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INTERPRETATION

OF ABNORMAL
LFTS
DR ALEX MOGERE
CONSULTANT PHYSICIAN
Principles of invx of abn LFTs

• 2.5 of population have raised LFTs


• Normal LFTs do not exclude liver disease
• Interpret LFTs in clinical context
• Take a careful history for risk factors, drugs
(inc OTCs), alcohol, comorbidity, autoimmunity
• Physical examination for liver disease
• Chase likely diagnosis rather than follow
algorithm unless there are no clues
• If mild abnormalities and no risk factors or
suggestion of serious liver disease , repeat LFTs
after an interval (with lifestyle modification)
LFTS
• LFTsMarkers of hepatocellular damage
• Cholestasis
• Liver synthetic function
Markers of hepatocellular damage
• AST- liver, heart skeletal muscle, kidneys,
brain, RBCs
• In liver 20 %activity is cytosolic and 80 %
mitochondrial
• Clearance performed by sinusoidal cells,
half-life 17hrs
• ALT more specific to liver, v.low
concentrations in kidney and skeletal muscles.
• Half-life 47hrs
GGT
• Gamma-GT hepatocytes and biliary epithelial
cells, pancreas, renal tubules and intestine
• Very sensitive but Non-specific
• Raised in ANY liver disease hepatocellular or
cholestatic
• Usefulness limited
• Confirm hepatic source for a raised ALP
• Alcohol
• Isolated increase does not require any further
evaluation, suggest watch and rpt 3/12 only if
other LFTs become abnormal then investigate
CHOLESTASIS
• ALP liver and bone (placenta, kidneys,
intestines or WCC)
• Hepatic ALP present on surface of bile duct
epithelia and accumulating bile salts increase
its release from cell surface. Takes time for
induction of enzyme levels so may not be first
enzyme to rise and half-life is 1 week.
• ALP isoenzymes, 5-NT or gamma GT may be necessary
to evaluate the origin of ALP
Cont. cholestasis
•Isolated ALP 3rd trimester, adolescents
•Bone exclude by raised GGT, 5-NT or isoenzymes
•May suggest biliary obstruction, chronic liver
disease or hepatic mass/tumour
•Liver USS/CT most important investigation-dilated
ducts
•Ca pancreas, CBD stones, cholangioca or liver
mets
Cont . Cholestasis(non-dilated ducts)
• Cholestatic jaundice Drugs- Antibiotics,
Nsaids, Hormones, ACEI
• PBC anti- mitochondrial Ab, M2 fraction, IgM
• PSC associated with IBD 70, p-ANCA, MRCP and
liver biopsy
• Chronic liver disease
• Cholangiocarcinoma beware fluctuating levels
• Primary or Metastatic cancer, lymphoma
• Infiltrative sarcoid, inflammatory-PMR, IBD
• Liver biopsy often required
Bilirubin, albumin and PTI(INR)
• Useful indicators of liver synthetic function
• In primary care when associated with liver
disease abnormalities should raise concern
• Thrombocytopenia is a sensitive indicator of
liver fibrosis
• Unconjugated bilirubin is raised in Haemolysis,Gilbert’s syndrome, a
benign, inherited disease
Acute hepatitis
• Viral Hep A, B, C, E, CMV, EBV
• ALT levels usually peak before jaundice appears.
• Jaundice occurs in 70% Hep A, 35% acute Hep B,
25% Hep C
• Check for exposure
• Check Hep A IgM, Hep B core IgM and HepBsAg, Hep
C IgG or Hep C RNA
Investigation of Abnormal LFTs - ALT/AST 2-5x
normal (100-200)

• History and Examination


• Discontinue hepatotoxic drugs
• Continue statins but monitor LFTs monthly
• Lifestyle modification (lose wt, reduce alcohol,
diabetic control)
• Repeat LFTs at 1 month and 6 months
Cont.Investigation of Abnormal LFTs - ALT/AST 2-5x
normal (100-200)

• If still abnormal at 6 months


• Consider referral to secondary care
• Hepatitis serology (B, C)
• Iron studies: transferrin saturation .ferritin
• Autoantibodies immunoglobulins
• Consider caeruloplasmin
• Alpha-1- antitrypsin
• Coeliac serology
• TFTs, lipids/glucose
• Consider liver biopsy esp if ALT gt 100)
Value of liver biopsy in deranged LFT
• The most accurate way to grade the severity of
liver disease
• Aminotransferase levels correlate poorly with
histological activity
• Narrows the diagnostic options, if not diagnostic
THANK YOU!

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