Hemoglobin (Hb) Stanleyville II causes gross overestimation of the Hb A1c proportion in routine HPLC.

duction in neutrophils is induced by G-CSF, and NAP is released into the bloodstream, perhaps through leakage of ALP from damaged or dead neutrophils. Fossa et al. (9 ) reported leukocytosis and increased serum ALP in response to G-CSF treatment and suggested that increased serum ALP activity was related to release of the enzyme from the increased numbers of leukocytes. Neutrophils were reported to be the source of increased serum ALP activity in experiments in which G-CSF was administered to rats (10 ). Our present results reflect a common phenomenon caused by disease, such as granulocytic leukemia or PV. We conclude that neutrophils may be an important source of increased serum ALP activity or bone-type ALP isoenzyme. Increased bone-type ALP should not be misdiagnosed as representing a pathologic condition, such as thyroid disease (hyperthyroidism), in which there is osteomalacia; hyperparathyroidism (either primary or secondary); chronic renal failure with renal osteodystrophy; diabetes mellitus with osteomyelitis; or metastatic cancer in which there is osteoblastic activity, such as prostate cancer. The present report describes indirect evidence that NAP might explain high bone-type ALP activity in patients without osteoblastic bone disease. Direct evidence is needed of the biochemical and immunochemical properties of ALP in the sera of patients with leukocytosis.