Alkaline phosphatase in serum consists of four structural genotypes: the liver-bone-kidney type, the intestinal type, the placental type and the variant from the germ cells. It occurs in osteoblasts, hepatocytes, leukocytes, the kidneys, spleen, placenta, prostate and the small intestine. The liver-bone- kidney type is particularly important.
The precise metabolic function of ALP has not yet been fully elucidated, however the enzyme is associated with intestinal lipid transport and bone calcification. ALP originates in approximately equal proportions from the liver and the skeletal system. Approximately 25% of healthy individuals also have intestinal ALP which accounts for approximately 10% of the total ALP in a fasting sample. Increases in total ALP are either due to physiological causes, or are caused by diseases of the liver or bone. Physiological increases in ALP are found in pregnancy from the 2nd trimester onwards due to placental ALP, in growing children due to bone ALP and postprandially in individuals with blood groups B and O, who are secretors of blood group substance H (intestinal ALP).
The most common cause of elevated ALP is hepatobiliary disease, with pathological ALP levels found in approximately 60% of patients with disease of the liver or biliary tract. A rise in the alkaline phosphatase occurs with all forms of cholestasis, particularly with obstructive jaundice.
ALP levels may also be elevated in primary bone diseases, such as osteomalacia, osteogenesis imperfecta, vitamin D intoxication and primary bone tumours. ALP levels may also be increased in secondary bone diseases, such as skeletal metastases, and in diseases such as multiple myeloma, acromegaly, renal insufficiency, hyperthyroidism, ectopic ossification, sarcoidosis, bone tuberculosis and healing fractures. In bone diseases such as Paget’s disease, vitamin D deficiency rickets and metastatic bone disease, ALP activity is a good indicator of bone activity, in the absence of co-existing chronic liver disease. Total ALP is only occasionally elevated in some metabolic bone diseases such as hyperparathyroidism, osteopenia or osteoporosis. Reduced levels of ALP are found in familial hypophosphatasia, hypoparathyroidism, achondroplasia, adynamic bone disease in dialysis patients, pituitary dwarfism, chronic radiation sickness and malnutrition.
Adults Males 40-129 U/L (0.67-2.15 μkat/L) Females 35-104 U/L (0.58-1.74 μkat/L) Children Male 0 - 14 days 83-248 U/L (1.39-4.14 μkat/L) 15 days - <1 year 122-469 U/L (2.04-7.83 μkat/L) 1 - < 10 years 142-335 U/L (2.37-5.59 μkat/L) 10 - < 13 years 129-417 U/L (2.15-6.96 μkat/L) 13 - < 15 years 116-468 U/L (1.94-7.82 μkat/L) 15 - < 17 years 82-331 U/L (1.37-5.53 μkat/L) 17 - < 19 years 55-149 U/L (0.92-2.49 μkat/L) Female 0 - 14 days 83-248 U/L (1.39-4.14 μkat/L) 15 days - < 1 year 122-469 U/L (2.04-7.83 μkat/L) 1 - < 10 years 142-335 U/L (2.37-5.59 μkat/L) 10 - < 13 years 129-417 U/L (2.15-6.96 μkat/L) 13 - < 15 years 57-254 U/L (0.95-4.24 μkat/L) 15 - < 17 years 50-117 U/L (0.84-1.95 μkat/L) 17 - < 19 years 45-87 U/L (0.75-1.45 μkat/L)