Samples with a total alkaline phosphatase less than 2x the upper limit of the reference interval will not be tested for alkaline phosphatase isoenzymes because analysis is unhelpful in this situation.
The alkaline phosphatase isoenzymes are separated by electrophoresis into different bands. The relative position and colour intensity of the bands with and without lectin ( a migration retarding sugar-binding protein ) can provide a qualitative impression as to the organ origin of the alkaline phosphatase isoenzyme(s).
Uncertainty of Measurement: Not applicable: a qualitative test with report comment
.
Requests for ALP isoenzymes will be vetted by Labplus chemical pathologists taking account of the following considerations:
If ALP is less than 2x the upper limit of the age-related range, ALP isoenzyme determination is rarely helpful in determining the cause. Transient non specific increases are common during acute illness in adults and children and often return to normal within a few months.
When other liver enzymes are normal P1NP may be a more helpful marker than ALP isoenzymes for detection of bone disease.
ALP isoenzyme determination is most likely to be helpful with sustained increase (>6 months) in total ALP when liver and bone markers are normal, and no cause for the increase is apparent clinically. If you wish to discuss the value of this investigation please contact one of the chemical pathologists vie email chemicalpathologist@adhb.govt.nz
To assist in the reporting of ALP isoenzymes full clinical details and recent LFT, ALP and P1NP results must accompany the request . If LFT and P1NP results are not provided LabPlus will perform these tests before completing ALP isoenzyme analysis.
CAUSES OF ISOLATED ALP ELEVATION
Benign familial hyperphosphatasemia is a cause for an unexplained isolated increased ALP and is seen at any age. Typically the intestinal isoenzyme is increased, with or without increased bone or liver isoenzyme as well. This is an asymptomatic genetic variant; all other liver enzymes are normal, and there is no evidence for increased bone turnover (normal P1NP). Other 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.
Apart from liver and bone, this test may identify other ALP isoenzymes:
a. Placental type - from pregnancy or Regan isoenzymes from tumours (e.g. pancreas, ovary, lung, breast)
b. Placental-like ALP type - from smoking or germ cell tumours e.g. from testis, thymus, lung
c. 'Fast liver' type - seen in transient hyperphosphatasaemia of infancy
d. 'Atypical bone' type - from raised neutrophils in some patients with e.g. polycythaemia rubra vera, chronic neutrophilic leukaemia, malignant lymphoma, lung cancer
e. Intestinal type - may be benign (e.g. related to a recent fatty meal, some families have detectable intestinal ALP), or related to liver cirrhosis, colitis or some tumours
f. Stauffer's syndrome e.g. in renal cell cancer (predominantly liver isoenzyme)
This test does not have the sensitivity to detect CSF placental ALP for the diagnosis of primary intracranial germinomas.
Only in very selected cases with equivocal presence of placental isoenzyme on electrophoresis or suspected low activity placental isoenzyme, the Placental Alkaline Phosphatase Test (heat denaturation) may provide additional information :
- 5 mL blood either in plain or heparin tube (minimum of 0.5 mL of serum or plasma) is required
- Result is usually available within 3 hours, but not outside 0800-1700 weekdays
-
If the remaining ALP activity after heat denaturation is close to 90-100%, it is suggestive of placental or Regan isoenzyme
References
1. Rosalki SB, Foo AY, Dooley JS. Benign familial hyperphosphatasaemia as a cause of unexplained increase in plasma alkaline phosphatase activity. J Clin Pathol. 1993;46:738-741
2. Stein, P., S. B. Rosalki, et al. (1987). "Transient hyperphosphatasemia of infancy and early childhood: clinical and biochemical features of 21 cases and literature review." Clin Chem 33(2 Pt 1): 313-318.
Emails to chemicalpathologist@adhb.govt.nz will receive priority attention from the on-call chemical pathologist.
If the query concerns a specific patient please include the NHI number in your email.
If email is not a suitable option, please contact the on-call chemical pathologist via Lablink (Auckland City Hospital ext. 22000 or 09-3078995).
Individual chemical pathologists may be contacted but will not be available at all times.
After-hours : contact Lablink (Auckland City Hospital ext. 22000 or 09-3078995) or hospital operator for on duty staff after hours.
Dr Samarina Musaad (Clinical Lead) : SamarinaM@adhb.govt.nz ext. 22402
Dr Cam Kyle: CampbellK@adhb.govt.nz ext 22052
Dr Weldon Chiu: WeldonC@adhb.govt.nz ext. 23427
Dr Campbell Heron: CHeron@adhb.govt.nz ext. 23427