Leukocyte histidine decarboxylase: properties and activity in myeloproliferative disorders.

E ARLIER OBSERVATIONS of elevated blood and urine histamine levels in myeloproliferative disorders1’2 have recently been confirmed and extended in this laboratory using a sensitive and specific spectrophotofluorometric assay.3 Whole blood and urine histamine content was demonstrated to be increased in uncontrolled polycythemia vera, “spent” polycythemia, and myelofibrosis with myeloid metaplasia. Leukocyte histamine content was also measured, since the histamine in whole blood in man is contained almost entirely within circulating leukocytes.4 Patients with active myeloproliferative states, including chronic myelocytic leukemia, who had elevated blood and urine histamine levels, had increased leukocyte histamine as well.5 When remission was induced by myelosuppressive therapy, elevated levels of whole blood, leukocyte and urine histamine fell, reaching normal in most cases. Increased leukocyte histamine content could result from increased formation of the amine, decreased release or intracellular catabolism, or some combination of the two processes. Since the only known pathway for histamine synthesis in mammals is by the intracellular decarboxylation of histidine,#{176} a study of the ability of normal leukocytes and those from patients with myeloproliferative disorders to decarboxylate histidine was undertaken to see if increased enzyme activity might account, at least in part, for the observed increases in leukocyte and urine histamine content in myeloproliferative states.