Bedside Snapshot
- Normal (Adult)
- 10–40 U/L (0.17–0.67 µkat/L). The ACG healthy ULN is lower: ≤33 U/L men, ≤25 U/L women. Use the ULN on your report
- Critical Values
- No universal critical value: interpret by trend and clinical context. Severe >15× ULN; massive >10,000 U/L (>167 µkat/L)
- High Suggests
- Acetaminophen toxicity, ischemic hepatitis (shock liver), acute viral hepatitis, drug-induced injury; fatty liver disease is the most common mild cause
- Low Suggests
- Rarely clinically significant: vitamin B6 deficiency, dialysis, frailty. A normal ALT does not exclude cirrhosis or late liver failure
- Act Now If
- ALT >15× ULN, or any rise with INR ≥1.5, confusion or hypoglycemia: check glucose, INR, APAP level; start NAC if acetaminophen possible; contact a transplant center
- Watch Out For
- A falling ALT with rising INR, bilirubin or confusion is liver failure, not recovery
Reference & Critical Ranges
Lab-specific ranges: Every lab sets its own interval, by analyzer and by population. Your lab report's range is the one that counts. The values below are typical, not a rule for your lab.
Reference ranges
| Population | Conventional | SI | Notes |
|---|---|---|---|
| Adult | 10–40 U/L | 0.17–0.67 µkat/L | Critical Care Transport reference range; many lab reports print an upper limit near 40–55 U/L |
| ACG 2017 healthy ULN, men | ≤33 U/L | ≤0.55 µkat/L | Healthy upper limit of normal 29–33 U/L per the ACG 2017 guideline, below most lab ULNs |
| ACG 2017 healthy ULN, women | ≤25 U/L | ≤0.42 µkat/L | Healthy ULN 19–25 U/L. ALT runs lower in women than in men |
| Pregnancy | Same as nonpregnant women: 10–40 U/L on the Critical Care Transport range (ACG healthy ULN ≤25 U/L) | 0.17–0.67 µkat/L (ACG ≤0.42) | ALT does not rise in normal pregnancy (alkaline phosphatase does). Any elevation needs a cause |
| Older adult | Same as adult | Same as adult | Very low values can reflect frailty or low muscle mass |
| Child 10 y and older, adolescent | ≤26 U/L boys, ≤22 U/L girls | ≤0.43 / ≤0.37 µkat/L | NASPGHAN 2017 pediatric ULN (95th percentile); use these, not the lab ULN, when screening for fatty liver disease |
| Child under 10 y | Age-specific lab interval | — | No verified pediatric cutoff is cited here; use the reporting lab's interval for age |
| Neonate and infant | Age-specific lab interval | — | Some reference laboratories publish no interval under 12 months; interpret with the reporting lab's range |
Severity & critical values
| Level | Conventional | SI | What it means |
|---|---|---|---|
| Borderline | Above the ULN to <2× ULN (men 34–65, women 26–49 U/L on the ACG limits; 41–79 U/L at a lab ULN of 40) | Above the ULN to <2× ULN | Repeat to confirm. Fatty liver, alcohol, medications, chronic hepatitis B or C |
| Mild | 2–5× ULN (men 66–165, women 50–125 U/L) | 2–5× ULN | Same causes as borderline; outpatient workup if the patient is well |
| Moderate | 5–15× ULN (men 165–495, women 125–375 U/L) | 5–15× ULN | Add acute viral hepatitis. Evaluate promptly |
| Severe | >15× ULN (men >495, women >375 U/L) | >15× ULN | Acetaminophen, ischemia, acute viral, drug or autoimmune hepatitis, acute biliary obstruction, Budd-Chiari, HELLP. Same-day evaluation |
| Massive | >10,000 U/L | >167 µkat/L | Mainly ischemic hepatitis (shock liver) or acetaminophen or other toxin injury; rarely HSV or other acute hepatitis |
Critical values: There is no universal lab critical value for ALT. Severe (>15× ULN) or massive (>10,000 U/L) elevations are emergencies. So is any ALT rise with an INR ≥1.5, new confusion or hypoglycemia.
Conversion: U/L × 0.0167 = µkat/L (1 µkat/L = 60 U/L)
Causes of Abnormal Results
High (ALT above your lab's upper limit: 40 U/L on the Critical Care Transport range, lower on the ACG 2017 healthy ULN of 33 U/L men and 25 U/L women)
| Mechanism | Common causes | Bedside clue |
|---|---|---|
| Direct toxic injury | Acetaminophen (APAP), single or repeated supratherapeutic doses; Amanita mushrooms | ALT in the thousands 1–4 days after ingestion; the APAP level may already be low or undetectable |
| Hypoperfusion or hypoxia | Ischemic hepatitis (shock liver): cardiac arrest, shock, sepsis, severe hypoxemia, acute heart failure | Recent hypotension; AST and lactate dehydrogenase (LDH) very high early; creatinine often rises |
| Acute viral hepatitis | Hepatitis A, B (new or reactivated), C, E; herpes simplex virus (HSV), Epstein-Barr virus, cytomegalovirus | Prodrome, jaundice. HSV: fever, often no jaundice, in pregnancy or immunosuppression |
| Idiosyncratic drug-induced liver injury (DILI) | Antibiotics (amoxicillin-clavulanate, isoniazid, nitrofurantoin), antiepileptics, NSAIDs, anabolic steroids, herbal and dietary supplements | New drug or supplement in the past weeks to months; ask about over-the-counter products |
| Pregnancy-specific | HELLP syndrome (hemolysis, elevated liver enzymes, low platelets), acute fatty liver of pregnancy (AFLP), preeclampsia | Second half of pregnancy or postpartum; hypertension, low platelets; hypoglycemia in AFLP |
| Vascular or biliary | Acute Budd-Chiari syndrome, hepatic artery thrombosis, a passing common bile duct stone | Right upper quadrant pain, ascites; after a stone, the spike fades as alkaline phosphatase (ALP) and bilirubin rise |
| Chronic liver disease | Metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD), alcohol-associated disease, chronic hepatitis B or C, hemochromatosis, autoimmune hepatitis, Wilson disease, alpha-1 antitrypsin deficiency | Usually <5× ULN; obesity, diabetes, alcohol use; Wilson disease in younger patients |
| Nonhepatic or systemic | Rhabdomyolysis, strenuous exercise, heat stroke, celiac disease, thyroid disease, adrenal insufficiency | High creatine kinase (CK) with AST well above ALT; recent exertion or heat exposure |
Acute liver failure (ALF): Liver injury, an INR ≥1.5 and any encephalopathy at all? If there is no pre-existing cirrhosis and the illness is under 26 weeks, that is ALF, and the ALT value does not matter. Wilson disease, autoimmune hepatitis and vertically acquired hepatitis B may still qualify. Start the ALF workup. Call a transplant center within hours.
Low (below the lab's lower limit)
A low ALT rarely matters on its own. It can hide liver injury. It can also mark poor health.
| Mechanism | Common causes | Bedside clue |
|---|---|---|
| Cofactor deficiency | Pyridoxine (vitamin B6) deficiency: alcohol use disorder, malnutrition | Assays without added pyridoxal phosphate read low; ALT understates injury |
| Kidney failure | Chronic kidney disease, hemodialysis | ALT runs low; a value inside the range may still be raised for that patient |
| Low muscle mass | Frailty and sarcopenia in older adults | Very low ALT is linked to frailty and higher mortality in observational studies |
| Few hepatocytes left | Advanced cirrhosis, late acute liver failure | Normal or falling ALT with low albumin, high INR or bilirubin |
Interpretation & Bedside Approach
Step-by-step approach
- Is it real? Well patient? Repeat the panel before you work it up. Marked hemolysis, recent strenuous exercise or a high CK point away from the liver.
- How sick is the patient? Check mental status, glucose, INR, bilirubin, blood pressure and lactate. In acute hepatitis, encephalopathy with an INR ≥1.5 means acute liver failure.
- Acute or chronic, and which way is it going? Compare with old results. ALT clears with a half-life of about 2 days. After one ischemic insult it peaks within 1–3 days, then falls steadily. A fall with a worsening INR or bilirubin means hepatocyte loss.
- Calculate derived values: the multiple of ULN, the R ratio (pattern) and the AST:ALT ratio.
- Classify: grade severity with the ACG 2017 bands and the pattern with the R ratio, then apply named criteria: acute liver failure (ACG 2023 guideline), Hy's law for drug injury (ACG 2021 DILI guideline) and the NIAAA criteria for alcohol-associated hepatitis (ACG 2024 guideline).
- Escalate or dispose: Moderate, severe and massive elevations all need immediate evaluation. Possible ALF needs ICU care and early transplant-center contact. A borderline or mild value in a well patient can be repeated as an outpatient.
R ratio (pattern of injury)
R = (ALT ÷ ALT ULN) ÷ (ALP ÷ ALP ULN)
R >5 hepatocellular; R 2–5 mixed; R <2 cholestatic.
AST:ALT ratio: usually <1 in viral hepatitis and MASLD. A ratio of ≥2, with both values under about 300 U/L, points toward alcohol-associated liver disease.
Pattern recognition
| Pattern | Suggests |
|---|---|
| ALT and AST in the thousands within 1–3 days of shock or arrest, very high LDH, rising creatinine | Ischemic hepatitis; enzymes fall quickly once perfusion is restored |
| ALT in the thousands with possible acetaminophen use, or no clear cause | APAP hepatotoxicity until proven otherwise: APAP level, start acetylcysteine (NAC) |
| ALT greater than AST, hundreds to thousands, jaundice, prodrome | Acute viral hepatitis, DILI or autoimmune hepatitis |
| AST:ALT >1.5, AST >50 U/L, AST and ALT both <400 U/L, bilirubin >3 mg/dL, jaundice onset within 60 days of heavy drinking (>40 g/day women, >60 g/day men, for 6 months or more), with less than 60 days of abstinence before jaundice | Probable alcohol-associated hepatitis (NIAAA criteria) after other causes are excluded |
| AST far above ALT with a very high CK | Muscle source: rhabdomyolysis, exertion, heat stroke |
| ALT or AST >3× ULN plus bilirubin >2× ULN without a cholestatic (high ALP) start | Hy's law: about 10% mortality in drug-induced injury; stop the drug and escalate |
| ALT falling while INR, bilirubin or confusion worsen | Massive hepatocyte loss: impending liver failure, not recovery |
Massive rise, unclear cause: Even with no reported ingestion, a severe or massive ALT rise gets an acetaminophen level. Cold and opioid combination products hide easily. Repeated dosing hides too. NAC helps most when it starts early.
Management Priorities
Emergency: Possible acute liver failure (acute hepatitis with INR ≥1.5 or any encephalopathy)
- Glucose first: check point-of-care glucose now and repeatedly; treat hypoglycemia with IV dextrose.
- Send the core labs: INR, glucose, APAP level, lactate, creatinine, electrolytes, bilirubin, ammonia, blood gas, pregnancy test, viral hepatitis serologies.
- Antidote early: start IV NAC whenever acetaminophen could be involved, without waiting for the level. In adults with non-APAP ALF, ACG 2023 suggests IV NAC (hepatology-directed).
- Call the transplant center: within the first hours; King's College criteria or the Model for End-Stage Liver Disease (MELD) score guide transplant prognosis.
- Monitor & repeat: mental status, glucose, INR and ALT/AST trend; ICU-level care for any encephalopathy.
Medications
Doses vary by protocol; follow local protocols and medical direction.
| Drug | Adult dose | Pediatric dose (max) | Onset / key notes |
|---|---|---|---|
| Acetylcysteine (NAC): APAP-related injury | 300 mg/kg IV over 20–21 hr: two-bag (200 mg/kg over 4 hr, then 100 mg/kg over 16 hr) or three-bag (150 mg/kg over 1 hr, 50 mg/kg over 4 hr, 100 mg/kg over 16 hr); dosing weight max 100 kg | Same mg/kg; 40 kg or less: three-bag regimen using the label's diluent-volume table (weight-based for 5–20 kg, fixed mL for 21–40 kg; watch for fluid overload and hyponatremia) (dosing weight max 100 kg) | Continue past 20–21 hr at the final-bag rate until stopping criteria are met; watch for anaphylactoid reactions during the load |
| Acetylcysteine (NAC): non-APAP ALF | IV regimen per hepatology or transplant center (off-label); trial benefit limited to early (grade I–II) encephalopathy | Not recommended in children (no benefit in the pediatric trial) | ACG 2023 suggests it; other guidance is less certain |
| Dextrose 10% (D10): hypoglycemia | 10 g IV (100 mL D10), or 5 g steps, until alert (field max 25 g) | 0.5–1 g/kg IV/IO as D10 5–10 mL/kg (max 25 g) | Recheck glucose at 15 min. Lows recur in ALF because the failing liver cannot release glucose; a continuous infusion may be needed |
Definitive care & disposition
- Acute liver failure or rising INR: ICU admission and early transfer to a transplant center.
- Acetaminophen: poison center (1-800-222-1222) or toxicology; NAC until stopping criteria are met (see the acetylcysteine page).
- Amanita mushroom ingestion: call the poison center or toxicology early; specific antidotal therapy is protocol-dependent.
- Ischemic hepatitis: treat the cause (shock, arrest, heart failure); the liver usually recovers once perfusion is restored.
- HELLP or AFLP: emergency obstetric consult; AFLP needs prompt delivery regardless of gestational age.
- Severe or massive rise without ALF: admit or complete a same-day workup (APAP, viral, autoimmune, Doppler ultrasound); stop hepatotoxic drugs and alcohol.
Doses are typical references. Follow local protocols, medical direction and institutional policy.
Special Populations
| Population | What changes | Clinical implication |
|---|---|---|
| Neonates & infants | Age-specific intervals; ALT also rises with birth-related hypoperfusion | In a febrile or septic neonate, a raised ALT is part of the workup for disseminated HSV; involve pediatric infectious disease |
| Children & adolescents | Healthy ULN 26 U/L boys, 22 U/L girls (age 10 and older); use the lab's age-specific interval under 10 | Lab ULNs miss pediatric fatty liver disease; screening starts at 10 years in children with obesity or cardiometabolic risk |
| Pregnancy | ALT unchanged; ALP rises; albumin falls | Any ALT elevation is abnormal: hyperemesis (first trimester), intrahepatic cholestasis (second or third), preeclampsia, HELLP, AFLP (third) |
| Older adults | No change in ULN; very low values more common | Low ALT can mark frailty; a normal ALT does not rule out drug injury |
| CKD / dialysis | ALT runs lower (pyridoxine deficiency is one reason) | Mild elevations within the range may still be meaningful |
| Liver disease (cirrhosis) | Few hepatocytes left; AST often exceeds ALT | Judge severity by INR, bilirubin, albumin and encephalopathy, not ALT |
| Other: athletes, alcohol use disorder, obesity | Exertion raises ALT and AST; B6 deficiency lowers ALT; ALT rises with body mass index (BMI) | Ask about training and drinking; check CK; interpret against metabolic risk |
Interfering Factors & Pitfalls
Collection & handling
| Factor | Effect | Why | Avoid / fix |
|---|---|---|---|
| Hemolysis | ↑ (small) | Red cells contain some ALT; AST, LDH and K⁺ rise much more | Recollect if markedly hemolyzed; a normal ALT with a high AST in a hemolyzed sample suggests artifact |
Medications & supplements
| Factor | Effect | Why | Avoid / fix |
|---|---|---|---|
| Hepatotoxic drugs and supplements | ↑ (true injury) | Direct (APAP) or idiosyncratic injury | Full medication, over-the-counter and supplement history; stop the suspect agent |
| Statins | ↑ (mild) | Common, usually benign enzyme rise | Serious statin liver injury is rare; interpret a mild rise in context rather than stopping reflexively |
Physiologic / biologic
| Factor | Effect | Why | Avoid / fix |
|---|---|---|---|
| Strenuous exercise, muscle injury | ↑ | Skeletal muscle releases ALT and much more AST | Check CK; repeat after a period without strenuous exercise |
| Pyridoxine (B6) deficiency | False − | ALT needs pyridoxal phosphate as a cofactor | Expect low readings in alcohol use disorder, malnutrition and dialysis; consider an assay with added cofactor |
Assay & device-specific
| Factor | Effect | Why | Avoid / fix |
|---|---|---|---|
| Different lab ULNs | Varies | Labs set ULNs from different populations (31–72 U/L in one survey) | Express results as multiples of ULN; compare serial values from the same lab |
Common misinterpretations
- “Inside the printed range means healthy”: Many lab ULNs sit above the healthy ULN, so a value inside the printed range is not proof of health.
- “Higher ALT means a worse outcome”: ALT measures injury, not function. It is INR, bilirubin, encephalopathy and glucose that predict outcome.
- “Normal ALT rules out liver disease”: Cirrhosis, B6 deficiency and late liver failure can all produce a normal ALT.
- “AST:ALT >2 is always alcohol”: The ratio helps only when the values are modest. Ischemic, muscle and early acute injury also raise AST first.
Physiology & Test Basics
What it measures
ALT (alanine aminotransferase, formerly SGPT) measures an enzyme that leaks into the blood when hepatocytes are injured. It marks liver cell injury. It does not measure liver function. AST lives in many more tissues. That is why ALT is the more liver-specific of the two.
Physiology & regulation
- Location: mainly in the cytoplasm of hepatocytes; small amounts in kidney, skeletal muscle and heart.
- Reaction: It moves an amino group from alanine to alpha-ketoglutarate. That links amino acid and glucose metabolism.
- Cofactor: needs pyridoxal phosphate (vitamin B6).
- Release: The enzyme leaks out when a hepatocyte membrane is damaged or the cell dies.
- Clearance: half-life about 2 days. That is longer than AST, so ALT stays high longer during recovery.
How it is measured
- Specimen: serum (gold or red top) or lithium-heparin plasma (light-green top); avoid hemolysis. No fasting needed.
- Panels: part of the comprehensive metabolic panel and the hepatic function panel.
- Method: Automated enzymatic rate assay on the main chemistry analyzer, reported in U/L. Some methods add pyridoxal phosphate. That corrects the low readings seen in B6 deficiency.
- Setting: A hospital lab test. It is not on most prehospital or transport point-of-care devices.
Why it matters
In the emergency department and ICU, ALT is the first clue to acetaminophen poisoning, shock liver and acute hepatitis. Three things decide how fast a patient needs an antidote, intensive care or a transplant center. The size of the rise. Its pattern against ALP and AST. Its trend alongside INR and bilirubin.
Clinical Pearls
Three questions for an ALT in the thousands: Ask these first. Could this be acetaminophen? Was there shock, arrest or hypoxia? Acute viral or drug hepatitis? Toxic mushrooms and HELLP round out the list. Between them, those causes cover almost every case.
Transport handoff for suspected liver failure: Hand over the timed glucose trend, INR, ALT/AST and bilirubin, each with its draw time. Include the APAP level, the ingestion time, and the NAC bag number and start time. Recheck glucose en route. Hypoglycemia can recur during the flight or drive.
Confusion with liver injury: check glucose first: Hypoglycemia and hepatic encephalopathy look alike. Check point-of-care glucose before any sedative. Report new drowsiness or confusion at once, because it changes the diagnosis to acute liver failure.
Late acetaminophen presenters: More than a day after ingestion, the APAP level can read undetectable while ALT climbs. The nomogram does not apply here. Per the 2023 US/Canada consensus, start NAC for elevated ALT/AST or signs of toxicity after a possible overdose.
Cardiac arrest survivors: On day 1–3 after return of circulation, ALT and AST spike with very high LDH. Usually that is ischemic hepatitis. The spike should fall quickly. A slow fall, or a rising INR, needs another explanation.
A normal ALT early after an overdose is expected: ALT rarely rises in the first day after an acute acetaminophen ingestion. So a normal early ALT does not exclude toxicity. The timed APAP level on the nomogram decides treatment.
References
- Kwo, P. Y., Cohen, S. M., & Lim, J. K. (2017). ACG clinical guideline: Evaluation of abnormal liver chemistries. American Journal of Gastroenterology, 112(1), 18–35. https://doi.org/10.1038/ajg.2016.517
- Shingina, A., Mukhtar, N., Wakim-Fleming, J., et al. (2023). Acute liver failure guidelines (American College of Gastroenterology). American Journal of Gastroenterology, 118(7), 1128–1153. https://doi.org/10.14309/ajg.0000000000002340
- Chalasani, N. P., Maddur, H., Russo, M. W., et al. (2021). ACG clinical guideline: Diagnosis and management of idiosyncratic drug-induced liver injury. American Journal of Gastroenterology, 116(5), 878–898. https://doi.org/10.14309/ajg.0000000000001259
- Jophlin, L. L., Singal, A. K., Bataller, R., et al. (2024). ACG clinical guideline: Alcohol-associated liver disease. American Journal of Gastroenterology, 119(1), 30–54. https://doi.org/10.14309/ajg.0000000000002572
- Dart, R. C., Mullins, M. E., Matoushek, T., et al. (2023). Management of acetaminophen poisoning in the US and Canada: A consensus statement. JAMA Network Open, 6(8), e2327739. https://doi.org/10.1001/jamanetworkopen.2023.27739
- Xanthakos, S. A., Ibrahim, S. H., Adams, K., et al. (2025). AASLD practice statement on the evaluation and management of metabolic dysfunction-associated steatotic liver disease in children. Hepatology, 82(5), 1352–1394. https://doi.org/10.1097/HEP.0000000000001368
- Verma, D., Saab, A. M., Saab, S., & El-Kabany, M. (2021). A systematic approach to pregnancy-specific liver disorders. Gastroenterology & Hepatology (N Y), 17(7), 322–329. https://pmc.ncbi.nlm.nih.gov/articles/PMC8475247/
- Lim, Y. T., Lau, S., Cheng, A., et al. (2025). Pictorial review of ischaemic hepatitis and its mimics. Singapore Medical Journal, 66(1), 47–53. https://doi.org/10.4103/singaporemedj.SMJ-2022-071
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