Liver Function Tests (LFT) - Overview, Normal Ranges, and Interpretation

Since you haven't shared specific values yet, here's a complete picture covering the panel itself, normal ranges, what abnormal patterns mean, and how to interpret them. Share your actual numbers any time and I'll walk through them directly.

1. What's in a standard LFT panel

The "hepatic function panel" typically includes - Henry's Clinical Diagnosis and Management by Laboratory Methods, p. 3044:

Test	What it reflects
ALT (alanine aminotransferase)	Liver cell (hepatocyte) injury - fairly liver-specific
AST (aspartate aminotransferase)	Hepatocyte injury - also found in muscle, heart, RBCs
Alkaline phosphatase (ALP)	Biliary tract/cholestasis, also bone
GGT (gamma-glutamyl transferase)	Confirms hepatobiliary origin of a raised ALP; sensitive to alcohol use
Total & direct bilirubin	Bile pigment excretion/conjugation
Albumin	Synthetic liver function (long half-life, ~20 days)
Total protein	Overall protein status
Prothrombin time (PT/INR)	Synthetic function - clotting factors (short half-life, more acute marker)

Note: "LFTs" is a bit of a misnomer - ALT, AST, ALP and GGT are actually markers of liver injury, not function. Albumin and PT/INR are the true functional tests.

2. Typical normal reference ranges (adult, may vary slightly by lab)

ALT: ~7-56 U/L
AST: ~10-40 U/L
ALP: ~44-147 U/L (higher in children/pregnancy - bone growth/placenta)
GGT: ~9-48 U/L
Total bilirubin: ~0.3-1.2 mg/dL (direct/conjugated: ~0-0.3 mg/dL)
Albumin: ~3.5-5.0 g/dL
Total protein: ~6.0-8.3 g/dL
PT: ~11-13.5 seconds (INR ~0.8-1.1)

Always check the specific reference range printed on your report, since assay methods differ between labs.

3. The key interpretive step: pattern recognition

The most useful clinical approach is to classify the abnormality as hepatocellular vs cholestatic vs isolated hyperbilirubinemia, then judge severity.

Hepatocellular pattern (ALT/AST rise disproportionately more than ALP):

Mild-moderate (<5x ULN): fatty liver (NAFLD/NASH), chronic viral hepatitis, alcohol, medications
Marked (often >1000-10,000 U/L, with ALT > AST): acute viral hepatitis (e.g., Hepatitis A - Symptom to Diagnosis, p. 464), drug-induced liver injury (acetaminophen overdose), ischemic hepatitis, autoimmune hepatitis
AST > ALT ratio >2:1 classically suggests alcoholic hepatitis

Cholestatic pattern (ALP rises disproportionately more than ALT/AST, often with elevated GGT and bilirubin):

Biliary obstruction (gallstones, stricture, tumor), primary biliary cholangitis, primary sclerosing cholangitis, drug-induced cholestasis, infiltrative disease (metastases, granulomas)
GGT elevation confirms the ALP is coming from liver/bile ducts, not bone - Quick Compendium of Clinical Pathology, p. 4-5

Isolated bilirubin elevation (normal ALT/AST/ALP):

Unconjugated: hemolysis, Gilbert syndrome
Conjugated: hepatocellular dysfunction or early cholestasis

Low albumin / prolonged PT/INR with otherwise normal enzymes suggests chronic liver disease with impaired synthetic function (e.g., cirrhosis) rather than acute injury.

4. Severity clues worth flagging

Transaminases in the thousands + coagulopathy + encephalopathy = acute liver failure - urgent.
Transaminases normalize faster than bilirubin during recovery from viral hepatitis (a normal recovery pattern, not a red flag by itself).
Alkaline phosphatase is the most sensitive single marker for hepatic metastases.

Recent evidence check

A 2025 review, Management of asymptomatic patients with abnormal liver function tests (Gabeta et al., European Journal of Internal Medicine, PMID 40784812), reinforces this same stepwise approach: confirm persistence of the abnormality, classify the pattern (hepatocellular vs. cholestatic), then use targeted history, exam, and second-line testing (viral serologies, autoimmune markers, imaging) before invasive workup. This aligns with the textbook approach above, no major contradiction.

If you have an actual report with numbers, paste them (or describe the values) and I'll interpret the specific pattern, likely causes, and what follow-up testing might be reasonable.

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