Reference — Gastrointestinal
Liver Laboratory Values
Quick reference for hepatic laboratory interpretation — hepatocellular injury markers, cholestatic markers, and synthetic function tests with normal ranges and clinical significance.
Educational use only. Reference ranges vary by laboratory and patient population. Always interpret results in the 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 Markers
AST (Aspartate Aminotransferase)Normal: 10–40 U/L
| Elevated causes | Hepatitis (viral, alcoholic, autoimmune), ischemic hepatitis, drug-induced liver injury, muscle injury (myocardial infarction, rhabdomyolysis), hemolysis |
| Decreased causes | B6 deficiency (pyridoxine — cofactor for AST synthesis) |
| Clinical note | AST:ALT ratio >2:1 with GGT elevation strongly suggests alcoholic hepatitis. Less specific than ALT for hepatic disease (found in heart, muscle, kidney). |
ALT (Alanine Aminotransferase)Normal: 7–56 U/L
| Elevated causes | Hepatitis (viral, alcoholic, NASH, autoimmune), drug/toxin-induced liver injury, biliary obstruction, celiac disease |
| Decreased causes | Not clinically significant |
| Clinical note | More specific to liver than AST. ALT >10× normal = acute hepatic necrosis (ischemia, acetaminophen toxicity, viral hepatitis). Serial trending more important than single value. |
AST:ALT RatioNormal: ~1:1
| Elevated causes | >2:1 = alcoholic hepatitis (especially with GGT elevation). >3:1 = highly suggestive of alcohol etiology. |
| Decreased causes | Not applicable |
| Clinical note | Useful pattern: ALT > AST in viral hepatitis. AST > ALT in alcoholic hepatitis (alcohol depletes pyridoxine needed for ALT synthesis). |
Cholestatic / Biliary Markers
ALP (Alkaline Phosphatase)Normal: 44–147 U/L (adult)
| Elevated causes | Biliary obstruction (choledocholithiasis, cholangiocarcinoma, PSC, PBC), liver metastases, Paget's disease of bone, bone growth (adolescents), pregnancy (placental ALP) |
| Decreased causes | Zinc deficiency, hypothyroidism, pernicious anemia, cardiac surgery with bypass |
| Clinical note | ALP alone does not diagnose liver disease — must correlate with GGT. Isolated elevated ALP with elevated GGT = biliary/hepatic source. Isolated ALP = consider bone disease. |
GGT (Gamma-Glutamyl Transferase)Normal: 8–61 U/L (M); 5–36 U/L (F)
| Elevated causes | Alcohol use (sensitive marker for chronic use), biliary obstruction, liver disease, pancreatitis, drug-induced liver injury (phenytoin, carbamazepine) |
| Decreased causes | Not clinically significant |
| Clinical note | Most sensitive liver enzyme for alcohol use. GGT + elevated ALP = biliary disease. GGT elevated with normal ALP = consider alcohol. |
Total BilirubinNormal: 0.2–1.2 mg/dL
| Elevated causes | Hepatic: hepatitis, cirrhosis, cholestasis. Prehepatic: hemolysis, ineffective erythropoiesis. Posthepatic: bile duct obstruction. Jaundice visible when >2.5 mg/dL. |
| Decreased causes | Not clinically significant |
| Clinical note | Distinguish indirect (unconjugated, prehepatic) vs direct (conjugated, hepatic/posthepatic) bilirubin. Dark urine + jaundice = direct hyperbilirubinemia (conjugated = water-soluble). |
Direct Bilirubin (Conjugated)Normal: 0–0.3 mg/dL
| Elevated causes | Hepatocellular disease (hepatitis, cirrhosis), biliary obstruction (gallstones, malignancy), Dubin-Johnson syndrome |
| Decreased causes | Not applicable |
| Clinical note | Elevated direct bilirubin = problem conjugating or excreting bilirubin. Associated with dark (tea-colored) urine and clay-colored stools in biliary obstruction. |
Indirect Bilirubin (Unconjugated)Normal: 0.2–0.9 mg/dL
| Elevated causes | Hemolysis (sickle cell, transfusion reaction, autoimmune hemolytic anemia), Gilbert's syndrome, Crigler-Najjar syndrome, neonatal jaundice |
| Decreased causes | Not applicable |
| Clinical note | Elevated indirect bilirubin = unconjugated (fat-soluble). Does NOT appear in urine (not water-soluble). Stool color normal (conjugation and excretion are intact). |
Hepatic Synthetic Function
AlbuminNormal: 3.5–5.0 g/dL
| Elevated causes | Dehydration (hemoconcentration) — not a clinically significant elevation |
| Decreased causes | Cirrhosis and liver failure (decreased synthesis), malnutrition, nephrotic syndrome (urinary losses), severe burns, protein-losing enteropathy, malabsorption |
| Clinical note | Albumin half-life = 20 days — reflects chronic liver function, not acute. Better marker of chronic disease severity than acute injury. Low albumin = ascites risk (decreased oncotic pressure). |
INR (International Normalized Ratio)Normal: 0.8–1.2
| Elevated causes | Liver disease (decreased factor synthesis), warfarin therapy, DIC, vitamin K deficiency (malabsorption, prolonged antibiotics), massive blood transfusion |
| Decreased causes | Not clinically significant |
| Clinical note | INR reflects hepatic synthesis of clotting factors II, VII, IX, X, and Protein C/S. INR is part of the MELD score for liver transplant prioritization. Elevated INR ≠ always anticoagulated — check clinical context. |
PT (Prothrombin Time)Normal: 11–13.5 seconds
| Elevated causes | Same as INR — liver failure, warfarin, DIC, vitamin K deficiency. More sensitive to factor VII (short half-life 4–6 hours) = early marker of acute liver failure. |
| Decreased causes | Not clinically significant |
| Clinical note | PT/INR are the best markers of acute hepatic synthetic failure. In acute liver failure, PT >15 sec or INR >1.5 indicates significant synthetic impairment. |
AmmoniaNormal: 15–45 mcg/dL (may vary by lab)
| Elevated causes | Hepatic encephalopathy (liver failure impairs urea cycle), GI bleed (blood = protein substrate), constipation, high-protein diet, urease-producing bacteria (H. pylori, UTI), renal failure |
| Decreased causes | Not clinically significant in isolation |
| Clinical note | Elevated ammonia alone does not diagnose HE — must correlate with clinical presentation. Ammonia does not reliably track HE severity. Arterial ammonia more reliable than venous. |
Related Resources
Liver Lab Values ChartAll liver labs in a single comparison table with normal ranges
Open →Cirrhosis & Portal HypertensionAscites, varices, hepatic encephalopathy, nursing priorities
Open →Hepatic Encephalopathy ReferenceCauses, ammonia, asterixis, grading, and nursing considerations
Open →Upper GI BleedingVariceal hemorrhage, assessment, and nursing management
Open →Renal Laboratory ValuesBUN, creatinine, eGFR — for hepatorenal syndrome comparison
Open →Standards & sources
Fact-checked Jun 21, 2026This page is written to align with American College of Gastroenterology (ACG) / AGA · ASPEN (nutrition support). 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 →