| First Author | Baker GR | Year | 1998 |
| Journal | Blood | Volume | 91 |
| Issue | 1 | Pages | 89-99 |
| PubMed ID | 9414272 | Mgi Jnum | J:45066 |
| Mgi Id | MGI:1101683 | Doi | 10.1182/blood.v91.1.89.89_89_99 |
| Citation | Baker GR, et al. (1998) Transient thrombocytopenia produced by administration of macrophage colony-stimulating factor: investigations of the mechanism. Blood 91(1):89-99 |
| abstractText | Administration of macrophage colony-stimulating factor (M-CSF) to mice (2 to 8 mg/kg/d x 5d) produced dose-dependent thrombocytopenia, which reached its nadir on days 4 to 5, followed by rapid recovery. Surprisingly, when administration of M-CSF was prolonged, the thrombocytopenia completely resolved, despite continued treatment. Splenectomy did not prevent the thrombocytopenia. Readministration of M-CSF after various intervals continued to produce the thrombocytopenic effect, even after 35 days. Measurements of Meg-CFC and megakaryocyte ploidy during the periods of M-CSF treatment and recovery of normal platelet levels showed no evidence of bone marrow suppression. Platelet survival was markedly decreased after 5 days of M-CSF (at the platelet count nadir) and after 9 days of continued M-CSF treatment, when the platelet count had returned to normal. Platelets from M-CSF-treated donors demonstrated normal survival when transfused into normal recipients. We concluded that thrombocytopenia produced by M-CSF was not due to suppression of thrombopoiesis, but to increased activity of the monocyte/macrophage system, which caused shortened platelet survival, and that subsequently, increased platelet production compensated for ongoing platelet destruction and resulted in normal platelet levels. |
