What is a dangerous alkaline phosphatase level?

ALP levels more than 3 times the upper limit of normal (roughly >400 IU/L in adults) are considered significantly elevated and warrant urgent evaluation. Very high ALP (>1,000 IU/L) is most commonly seen in Paget disease of bone, biliary obstruction, or metastatic bone disease. However, the danger depends on the underlying cause rather than the number alone — even mildly elevated ALP in the setting of other liver test abnormalities may indicate serious disease.

What causes high alkaline phosphatase?

The most common causes of elevated ALP are liver disease (especially cholestasis and biliary obstruction) and bone disease (Paget disease, fracture healing, bone metastases). Other causes include pregnancy (third trimester — placental ALP), growing children and adolescents (bone growth), medications (e.g., phenytoin, carbamazepine), heart failure, and certain malignancies. In isolation, a mildly elevated ALP is often benign.

Is alkaline phosphatase related to liver or bone?

Both. ALP is found in many tissues, but the two major sources are liver (biliary epithelium) and bone (osteoblasts). To determine the source, clinicians use GGT (gamma-glutamyl transferase) or 5'-nucleotidase — if these are also elevated, the ALP is likely hepatic in origin. ALP isoenzyme fractionation can also be performed. Elevated ALP with normal GGT suggests a bone source.

What is the normal ALP range by age?

Normal ALP varies significantly by age. Adults: 44–147 IU/L. Children have much higher levels due to active bone growth — infants may have ALP of 150–420 IU/L, and adolescents during growth spurts can reach 100–390 IU/L. ALP normally rises slightly in healthy adults over age 60, particularly in women after menopause. Pregnancy (third trimester) can double or triple ALP due to placental production.

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Alkaline Phosphatase (ALP) Levels

Comprehensive reference for alkaline phosphatase normal ranges, causes of elevated or low ALP, and clinical interpretation for liver and bone disease.

⚡ Quick Answer — Normal ALP Range

Adults: 44–147 IU/L (0.73–2.44 µkat/L)

Ranges vary by laboratory, age, and sex. Children and adolescents have significantly higher ALP due to active bone growth.

What Is Alkaline Phosphatase?

Alkaline phosphatase (ALP) is a group of isoenzymes found in nearly all body tissues, with the highest concentrations in liver (biliary epithelium), bone (osteoblasts), kidney, intestine, and placenta. The enzyme catalyzes the hydrolysis of phosphate esters in an alkaline environment and plays a role in bone mineralization and hepatic bile transport.

In clinical practice, serum ALP is primarily used as a marker of cholestatic liver disease and bone turnover disorders. It is part of the standard hepatic function panel (liver function tests). When ALP is elevated, the clinical challenge is determining whether the source is hepatic, osseous, or physiological.

ALP levels are influenced by age, sex, blood type, and pregnancy status. Because children and adolescents have high osteoblastic activity during growth, their ALP levels are normally 2–3 times higher than adult reference ranges. Levels also rise in the third trimester of pregnancy due to placental ALP production.

Normal Alkaline Phosphatase Range by Age

Age Group	Conventional (IU/L)	SI (µkat/L)
Newborns (0–14 days)	83–248	1.38–4.13
Infants (15 days–1 year)	122–469	2.03–7.82
Children (1–9 years)	142–335	2.37–5.58
Adolescents (10–17 years, male)	116–468	1.93–7.80
Adolescents (10–17 years, female)	57–254	0.95–4.23
Adults (≥18 years, male)	44–147	0.73–2.44
Adults (≥18 years, female)	35–104	0.58–1.73
Older adults (≥60 years)	Up to 170 (women post-menopause)	Up to 2.83
Pregnancy (3rd trimester)	Up to 2–3× normal	—

Reference ranges from Tietz Clinical Guide to Laboratory Tests, 4th edition. Ranges vary by assay method and laboratory. 1 IU/L ≈ 0.0167 µkat/L.

What Does a High Alkaline Phosphatase Mean?

Elevated ALP is a common laboratory finding. The degree of elevation and clinical context guide the differential diagnosis.

Hepatobiliary Causes (Most Common in Adults)

Cholestasis / biliary obstruction — gallstones, pancreatic head tumors, primary biliary cholangitis, primary sclerosing cholangitis. ALP may reach 3–10× normal.
Hepatitis — viral, alcoholic, or drug-induced. ALP is typically mildly elevated (1–3× normal), with AST/ALT more prominently raised.
Infiltrative liver disease — granulomatous hepatitis (sarcoidosis, TB), hepatic amyloidosis, metastatic cancer to the liver.
Medications — phenytoin, carbamazepine, rifampin, and others can induce ALP synthesis.

Bone Causes

Paget disease of bone — often dramatically elevated (>1,000 IU/L in severe disease).
Fracture healing — transient elevation during callus formation.
Bone metastases — prostate, breast, lung carcinomas with osteoblastic metastases.
Osteomalacia / rickets — from vitamin D deficiency or phosphate wasting.
Hyperparathyroidism — with associated osteitis fibrosa cystica.

Physiological Causes

Pregnancy (third trimester) — placental ALP isoenzyme; can double or triple total ALP.
Children and adolescents — normal bone growth produces elevated bone ALP.
After a fatty meal — transient rise in intestinal ALP (blood groups B and O).

Symptoms of Conditions Causing High ALP

ALP elevation itself is asymptomatic. Symptoms depend on the underlying cause: jaundice, pruritus, and dark urine (cholestasis); bone pain, fractures, or deformity (Paget disease, metastases); fatigue, weight loss (malignancy).

What Does a Low Alkaline Phosphatase Mean?

Low ALP is less common but can be clinically significant. Causes include:

Hypophosphatasia — a rare genetic disorder of ALP deficiency causing impaired bone mineralization. The most specific cause of persistently low ALP.
Malnutrition / protein deficiency — reduced hepatic protein synthesis.
Hypothyroidism — decreased metabolic activity reduces ALP production.
Pernicious anemia (vitamin B12 deficiency) — mechanism not fully understood.
Wilson disease — copper overload may suppress ALP in fulminant hepatic failure (low ALP with high bilirubin is a classic Wilson disease clue).
Zinc deficiency — ALP is a zinc-dependent metalloenzyme.
Cardiac bypass surgery — transient decrease postoperatively.

Clinical pearl: In the setting of acute liver failure, a disproportionately low ALP relative to bilirubin (ALP:bilirubin ratio <4 with high bilirubin) is suggestive of Wilson disease and should prompt urgent ceruloplasmin and copper studies.

Related Tests & Calculators

ALP is best interpreted alongside other liver and bone markers:

GGT (gamma-glutamyl transferase) — elevated GGT with elevated ALP suggests a hepatobiliary source. Normal GGT with elevated ALP points to bone.
5'-Nucleotidase — another liver-specific enzyme to differentiate hepatic vs. bone ALP.
AST and ALT — AST & ALT Levels Reference — help distinguish cholestatic (ALP-predominant) from hepatocellular (aminotransferase-predominant) injury.
Bilirubin — Bilirubin Levels Reference — elevated with ALP in cholestatic disease.
Calcium, phosphate, vitamin D, PTH — to evaluate bone causes.
ALP isoenzyme fractionation — electrophoresis or heat stability testing to identify the tissue source.

About This Test

Clinical Pearls

🔑 Key Points for Clinicians

Isolated ALP elevation (all other LFTs normal) in an otherwise healthy patient is often benign. Recheck in 3–6 months; if persistent, obtain GGT and consider ALP isoenzymes.
The R-ratio (ALT/ULN ÷ ALP/ULN) helps classify liver injury: R <2 = cholestatic, R >5 = hepatocellular, R 2–5 = mixed.
ALP from bone is heat-labile (degrades at 56°C for 10 min); liver ALP is heat-stable. This simple heat inactivation test can help determine the source.
Blood group B and O individuals have transient post-prandial intestinal ALP elevations — draw fasting for accurate results.
In pregnancy, total ALP can reach 2–3× normal in the third trimester. This is physiological and due to placental ALP. Liver-specific ALP or GGT can be used if hepatic pathology is suspected.
Markedly elevated ALP (>10× ULN) has a short differential: biliary obstruction, infiltrative liver disease, Paget disease, and rarely, hepatic metastases.

Specimen and Assay Notes

ALP is measured from a serum or heparinized plasma specimen. EDTA and oxalate anticoagulants chelate the zinc and magnesium cofactors, causing falsely low results — these tubes should not be used. Hemolysis does not significantly interfere. Most modern assays use IFCC-standardized methods at 37°C with p-nitrophenylphosphate as substrate.

References

Burtis CA, Ashwood ER, Bruns DE. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 6th ed. Elsevier; 2018:503-507.
Pratt DS, Kaplan MM. Evaluation of abnormal liver-enzyme results in asymptomatic patients. N Engl J Med. 2000;342(17):1266-1271.
Friedman LS. Approach to the patient with elevated alkaline phosphatase. UpToDate. Accessed January 2025.
Lowe D, Sanvictores T, Zubair M, John S. Alkaline Phosphatase. In: StatPearls. StatPearls Publishing; 2024.
Green J, Czanner G, Reeves G, et al. Oral bisphosphonates and risk of cancer of oesophagus, stomach, and colorectum: case-control analysis within a UK primary care cohort. BMJ. 2010;341:c4444.
Whyte MP. Hypophosphatasia — aetiology, nosology, pathogenesis, diagnosis and treatment. Nat Rev Endocrinol. 2016;12(4):233-246.

References last verified: February 2026