAg
ASMA, ANA, AMA
ferritin
caeruloplasmin (<55y)
glucose, lipids
(TTG, TFTs)
Staging AST
platelets
albumin
Action? Refer if +ve aetiology screen
fibrosis/cirrhosis ↓platelets
AST/ALT>0.8
splenomegaly
unexplained
ALD ↓alcohol
NAFLD ↓weight

16. Sub-groups ↑bilirubin alone: usually Gilbert’s (exclude haemolysis)
(check unconjugated)
↑GGT alone: think alcohol
(think NAFLD)
AP alone: probably not liver
consider isoenzymes
↑AP + GGT: usually biliary
USS for biliary obstruction
Check AMA for PBC

17. So…for the next patient with asymptomatic abnormal LFTs….
investigate?
if persistent
according to clinical picture
don’t miss treatable disease
refer?
if require treatment, suspect advanced disease or diagnosis unclear
reassure?
if negative screen and
no suspicion of advanced disease
ignore?
never!

18. and…..
…..a very big thanks to Simon, Sara, Emily and Thulani
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