Liver Function Tests
“Liver function tests” (LFTs) are a group of blood tests that reflect different aspects of liver and biliary tract health. In practice they help you:
- Detect and characterise liver injury (hepatocellular vs cholestatic vs mixed).
- Assess synthetic function (albumin, clotting factors).
- Monitor progression or resolution of liver disease and the effect of treatment.
Always interpret LFTs in context of the patient’s history, examination, medicines and local reference ranges.
Common LFT Components
The table below summarises what each main test reflects and typical causes of abnormal results.
| Parameter | Predominantly Reflects | Common Causes of Elevation | Comments / Low Values |
|---|---|---|---|
| Alanine aminotransferase (ALT) | Hepatocellular injury (enzyme mainly in liver cells). | Acute viral hepatitis, drug-induced liver injury (e.g. paracetamol), ischaemic hepatitis (“shock liver”), non-alcoholic fatty liver disease, autoimmune hepatitis, chronic viral hepatitis. | Very low ALT is rarely clinically significant. Mild elevations can occur with metabolic syndrome or medications. |
| Aspartate aminotransferase (AST) | Hepatocellular injury, but also present in muscle and heart. | Similar to ALT. AST:ALT ratio > 2 suggests alcoholic liver disease; marked rises (> 1000 IU/L) can be seen in acute viral or ischaemic injury. Elevation can also be from muscle injury (myositis, rhabdomyolysis). | Low AST is usually not significant. Always consider muscle or cardiac sources if CK or troponins are abnormal. |
| Alkaline phosphatase (ALP) | Cholestasis (bile ducts) and bone turnover. | Cholestatic liver disease and biliary obstruction (stones, strictures, tumours), infiltrative liver disease (metastases, granulomas), pregnancy, bone disease (Paget’s disease, bone metastases, healing fractures). | Low ALP is uncommon; may be seen in severe malnutrition, zinc or magnesium deficiency, hypothyroidism, or rare conditions such as hypophosphatasia. |
| Gamma-glutamyl transferase (GGT) | Biliary enzyme; sensitive but not specific. | Cholestasis, alcohol use, many hepatotoxic drugs, non-alcoholic fatty liver disease, pancreatic or biliary disease. | Often used together with ALP – a raised ALP with raised GGT suggests hepatobiliary origin. Low GGT is usually not clinically significant. |
| Bilirubin (total) | Haem breakdown and hepatic excretion. |
Pre-hepatic: haemolysis, large haematomas. Hepatic: hepatitis, cirrhosis, drugs, sepsis. Post-hepatic: biliary obstruction (stones, tumours, strictures). |
Low bilirubin is not usually clinically relevant. An isolated mild unconjugated rise with normal other tests may suggest Gilbert’s syndrome. |
| Albumin | Liver synthetic function and chronic disease (long half-life). | “High” albumin is usually due to haemoconcentration/dehydration. | Low albumin suggests chronic liver disease, malnutrition, nephrotic syndrome, protein-losing enteropathy or chronic inflammation. It changes slowly and is less useful in acute illness. |
| Prothrombin time / INR | Liver synthesis of clotting factors (short half-life). | Prolonged PT/INR indicates impaired hepatic synthetic function (e.g. acute severe hepatitis, decompensated cirrhosis), vitamin K deficiency, warfarin therapy or DIC. | This is a key marker of severity in acute liver failure and chronic liver disease. Correction with vitamin K helps distinguish synthetic failure from vitamin K deficiency. |
Reference ranges vary between laboratories. Always check your local lab values rather than relying on fixed cut-offs.
Interpreting LFT Patterns
Instead of looking at each value in isolation, look for overall patterns: hepatocellular, cholestatic (“surgical-type” jaundice), mixed or isolated abnormalities.
| Pattern | ALT / AST | ALP / GGT | Bilirubin | Albumin / PT (synthetic) | Typical Causes |
|---|---|---|---|---|---|
| Normal | Within reference range | Within reference range | Normal (< ~20 μmol/L) | Normal | No biochemical evidence of liver disease, but does not exclude early or mild disease. |
|
Predominantly hepatocellular (“medical jaundice” pattern) |
Markedly raised (often > 10× normal), usually > ALP | Normal or mildly raised (up to ~2–3×) | Normal or raised (depending on severity and duration) | May be normal early; can be impaired in severe or chronic disease (low albumin, prolonged PT/INR). | Acute viral hepatitis, drug-induced liver injury (e.g. paracetamol), ischaemic hepatitis, autoimmune hepatitis, acute alcoholic hepatitis. |
|
Predominantly cholestatic (“surgical jaundice” pattern) |
Normal or mildly elevated (often < 5× normal) | Markedly raised ALP and GGT (often > 3× normal) | Raised conjugated bilirubin | Usually preserved early; may fall or PT may rise in prolonged obstruction or underlying chronic liver disease. | Extra-hepatic biliary obstruction (stones, strictures, pancreatic or biliary tumours), primary sclerosing cholangitis, primary biliary cholangitis, drug-induced cholestasis. |
| Mixed hepatocellular & cholestatic | Both ALT/AST and ALP/GGT raised significantly | Both sets of enzymes raised | Often raised | May be normal or impaired depending on severity | Many drug reactions, advanced biliary disease, infiltrative liver disease, severe alcoholic hepatitis, sepsis-associated liver dysfunction. |
| Isolated hyperbilirubinaemia | Normal | Normal | Raised (unconjugated or conjugated) | Usually normal |
Unconjugated: haemolysis, Gilbert’s syndrome, resorbing haematoma. Conjugated: early obstruction or hepatocellular disease before enzymes rise. |
| Synthetic failure (advanced disease) | May be only mildly elevated or even normal | Normal, high or low depending on cause | Often raised | Low albumin and prolonged PT/INR – key markers of poor prognosis | Decompensated cirrhosis, acute liver failure, severe sepsis with hepatic dysfunction. |
In the ED, the most urgent questions are: “Is this acute severe liver injury?”, “Is there biliary obstruction needing imaging/surgical input?” and “Is synthetic function impaired?”. The pattern and the PT/INR will usually guide you.