The standard liver function panel includes markers of hepatocyte injury, cholestasis, synthetic function, and bilirubin metabolism. Understanding what each measures clarifies what an abnormality means:
Transaminases (Hepatocellular Injury Markers)
- ALT (Alanine Aminotransferase): More liver-specific than AST. The primary marker of hepatocyte injury. Elevated in most forms of liver disease.
- AST (Aspartate Aminotransferase): Also found in cardiac muscle, skeletal muscle, kidney, and brain. Less specific for the liver. Important in the AST:ALT ratio.
Your lab's "normal" ALT is probably too high
Most laboratories report an ALT upper limit of normal around 40–55 IU/L, because those ranges were derived from populations that included people with undiagnosed liver disease. The ACG defines the true healthy normal ALT as 29–33 IU/L for males and 19–25 IU/L for females, and recommends that levels above this be assessed rather than dismissed.Practical consequence: a "normal-per-lab" ALT of 38 in a woman is above the healthy normal range and, with metabolic risk factors, still deserves evaluation. Do not let the lab's reference interval end the conversation.
Cholestatic Markers
- ALP (Alkaline Phosphatase): Elevated in biliary obstruction, infiltrative disease, and bone disease. Also elevated in pregnancy (placental isoform). Check GGT to confirm hepatic origin.
- GGT (Gamma-Glutamyl Transferase): Highly sensitive for hepatic origin of ALP elevation. Also elevated with alcohol use, fatty liver, and many medications. Poor specificity in isolation.
Bilirubin
- Total bilirubin: Sum of conjugated (direct) and unconjugated (indirect) fractions.
- Direct (conjugated) bilirubin elevation → hepatic or post-hepatic cause
- Indirect (unconjugated) bilirubin elevation → pre-hepatic (hemolysis) or Gilbert syndrome
Synthetic Function Markers
- Albumin: Synthesized exclusively by the liver. Low albumin reflects reduced hepatic synthetic capacity (half-life ~20 days — chronic marker).
- PT/INR: Reflects clotting factors made by the liver. Prolonged INR in liver disease indicates synthetic dysfunction (acute marker, half-life hours to days).