What each LFT measures
| Test | Normal Range | What it reflects |
|---|---|---|
| ALT (Alanine aminotransferase) | 7–56 U/L | Liver cell damage: most specific liver enzyme |
| AST (Aspartate aminotransferase) | 10–40 U/L | Liver cell damage: also raised in muscle and heart disease |
| ALP (Alkaline phosphatase) | 44–147 U/L | Liver or bile duct disease; bone disease |
| GGT (Gamma-GT) | Men: <71 U/L; Women: <42 U/L | Bile duct disease; alcohol use |
| Bilirubin (total) | 0.1–1.2 mg/dL | Jaundice: from red cell breakdown or bile duct obstruction |
| Albumin | 3.5–5.0 g/dL | Liver synthetic function: low in chronic liver disease |
| Total protein | 6.3–8.2 g/dL | Combined albumin and globulin |
| INR / Prothrombin time | INR 0.8–1.2 | Clotting factor production: impaired in severe liver disease |
How to read your LFT pattern
Hepatocellular vs cholestatic pattern
Hepatocellular pattern (liver cell damage): ALT and AST raised much more than ALP. Causes: hepatitis (viral, alcoholic, autoimmune), fatty liver disease, paracetamol overdose. Cholestatic pattern (bile duct obstruction): ALP and GGT raised more than ALT and AST. Causes: gallstones, bile duct cancer, primary biliary cholangitis. Mixed pattern: both groups raised, seen in severe hepatitis or drug reactions.
What does a raised ALT mean?
ALT is the most liver-specific enzyme. Causes of raised ALT by level: mild (1–3x normal): fatty liver (NAFLD), alcohol, medications, thyroid disease; moderate (3–10x): hepatitis B or C, drug-induced liver injury, autoimmune hepatitis; severe (>10x): acute viral hepatitis, ischaemic hepatitis ("shock liver"), paracetamol overdose, acute biliary obstruction. Isolated mild ALT elevation (1–2x normal) is very common and often from fatty liver.
LFT checklist for patients
Questions to discuss with your doctor
- Which tests are abnormal: liver enzymes or liver function?
- Is the pattern hepatocellular or cholestatic?
- Do I need a liver ultrasound?
- Should alcohol or medication be reviewed?
- Do I need tests for hepatitis B or C?
- Should I lose weight to help a fatty liver?
Frequently Asked Questions
What do liver function tests actually measure?
Can liver tests be abnormal without liver disease?
What does a raised ALT and AST indicate?
References
Sources cited on this page. PubMed links open the original abstract.
- Pratt DS, Kaplan MM. Evaluation of abnormal liver-enzyme results in asymptomatic patients. N Engl J Med. 2000;342(17):1266–1271. PMID 10781624 · doi:10.1056/NEJM200004273421707
ALT versus ALP – two different patterns of liver injury
Liver function tests (LFTs) include multiple enzymes that rise in different clinical situations. Understanding which enzyme pattern is elevated guides diagnosis efficiently:
- Hepatocellular pattern (ALT and AST predominant): ALT (alanine aminotransferase) and AST (aspartate aminotransferase) are enzymes inside liver cells (hepatocytes). They leak into the blood when hepatocytes are damaged or dying. A predominantly elevated ALT/AST points to hepatocellular injury: viral hepatitis (hepatitis B and C), alcohol-related hepatitis, drug-induced liver injury (paracetamol overdose, statins, isoniazid), non-alcoholic steatohepatitis (NASH), or ischaemic hepatitis ("shock liver"). ALT is more liver-specific; AST is also found in muscle and heart. An AST:ALT ratio above 2:1 suggests alcohol-related hepatitis (alcohol impairs pyridoxal phosphate, which favours AST over ALT production).
- Cholestatic pattern (ALP and GGT predominant): Alkaline phosphatase (ALP) and GGT are enzymes expressed in bile duct cells. They rise when bile cannot flow normally – biliary obstruction. Causes include gallstones in the common bile duct, bile duct strictures, pancreatic head cancer, primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC). ALP also rises from bone (Paget's disease, metastases, growing bones in children) – GGT is used to confirm the ALP is liver-derived rather than bone-derived.
Albumin and INR – synthetic function markers
ALT and ALP measure liver damage; albumin and prothrombin time (PT/INR) measure liver function – what the liver is actually producing. These markers are critical in assessing the severity of liver disease:
- Albumin: The main protein synthesised exclusively by the liver. Half-life approximately 20 days – so albumin falls only in more prolonged liver dysfunction. Serum albumin below 35 g/L indicates impaired synthetic function; below 25 g/L is severe hypoalbuminaemia with risk of oedema and ascites. Important caveat: albumin is a negative acute phase reactant – it falls in any inflammatory state, not just liver disease.
- Prothrombin time (PT) / INR: The liver synthesises clotting factors (I, II, V, VII, IX, X). A prolonged PT/INR in the context of liver disease indicates failing synthetic function. This is the most sensitive early marker of acute liver failure – rising INR alongside jaundice and confusion (encephalopathy) defines acute liver failure and triggers urgent transplant assessment (King's College criteria).
The Child-Pugh score and MELD (Model for End-Stage Liver Disease) score – both incorporating bilirubin, albumin, and INR – are used to stage chronic liver disease severity and prioritise patients for liver transplantation.
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