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Liver function tests: reading the pattern !

The liver panel mixes markers of cell injury, cholestasis and true function; the pattern points to the cause.

Updated 2026-11-01

Key facts

  • Hepatocellular injury: high ALT and AST, out of proportion to alkaline phosphatase.
  • Cholestasis: high alkaline phosphatase and GGT, with or without high direct bilirubin.
  • True synthetic function: albumin (half-life about 3 weeks) and prothrombin time/INR (factors with half-lives of hours).
  • High indirect bilirubin with normal enzymes: haemolysis or Gilbert syndrome; high direct bilirubin: cholestasis or failed excretion.
  • R factor = (ALT/ULN) ÷ (ALP/ULN): > 5 hepatocellular, < 2 cholestatic, 2–5 mixed (ULN = the laboratory's upper limit of normal).

In detail

  • 'Liver function tests' is a loose name: aminotransferases and alkaline phosphatase measure injury, not function.
  • Aminotransferases leak from hepatocytes when their membrane breaks: viral, toxic (paracetamol), ischaemic or autoimmune hepatitis, fatty liver.
  • Alkaline phosphatase and GGT are made in greater amounts by the bile canaliculi when there is obstruction or intrahepatic cholestasis.
  • Bilirubin comes from haem: the indirect (unconjugated) form needs hepatic UGT1A1; the direct (conjugated) form leaves into bile through the MRP2 transporter.
  • Albumin falls slowly in chronic disease; INR lengthens within hours in acute failure and is the best immediate prognostic marker.
  • The Child–Pugh and MELD scores use bilirubin, albumin, INR, creatinine and sodium to grade cirrhosis.
Also called
LFTs, Liver panel, Hepatic panel

Clinical notes

  • Aminotransferases in the thousands: acute viral hepatitis, paracetamol or ischaemic hepatitis ('shock liver').
  • An INR that does not correct with vitamin K means failed synthesis; if it corrects, it suggests cholestasis or malabsorption.
  • Normal aminotransferases do not exclude advanced cirrhosis, because little tissue is left to injure.

Pathways

Test yourself

Think of the answer, then tap the question to see it.

Which marker best reflects acute hepatic synthetic function?

Prothrombin time/INR, because clotting factors have half-lives of hours, against weeks for albumin.

Which pattern suggests biliary obstruction?

Alkaline phosphatase and GGT raised more than the aminotransferases, with high direct bilirubin.

Why can albumin be normal in severe acute hepatitis?

Its half-life is about three weeks: it takes time to fall even when synthesis is already failing.

What does isolated indirect hyperbilirubinaemia with normal enzymes suggest in a young adult?

Gilbert syndrome (low UGT1A1 activity) or haemolysis.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Liver Function Tests: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2026); Bilirubin Blood Test: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2026); Total Protein and Albumin/Globulin (A/G) Ratio : MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

← All of biochemistry

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Representative model, for educational purposes only.