Background. Chemotherapy is an essential modality of curative strategies in pediatric oncology. Dose and dose intensity are, above all, restricted by the myelosuppressive effects of cytotoxic drugs. Neutropenia constitutes an important risk of morbidity and mortality. Granulocytemacrophage-colony st
Alteration of colony-stimulating factor output, endotoxemia, and granulopoiesis in cyclic neutropenia
✍ Scribed by Peter L. Greenberg; Ine Bax; Jack Levin; Tony M. Andrews
- Publisher
- John Wiley and Sons
- Year
- 1976
- Tongue
- English
- Weight
- 734 KB
- Volume
- 1
- Category
- Article
- ISSN
- 0361-8609
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Cellular and humoral factors involved in the regulation of granulopoiesis were evaluated in two patients with cyclic neutropenia by utilizing the agar‐gel marrow culture technique to serially study marrow granulocytic colony‐forming capacity (CFC) and the urinary output of colony‐stimulating factor (CSF). CSF output varied inversely with peripheral neutrophil counts and directly with monocyte counts and evidence for infection (endotoxemia and/or staphylococcal abscesses). Following autologous infusion of one patient's plasma obtained during a period of neutropenia, increased urinary excretion of CSF occurred concomitant with increments in both marrow CFC and the proportion of granulocytic progenitor cells in DNA synthesis. Neutrophil periodicity was not altered by the administration of the neutropenic plasma. These findings are consistent with the hypothesis that cyclic neutropenia is caused by a quantitatively decreased entry of stem cells or granulocytic progenitor cells into granulopoiesis.
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