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Alkaline Phosphatase (ALP)

Blood Sciences Test



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Reference Range

Age (up until) Up to 29 days

  • Min : 70
  • Max : 380

Age (up until) 29 days-16 years

  • Min : 60
  • Max : 425

Age (up until) 16 years-120 years

  • Min : 30
  • Max : 130

Test Usage

Alkaline phosphatase refers to a family of enzymes that catalyze hydrolysis of phosphate esters at an alkaline pH. ALP is present (in decreasing order of abundance) in placenta, intestine, kidney, bone and liver. In adults, more than 80% of serum ALP activity derives from liver and bone. In late pregnancy, placental ALP is increased. In children and adolescents most serum ALP activity originates in osteoblasts and correlates with the rate of bone growth. The serum half life is seven days.

Familial benign hyperphosphatasaemia shows as a raised ALP throughout life.

Several caveats must be remembered in interpreting ALP results.

  • ALP levels should ideally be measured after fasting because enzyme levels increase as much as 30 U/L after food ingestion. Patients with blood group O and B who are secretors can have increased ALP levels after eating a fatty meal because of the release of intestinal enzyme.
  • Africans have 10 to 15% higher ALP serum levels than Caucasians.
  • In children, ALP is increased up to 3 times the upper limit of normal and in pregnant patients it can be increased up to 2 times normal.
  • ALP levels may double following bone fracture.
  • Smokers have 10% higher ALP levels than nonsmokers do.
  • ALP levels fluctuate approximately 6% from week to week in a healthy individual.

ALP is most useful in diagnosing cholestatic liver diseases. Bile duct obstruction results in increased synthesis of ALP by bile duct epithelial cells and release of ALP into the serum. Alkaline phosphatase may be increased even if only a few small bile ducts are obstructed and serum bilirubin is normal. Serum ALP often exceeds four times the upper limit of normal in extrahepatic and intrahepatic cholestasis. The most common causes of extrahepatic cholestasis are pancreatic cancer, common duct stones and strictures, and primary sclerosing cholangitis. Intrahepatic cholestasis is usually due to primary biliary cirrhosis or drug reactions (erythromycin, chlorpromazine, estrogens, and methyltestosterone). Patients with primary sclerosing cholangitis and primary biliary cirrhosis initially have elevated ALP and normal bilirubin levels.

When the ALP level is increased disproportionately to the bilirubin level (e.g. a bilirubin < 1.0 mg/dL and ALP > 1000 U/L), granulomatous or infiltrative diseases of the liver are likely. Possible diagnoses include sarcoidosis, fungal infections, tuberculosis, and lymphoma. ALP levels are also increased in hyperthyroidism, cardiac failure, lymphoma, and hypernephroma.

Lower ALP levels (< 3 times the upper limit of normal) are less specific for cholestatic liver disease and may be seen with hepatocellular diseases such as acute viral hepatitis, chronic hepatitis, and cirrhosis. However, it is important to remember that incomplete obstruction by gallstones may produce mildly elevated ALP levels. Intrahepatic cholestasis secondary to anabolic steroids or birth control pills may cause mild increases in ALP. Gamma glutamyltransferase (GGT) can be measured to determine if elevated ALP levels are of liver origin; increased GGT indicates that ALP is most likely from the liver.

Medications that have been reported to increase ALP include; allopurinol, anabolic steroids, captopril, carbamazepine, chlorpromazine, chlorpropamide, diltiazem, erythromycin, estrogens, flutamide, gold salts, methimazole, methyltestosterone, phenothiazines, phenylbutazone, phenytoin, quinidine, sulfonamides, tolazamide, tolbutamide, trimethoprim-sulfamethoxazole, valproic acid, and verapamil.

Sometimes it is useful to look at the relationship of ALP to bilirubin and lactate dehydrogenase (LD) levels.

Pathology ALP Bilirubin LD
Intra or extrahepatic cholestasis Increased Increased Normal
Focal benign cholestasis Increased Normal Normal
Focal malignant cholestasis Increased Normal Increased

Osteoblastic bone disease can also increase serum ALP. The most common bone disorders associated with elevated ALP are; Paget’s disease, osteomalacia, hyperparathyroidism, osteogenic sarcoma, and bone metastases.

Low alkaline phosphatase levels have been reported in patients with magnesium deficiency, hypothyroidism, malnutrition, hemolytic anemia, Wilson’s Disease, post coronary bypass surgery, estrogen replacement therapy, and congenital hypophosphatasia. Blood transfusion causes transient decreases in ALP, due to chelation of cations by citrate.

Specimen requirement is one SST tube of blood.

If blood is collected in a citrate or EDTA tube, ALP activity will be almost totally inhibited due to the chelation of zinc and magnesium, which are necessary enzyme cofactors.

Turnaround time

1 day


Local test

Can be added on to an existing request up to 4 days following sample receipt

Specimen Labelling Procedure
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