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09-02-2005, 02:33 PM

Julie,
First... 126 ALP when normal is 125 is NOT high! In fact, you will find regional differences in that "high" number, some suggesting that 135 is normal. Allow at least 10% margin for error.
ALP can be influenced by a variety of things: neulasta, neupogen, wine, etc.

I've attached below an article on reasons why it may be elevated:

Causes of high alkaline phosphatase include bone growth, healing fracture, acromegaly, osteogenic sarcoma, liver or bone metastases, leukemia, myelofibrosis, and rarely myeloma. Alkaline phosphatase is used as a tumor marker.1,2
In rickets and osteomalacia, serum calcium and phosphorus are low to normal, and alkaline phosphatase may be normal or increased.

Hypervitaminosis D may cause elevations in alkaline phosphatase.

In Paget disease of bone there is often isolated elevation of serum alkaline phosphatase. Some of the highest levels of serum ALP are seen in Paget disease.

Hyperthyroidism, by its effects upon bone, may elevate alkaline phosphatase. There is evidence that thyroid hormone (T3) acts to stimulate bone alkaline phosphatase activity through an osteoblast nuclear receptor-mediated process.3

Hyperparathyroidism, in some patients. Pseudohyperparathyroidism.

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

Biliary obstruction (tenfold increase may be seen with carcinoma of the head of pancreas, choledocholithiasis); cholestasis; GGT also high. 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 (eg, with ulcerative colitis), although importantly, 3% of cases of symptomatic sclerosing cholangitis may have normal serum ALP.4 Endoscopic retrograde cholangiography might be considered then in patients with diseases known to be associated with primary sclerosing cholangitis and with appropriate symptomatology even though ALP level is normal. Primary or metastatic tumor in liver: there may be marked increase and GGT 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, GGT and CEA.2

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

Gilbert syndrome: Increase in intestinal alkaline phosphatase is seen.5

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 (eg, sarcoid, TB, amyloidosis, abscess).

Sepsis. Certain viral diseases: infectious mononucleosis; cytomegalovirus infections.

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

Pulmonary infarct (1-3 weeks after embolism. Healing infarcts in other organs, including 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), birth control agents, methyltestosterone, phenothiazines, oral hypoglycemic agents, erythromycin, 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.

09-02-2005, 02:33 PM	#3
al from canada Guest Posts: n/a	Julie, First... 126 ALP when normal is 125 is NOT high! In fact, you will find regional differences in that "high" number, some suggesting that 135 is normal. Allow at least 10% margin for error. ALP can be influenced by a variety of things: neulasta, neupogen, wine, etc. I've attached below an article on reasons why it may be elevated: Causes of high alkaline phosphatase include bone growth, healing fracture, acromegaly, osteogenic sarcoma, liver or bone metastases, leukemia, myelofibrosis, and rarely myeloma. Alkaline phosphatase is used as a tumor marker.1,2 In rickets and osteomalacia, serum calcium and phosphorus are low to normal, and alkaline phosphatase may be normal or increased. Hypervitaminosis D may cause elevations in alkaline phosphatase. In Paget disease of bone there is often isolated elevation of serum alkaline phosphatase. Some of the highest levels of serum ALP are seen in Paget disease. Hyperthyroidism, by its effects upon bone, may elevate alkaline phosphatase. There is evidence that thyroid hormone (T3) acts to stimulate bone alkaline phosphatase activity through an osteoblast nuclear receptor-mediated process.3 Hyperparathyroidism, in some patients. Pseudohyperparathyroidism. Chronic alcohol ingestion (in chronic alcoholism, alkaline phosphatase may be normal or increased, but often with high AST (SGOT) and/or high bilirubin and especially with high GGT; MCV may be high). Biliary obstruction (tenfold increase may be seen with carcinoma of the head of pancreas, choledocholithiasis); cholestasis; GGT also high. 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 (eg, with ulcerative colitis), although importantly, 3% of cases of symptomatic sclerosing cholangitis may have normal serum ALP.4 Endoscopic retrograde cholangiography might be considered then in patients with diseases known to be associated with primary sclerosing cholangitis and with appropriate symptomatology even though ALP level is normal. Primary or metastatic tumor in liver: there may be marked increase and GGT 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, GGT and CEA.2 Cirrhosis, especially in primary biliary cirrhosis, in which fivefold or more increases are seen. Gilbert syndrome: Increase in intestinal alkaline phosphatase is seen.5 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 (eg, sarcoid, TB, amyloidosis, abscess). Sepsis. Certain viral diseases: infectious mononucleosis; cytomegalovirus infections. Postoperative cholestasis. Pancreatitis, carcinoma of pancreas, cystic fibrosis. Pulmonary infarct (1-3 weeks after embolism. Healing infarcts in other organs, including 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), birth control agents, methyltestosterone, phenothiazines, oral hypoglycemic agents, erythromycin, 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.