Interpretation
This enzyme is present in bone, liver, and placenta. This assay does not differentiate the source. To determine the source of a raised ALP, liver enzymes (GGT) and/or the bone turnover marker (P1NP) may be useful. If the source of a raised ALP is still unclear, ALP isoenzymes can be performed.
Bone – changes occur with age especially during childhood. Increased levels are seen in osteomalacia, rickets, secondary hyperparathyroidism, healing fractures and Paget’s disease.
Bone ALP activity is high in infants, decreases during the second year and remains increased until puberty.
Liver – increased levels are typically associated with cholestatic liver disease and obstructive jaundice, conditions include cirrhosis, hepatitis, liver abscess, tumours, drugs and toxins.
Placenta – ALP rises in the third trimester of pregnancy and may reach 5 times the URL. The placental isoform (Regan) may be secreted by some tumours.
Benign familial hyperphosphatasaemia – this condition may present as a persisting isolated raised ALP presenting at any age. All other liver enzymes are normal with no evidence of increased bone turnover (normal P1NP). Other family members may have a raised ALP. This is an asymptomatic genetic variant.
Transient hyperphosphatasaemia of infancy – an isolated elevated ALP (very high levels – thousands) persisting for a few months. The pathogenesis remains unknown, but may follow a viral infection. Diagnosis may be supported by examination of ALP isoenzymes.
Test Method
Kinetic colour test for the quantitative determination of alkaline phosphatase performed on Beckman Coulter AU5822 analyser using Beckman Coulter reagents.
