Lactoferrin in the myeloproliferative disorders: a search for granulopoietic regulator defects

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Abstract
Evidence of a defect in the negative feedback control of human granulopoiesis in the myeloproliferative disorders is presented. Neutrophil release of lactoferrin, plasma lactoferrin concentration, the number of lactoferrin receptor sites on mononuclear cells and granulocyte-monocyte colony stimulating factor (GM-CSF) release from peripheral blood cells were determined in patients with myeloproliferative disorders and compared with normal individuals. There was a significantly (P < 0.001) decreased release of lactoferrin from the neutrophils of patients with myeloproliferative disorders which could be responsible for a reduced suppression of GM-CSF release from mononuclear cells which in turn may be responsible for the increased myeloid proliferative activity in patients with myeloproliferative disorders.