American journal of hematology vol:36 issue:4 pages:285-7
We report a case of a patient who developed a fatal adult respiratory distress syndrome (ARDS) during treatment with rh granulocyte-macrophage colony stimulating factor (rhGM-CSF) (250 mcg/m2/day s.c.) and low-dose cytosine-arabinoside (Ara-C) (20 mg/m2/day s.c.). Several mechanisms which might explain the lung tissue damage in this patient were explored. GM-CSF increased the expression of the glycoproteins CD11B and CD18 on the surface of his neutrophils, which may have increased the adhesiveness of neutrophils to the pulmonary endothelium. In addition, GM-CSF primed the neutrophils of the patient to an enhanced release of superoxide anions. Both findings may at least partially explain why GM-CSF exerted a deleterious action on the pulmonary endothelial integrity in this patient. Other factors, such as increased platelet-activating factor production by the neutrophils or tumor necrosis factor-mediated mechanisms, may also have played a role. ARDS as a complication of low-dose Ara-C seems less plausible.