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Treatment with granulocyte‐macrophage colony stimulating factor and the adult respiratory distress syndrome
Author(s) -
Verhoef Gregor,
Boogaerts Marc
Publication year - 1991
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830360413
Subject(s) - ards , respiratory distress , medicine , granulocyte , granulocyte macrophage colony stimulating factor , immunology , tumor necrosis factor alpha , macrophage , respiratory disease , lung , cytokine , biology , anesthesia , biochemistry , in vitro
Abstract 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/m 2 /day s.c.) and low‐dose cytosine‐arabinoside (Ara‐C) (20 mg/m 2 /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 CD11 B 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.