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Alkaline Phosphatase (ALP)

Alkaline phosphatase refers to a family of enzymes that catalyze hydrolysis of phosphate estersat 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 andbone. In late pregnancy, placental ALP is increased. In children and adolescents most serumALP activity originates in osteoblasts and correlates with the rate of bone growth. The serumhalf life is seven days.

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Several caveats must be remembered in interpreting ALP results.

ALP levels should always be measured after fasting because enzyme levels increase asmuch as 30 U/L after food ingestion. Patients with blood group O and B who aresecretors can have increased ALP levels after eating a fatty meal because of the releaseof intestinal enzyme.African Americans 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 pregnantpatients 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 inincreased 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 andserum bilirubin is normal. Serum ALP often exceeds four times the upper limit of normal inextrahepatic and intrahepatic cholestasis. The most common causes of extrahepatic cholestasisare 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 primarysclerosing cholangitis and primary biliary cirrhosis initially have elevated ALP and normalbilirubin levels.

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When the ALP level is increased disproportionately to the bilirubin level (e.g. a bilirubin < 1.0mg/dL and ALP > 1000 U/L), granulomatous or infiltrative diseases of the liver are likely.Possible diagnoses include sarcoidosis, fungal infections, tuberculosis, and lymphoma. ALPlevels 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 liverdisease and may be seen with hepatocellular diseases such as acute viral hepatitis, chronichepatitis, and cirrhosis. However, it is important to remember that incomplete obstruction bygallstones may produce mildly elevated ALP levels. Intrahepatic cholestasis secondary toanabolic steroids or birth control pills may cause mild increases in ALP. Gammaglutamyltransferase (GGT) can be measured to determine if elevated ALP levels are of liverorigin; 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.

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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 disordersassociated 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 bypasssurgery, estrogen replacement therapy, and congenital hypophosphatasia. Blood transfusioncauses transient decreases in ALP, due to chelation of cations by citrate.

Reference range in adults is 40 - 125 IU/L (Vitros Analyzer).

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, whichare necessary enzyme cofactors.

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