LabCorp Test

Alkaline Phosphatase Blood Test

Quick Overview

Measures the level of alkaline phosphatase in the blood.

Test #001107


Availability: In stock

Also Known As ALK, ALP, Phosphatase, Alkaline
Preparation No special preparation required.
Test Results 1-2 days. May take longer based on weather, holiday or lab delays.

There are many reasons a person can experience high or low levels of alkaline phosphatase. Walk-In Lab’s ALP blood test is a convenient and cheap online solution for identifying your alkaline phosphatase levels.

Causes of high alkaline phosphatase:

  • High alkaline phosphatase levels can be caused by healing fracture, bone growth, acromegaly, liver or bone metastases, osteogenic sarcoma, myelofibrosis, leukemia, and rarely myeloma. A alkaline phosphatase is used as a tumor marker in the body.

  • Sometimes seen in rickets and osteomalacia, serum calcium and phosphorus will often have low to normal levels, while alkaline phosphatase may have normal or increased levels.

  • Hypervitaminosis D sometimes causes spikes in alkaline phosphatase (elevated alkaline phosphatase)

  • Isolated elevation of serum alkaline phosphatase is often see in Paget disease of bone. Some of the highest levels of serum ALP are seen in Paget disease.

  • With its effects upon bone, hyperthyroidism may cause elevate alkaline phosphatase. Evidence shows that the thyroid hormone (T3) acts to stimulate bone alkaline phosphatase activity through an osteoblast nuclear receptor-mediated process.

  • In some patients, Hyperparathyroidism may cause elevated alkaline phosphatase levels. Also, Pseudohyperparathyroidism.

  • Chronic alcohol ingestion can cause increased levels (in chronic alcoholism, alkaline phosphatase may be normal or increased, but often with high AST (SGOT) and/or high bilirubin and especially with high GT; MCV may be high).

  • Biliary obstruction (a tenfold increase in ALP may be seen with carcinoma of the head of pancreas, choledocholithiasis); cholestasis; GT is also elevated. Cholecystitis with cholangitis. (In most patients with cholecystitis and cholangitis who do not have a common duct stone, alkaline phosphatase is within normal limits or only slightly increased.) Sclerosing cholangitis (e.g., with ulcerative colitis), although importantly, 3 percent of cases of symptomatic sclerosing cholangitis may have normal serum ALP. Endoscopic retrograde cholangiography might be considered in patients with diseases known to be associated with primary sclerosing cholangitis and with appropriate symptomatology even though the ALP level is normal. If there is a primary or metastatic tumor in the liver there may be a marked increase, and GT is often high. Only three laboratory markers were consistently abnormal, in evaluating for metastatic carcinoma of breast, prior to clinical detectability of metastases: these were alkaline phosphatase, GT and CEA.

  • Cirrhosis, especially in primary biliary cirrhosis, in which fivefold or more increases in alkaline phosphatase are seen.

  • Gilbert syndrome: Increase in intestinal ALP is seen.

  • Hepatitis: Moderate increases in alkaline phosphatase occur in viral hepatitis, but greater elevations of the transaminases (AST (SGOT), ALT (SGPT)) are usually found.

  • Fatty metamorphosis of liver (moderate increase occurs in acute fatty liver).

  • Diabetes mellitus, diabetic hepatic lipidosis.

  • Infiltrative liver diseases can cause increased levels (e.g., sarcoid, amyloidosis, abscess, TB).

  • Sepsis. Certain viral diseases such as infectious mononucleosis and cytomegalovirus infections.

  • Postoperative cholestasis. Pancreatitis, carcinoma of pancreas, cystic fibrosis.

  • Pulmonary infarct (one to three weeks after embolism. Healing infarcts in other organs, including the kidney, may also cause increased alkaline phosphatase); other situations in which angiofibroplasia occurs, such as healing in a large decubitus ulcer.

  • Tumors, especially hypernephroma; neoplastic ectopic production (Regan, Nagao isoenzymes).

  • Fanconi syndrome.

  • Peptic ulcer, erosion. Intestinal strangulation or obstruction, or ulcerative lesion. Steatorrhea, malabsorption (from bone, secondary to vitamin D deficiency). Ulcerative colitis with pericholangitis, other erosive lesions of colon.

  • Congestive heart failure.

  • Parenteral hyperalimentation of glucose, intravenous albumin administration.

  • Familial hyperphosphatasemia.

  • Idiopathic.

  • Drugs − estrogens (large doses), methyltestosterone, birth control agents, phenothiazines, erythromycin, oral hypoglycemic agents, or any drug producing hypersensitivity or toxic cholestasis. Many commonly and uncommonly used drugs elevate alkaline phosphatase, and tenfold increases may be seen with drug cholestasis.

There are additionally many causes of low alkaline phosphatase levels:

  • Hypophosphatasia: Very low alkaline phosphatase values are found in the presence of normocalcemia or hypocalcemia. This diagnosis may be confirmed by quantitation of urinary phosphoethanolamine.

Hypothyroidism: But most hypothyroid patients have normal alkaline phosphatase.

  • In very few patients, Pernicious anemia can cause low levels of ALP.

  • Malnutrition has been reported to relate to low values, but in practice, diseases causing malnutrition relate often to high alkaline phosphatase results (e.g., disseminated neoplasia).

  • Some drugs such as azathioprine, clofibrate, estrogens and estrogens in combination with androgens) lower serum ALP activity.

  • Serum ALP activity of intestinal origin occurs only in individuals of ABO blood type O or A. They are secretors of ABH RBC antigens and additionally carry the Lewis red cell antigen. Serum intestinal ALP level increases in these individuals about two hours following consumption of a fatty meal.

  • Serum alkaline phosphatase is a member of a family of zinc metalloprotein enzymes that function to split off a terminal phosphate group from an organic phosphate ester. This enzyme functions in an alkaline environment (optimum pH of 10). Active center of ALP enzymes includes a serine residue. Mg and Zn ions are required for minimal activity. Enzyme activity is localized in the brush border of the proximal convoluted tubule of the kidney, hepatic sinusoidal membranes,intestinal mucosal epithelial cells, vascular endothelial cells and osteoblasts of bone. There are distinctive forms of ALP in the placenta and small intestine such as renal, hepatic and osteoblast (bone) ALP are similar molecules.

  • Liver alkaline phosphatase is increased in infiltrative liver disease as well as cholestasis and inflammatory liver disease. The enzyme is sensitive to obstructive biliary processes, even a small secondary bile duct obstruction, and thus may be increased in those patients when the bilirubin is normal due to compensatory bilirubin excretion by the rest of the liver. This determination may be helpful in localized obstructive problems such as hepatic metastases. An electrophoretically slow moving isoenzyme with high relative mass may occur in some patients with bile duct obstruction and hepatic metastases and may result in false elevation of CK-MB.

  • GT is an additional test that can be conducted to confirm biliary abnormality. GT is elevated in hepatobiliary disease, but not in uncomplicated bone disease.

  • Pregnancy increases Serum ALP. Marked decline of high ALP of pregnancy is seen with imminent fetal demise and placental insufficiency

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