Chart — Gastrointestinal
Liver Lab Values Chart
Complete liver function panel reference — hepatocellular injury, cholestatic markers, and hepatic synthetic function with normal ranges, elevated and decreased causes, and clinical interpretation flags.
Educational use only. Reference ranges vary by laboratory. Always interpret results in clinical context and per your institution's reference values. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Hepatocellular Injury
| Lab | Normal Range | Elevated Causes | Decreased Causes |
|---|---|---|---|
| AST | 10–40 U/L | Hepatitis, ischemic hepatitis, drug-induced injury, alcoholic hepatitis, myocardial infarction, rhabdomyolysis | Pyridoxine (B6) deficiency |
| AST:ALT >2:1 = alcoholic hepatitisLess liver-specific than ALT — found in heart, muscle, kidney. AST:ALT >2:1 suggests alcoholic hepatitis. | |||
| ALT | 7–56 U/L | Viral hepatitis, NASH, drug toxicity, autoimmune hepatitis, celiac disease, biliary obstruction | Not clinically significant |
| Most liver-specific aminotransferase. ALT >10× normal = severe hepatocellular necrosis (ischemia, acetaminophen, viral hepatitis). | |||
Cholestatic / Biliary Markers
| Lab | Normal Range | Elevated Causes | Decreased Causes |
|---|---|---|---|
| ALP | 44–147 U/L (adult) | Biliary obstruction, cholestasis, liver metastases, Paget's disease of bone, bone growth, pregnancy | Zinc deficiency, hypothyroidism, pernicious anemia |
| ALP + GGT both elevated = biliary/hepatic sourceCorrelate with GGT to confirm hepatic source. Elevated ALP + elevated GGT = biliary/hepatic. Elevated ALP alone = consider bone disease. | |||
| GGT | 8–61 U/L (M) / 5–36 U/L (F) | Alcohol use (most sensitive marker), biliary obstruction, liver disease, drug-induced (phenytoin, carbamazepine) | Not clinically significant |
| Most sensitive for chronic alcohol use. GGT + elevated ALP confirms hepatic origin of ALP elevation. | |||
| Total Bilirubin | 0.2–1.2 mg/dL | Hepatic disease, hemolysis, biliary obstruction, Gilbert's syndrome, Dubin-Johnson. Jaundice visible >2.5 mg/dL. | Not clinically significant |
| Jaundice visible when >2.5 mg/dLDifferentiate conjugated (direct) from unconjugated (indirect) to determine prehepatic vs hepatic vs posthepatic cause. | |||
| Direct Bilirubin (Conjugated) | 0–0.3 mg/dL | Hepatocellular disease (hepatitis, cirrhosis), biliary obstruction (gallstones, malignancy), Dubin-Johnson syndrome | Not applicable |
| Water-soluble → appears in urine (dark urine). Associated with clay-colored stool in complete biliary obstruction. | |||
| Indirect Bilirubin (Unconjugated) | 0.2–0.9 mg/dL | Hemolysis, Gilbert's syndrome, Crigler-Najjar, neonatal jaundice, ineffective erythropoiesis | Not applicable |
| Fat-soluble → does NOT appear in urine. Stool color normal (conjugation/excretion intact). Elevated indirect = pre-hepatic problem. | |||
Hepatic Synthetic Function
| Lab | Normal Range | Elevated Causes | Decreased Causes |
|---|---|---|---|
| Albumin | 3.5–5.0 g/dL | Hemoconcentration/dehydration (not significant elevation) | Cirrhosis/liver failure, malnutrition, nephrotic syndrome, burns, protein-losing enteropathy |
| Half-life 20 days — reflects chronic liver functionHalf-life = 20 days → reflects chronic function, not acute injury. Used in Child-Pugh score. Low albumin → ascites (decreased oncotic pressure). | |||
| INR / PT | INR: 0.8–1.2 / PT: 11–13.5 sec | Liver disease (decreased synthesis of factors II, VII, IX, X), warfarin, DIC, vitamin K deficiency | Not clinically significant |
| Used in MELD score for transplant prioritizationUsed in MELD score (along with bilirubin and creatinine). Factor VII (half-life 4–6 hr) makes PT the most sensitive early marker of acute liver failure. | |||
Metabolic / Additional Markers
| Lab | Normal Range | Elevated Causes | Decreased Causes |
|---|---|---|---|
| Ammonia | 15–45 mcg/dL | Hepatic encephalopathy, GI bleed, constipation, high-protein diet, urease-producing infections (H. pylori), renal failure | Not clinically significant |
| Level does not reliably predict HE severityDoes not need to be severely elevated to cause HE — serum level does not reliably correlate with grade of encephalopathy. | |||
| Platelets | 150,000–400,000/µL | Reactive thrombocytosis (infection, iron deficiency); not directly from liver disease | Cirrhosis with splenomegaly (hypersplenism — splenic sequestration); decreased thrombopoietin (TPO) from liver |
| Thrombocytopenia in cirrhosis = platelet sequestration in enlarged spleen + decreased TPO production. Increases bleeding risk. | |||
| Sodium | 136–145 mEq/L | Hypernatremia is rare in liver disease | Dilutional hyponatremia in cirrhosis — free water retention from ADH/RAAS activation. Na <125 in cirrhosis = poor prognosis. |
| Na <125 in cirrhosis = poor prognosis; consider transplant listingHyponatremia in cirrhosis is dilutional (not true sodium depletion). Fluid restriction, not aggressive sodium supplementation, is the treatment. | |||
Source: AASLD Practice Guidelines; UpToDate Liver Laboratory Tests; ACG Guidelines
Related Resources
Liver Laboratory Values ReferenceDetailed interpretation of each liver lab value
Open →Cirrhosis & Portal HypertensionHow liver labs change in cirrhosis and portal hypertension
Open →Hepatic Encephalopathy ReferenceAmmonia, West Haven grading, lactulose therapy
Open →Hepatic Encephalopathy Staging ChartClinical stages and nursing priorities
Open →Standards & sources
Fact-checked Jun 21, 2026This page is written to align with AASLD Practice Guidelines; ACG Guidelines; UpToDate Liver Laboratory Tests. It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →