IN 1923 Robison1 discovered alkaline phosphatase (AP) in bone, and subsequent observations indicated that increased osteoblastic activity resulted in a rise of serum alkaline phosphatase (SAP). Seven years later, Roberts2 noted increased SAP in hepatobiliary disease. Although AP is found in other tissues of the body (intestine, kidney), diseases of the skeletal or hepatobiliary systems are the only ones consistently accompanied by elevated SAP. It has been assumed3-5 that the skeletal system is the chief source of AP, that the liver serves as the excretory organ for this enzyme, and that its rise in the serum is due to reduced excretion by the liver, but this assumption is contrary to experimental and clinical observations.6-8 One of us (M.A.S.) has demonstrated in dogs with biliary fistulas that biliary excretion of AP rises while the serum enzyme rises, an observation that cannot be correlated with the retention (or
Allen H, Spellberg MA. Alkaline Phosphatase in Bile and Urine: Excretion in Patients With Hepatobiliary Disease. Arch Intern Med. 1967;120(6):667–671. doi:10.1001/archinte.1967.00300050023004
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