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Aids in the differential diagnosis of chronic myelocytic leukemia (CML) versus leukemoid reaction; aids in the evaluation of polycythemia vera, myelofibrosis with myeloid metaplasia, and paroxysmal nocturnal hemoglobinuria Low scores have been associated with CML, PNH, thrombocytopenic purpura, and hereditary hypophosphatasia. In CML regardless of the total white count, the score remains low. In CML, it has been demonstrated that the mRNA for leukocyte alkaline phosphatase by Northern blotting is undetectable.(1) This suggests either rapid degradation of the message or no transcription of the LAP gene. In nonleukemic neutrophilia, the LAP rises as the WBC rises. High scores have been seen in polycythemia vera, myelofibrosis, aplastic anemia, mongolism, hairy cell leukemia, leukemoid reactions, and neutrophilia either physiological or secondary to infection. It is also increased in Hodgkin's disease. Serial LAP activity can be a useful adjunct in evaluating the activity of Hodgkin's disease as well as its response to therapy. Increase in LAP does not occur in cases of sickle cell crisis, possibly due to zinc deficiency (leukocyte alkaline phosphatase is a zinc metalloenzyme) but more likely relating to a mild defect in the hypothalamic-pituitary-adrenal axis with decreased plasma cortisol response in patients in sickle cell crisis.(2)
Pregnancy, increased number of immature forms of neutrophils, and postoperative or "stressful" states are associated with increased scores. The differential must have adequate numbers of mature neutrophilic granulocytes to perform the LAP.
