The Curbside  ·  Stop 01  ·  Hepatology

String of Pearls

Reading liver function tests in three questions.

Framework adapted from Dr. M. Shujat Rasool. A bedside approach for attendings and trainees.

Never read LFTs as isolated values. Group them, then ask three questions in order. The sequence is the point: injury, then flow, then function.
01

Is the liver injured?

Hepatocyte enzymes: ALT, AST

ALT > AST
Viral hepatitis, MASLD, most drug-induced injury
AST > ALT (ratio >2:1)
Alcohol-associated liver disease
Both in the 1000s
Ischemic hepatitis, acute viral, acetaminophen toxicity

DOTake a drug, alcohol, and viral-risk history. Trend the values, don't react to a single number.

02

Is bile flowing?

Cholestasis markers: ALP, GGT, bilirubin

ALP + GGT both up
Cholestasis or biliary obstruction; GGT confirms the ALP is hepatic
ALP up, GGT normal
Bone source, not liver
Direct bilirubin up
Cholestasis or impaired excretion
Indirect up, rest normal
Hemolysis or Gilbert syndrome

DOIf obstruction is on the table, get a right upper quadrant POCUS.

03

Can the liver still work?

Synthetic function: albumin, INR

INR prolonged
Lost clotting-factor synthesis; your acute-severity marker. Rule out vitamin K deficiency and anticoagulants first
Albumin low
Chronic decline; also malnutrition, nephrotic syndrome, protein loss
Both abnormal
True synthetic failure. Look for decompensation (encephalopathy, ascites); calculate MELD

DOStage the severity. Synthetic failure changes disposition, not just the differential.

The one line to remember

ALT and AST measure damage. Albumin and INR measure function. A cirrhotic liver can show near-normal enzymes and still be failing, so always finish with Question 3.

Two pearls worth the detour

MASLD, the diagnosis behind most "ALT > AST" referrals

Hepatic steatosis on imaging plus at least one cardiometabolic risk factor (raised BMI or waist circumference, dysglycemia, hypertension, high triglycerides, low HDL), with no significant alcohol use or other cause. The rename from NAFLD isn't cosmetic: the diagnosis is now positive (metabolic criteria present) rather than a diagnosis of exclusion.

Wilson disease, the one you miss if you only follow the algorithm

Screen in unexplained liver disease under age 40, especially with neuropsychiatric features. Start with serum ceruloplasmin (low), 24-hour urinary copper (high), and slit-lamp for Kayser-Fleischer rings.

Lab clue: in acute Wilsonian liver failure, a disproportionately low ALP against a very high bilirubin (low ALP:bilirubin ratio), often with Coombs-negative hemolysis.