Diagnostic Use
This enzyme is present in bone, liver, and placenta. The ALP assay does not differentiate the source. To determine the source of a raised ALP, liver enzymes and P1NP are usually sufficient. 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 of activity are found in rickets, osteomalacia, secondary hyperparathyroidism, healing fractures and Paget’s disease. It is variably increased with malignant deposits in bone.
ALP activity is high in infants, decreases during the second year, and remains increased until puberty.
P1NP (procollagen-1 N-terminal propeptide) is an independent marker of bone turnover which is specific for bone (not increased in liver disease)
Liver:
Increased ALP may be caused by any disease which causes cholestasis including tumours, cirrhosis, hepatitis, liver abscess, drugs or toxins (see Hepatotoxic drug reactions ). An increased ALP and GGT in the absence of a raised bilirubin may indicate mass lesions (e.g. secondary tumours) which leave sufficient unaffected liver for bilirubin excretion to continue at an adequate rate.
Placenta:
ALP from this source increases in the final trimester of pregnancy (up to 5x the upper limit of the reference interval).
Tumours:
Some tumours secrete the placental isoenzyme of ALP (Regan isoenzyne)
Isolated raised ALP
Benign familial hyperphosphatasemia is a cause for a persistent isolated increased ALP and is seen at any age. This is an asymptomatic genetic variant; all other liver enzymes are normal, and there is no evidence for increased bone turnover (normal P1NP). Family members may also have a raised ALP.
In transient hyperphosphatasaemia of infancy the ALP level may be very high (thousands), and typically persists for a few months. The pathogenesis is not known, but it has been suggested to follow viral infections.
Reference Intervals
Serum/plasma ALP reference intervals have been updated on 05/12/17. The predominant change is in paediatrics, to better reflect the physiological changes seen during adolescent years.
While the analytical method has not changed for individual laboratories, this update has incorporated information from recent high-quality publications on population reference interval studies, recommendations by Australasian Association of Clinical Biochemists (AACB) and data mining of laboratory results from NZ adults. If previously used reference intervals are needed or to discuss this further, please contact a chemical pathologist (see below for contact details).
Units: U/L
|
Age
|
Female
|
|
0 to <6 months
|
80 – 600
|
|
6 months to <10 years
|
80 – 450
|
|
10 to <13 years
|
45 – 460
|
|
13 to <15 years
|
45 – 300
|
|
15 to <22 years
|
45 – 150
|
|
22 to <50 years
|
40 – 110
|
|
50 to <60 years
|
40 – 120
|
|
60 years and over
|
40 – 130
|
|
Age
|
Male
|
|
0 to <6 months
|
80 – 600
|
|
6 months to <10 years
|
80 – 450
|
|
10 to <15 years
|
45 – 500
|
|
15 to <17 years
|
45 – 380
|
|
17 to <19 years
|
45 – 220
|
|
19 to <22 years
|
45 – 150
|
|
22 to <50 years
|
40 – 110
|
|
50 to <60 years
|
40 – 120
|
|
60 years and over
|
40 – 130
|
Uncertainty of Measurement
2 U/L for results around 25 U/L
6% for results around 300 U/L