scholarly journals Utilization of G-CSF and GM-CSF as an alternative to discontinuation in clozapine-induced neutropenia or leukopenia: A case report and discussion

2018 ◽  
Vol 8 (5) ◽  
pp. 250-255 ◽  
Author(s):  
Allison Karst ◽  
Jonathan Lister
Keyword(s):  
Case Report ◽  
Treatment Resistant ◽  
Colony Stimulating Factors ◽  
Gm Csf ◽  
Clozapine Treatment ◽  
Increased Risk ◽  
Proliferation And Differentiation ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract Clozapine remains the definitive gold standard for treatment-resistant schizophrenia despite limitations in use because of hematological abnormalities. Neutropenia or leukopenia are often treated with interruption of clozapine treatment, frequently resulting in clinical decompensation, hospitalization, increased burden to patient care, and increased risk of suicide. Colony-stimulating factors, including granulocyte colony-stimulating factors and granulocyte-macrophage colony-stimulating factors, are cytokines that stimulate proliferation and differentiation of myeloid precursor cells. Their use in the prevention and treatment of clozapine-associated neutropenia presents an alternative to clozapine discontinuation in certain cases. We present a case report of successful periodic granulocyte-macrophage colony-stimulating factor use with clozapine in a patient with treatment-resistant schizophrenia, as well as discussion of a practical approach to patients with possible clozapine-induced neutropenia or leukopenia.

scholarly journals Effect of priming polymorphonuclear leukocytes with cytokines (granulocyte-macrophage colony-stimulating factor [GM-CSF] and G-CSF) on the host resistance to Streptococcus pneumoniae in chinchillas infected with influenza A virus

Blood ◽  
1994 ◽  
Vol 83 (7) ◽  
pp. 1929-1934
Author(s):  
JS Abramson ◽  
HR Hudnor
Keyword(s):  
Streptococcus Pneumoniae ◽  
Influenza A Virus ◽  
Influenza A ◽  
Pneumococcal Disease ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Increased Risk ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Patients infected with influenza A virus (IAV) are at increased risk for bacterial superinfections, and this occurs in association with depressed polymorphonuclear leukocyte (PMNL) function. Recently, we reported that in vitro exposure of human PMNL to granulocyte-macrophage colony-stimulating factor (GM-CSF) reverses IAV-induced cell dysfunction. The present study used an established animal model of IAV infection to examine whether G-CSF and/or GM-CSF can overcome IAV- induced PMNL dysfunction and thereby prevent secondary infections. Preliminary studies determined a dosing schedule of these cytokines that caused significant priming of chinchilla PMNL. In subsequent studies, animals were inoculated intranasally with IAV (day 1) followed 3 days later by Streptococcus pneumoniae, and administered daily intraperitoneal injections with a cytokine or placebo on days 3 through 9. Animals had blood obtained on multiple occasions for PMNL studies, and were followed-up for evidence of pneumococcal disease. Both cytokines caused significant priming of the PMNL chemiluminescence response and this was associated with reversal of the IAV-induced PMNL dysfunction. However, neither cytokine decreased the incidence of pneumococcal disease.

scholarly journals Mammalian Granulocyte–Macrophage Colony-stimulating Factor Receptor Expressed in Primary Avian Hematopoietic Progenitors: Lineage-specific Regulation of Proliferation and Differentiation

1998 ◽  
Vol 141 (4) ◽  
pp. 1041-1051
Author(s):  
Oliver Wessely ◽  
Eva-Maria Deiner ◽  
Kim Chew Lim ◽  
Georg Mellitzer ◽  
Peter Steinlein ◽  
...  
Keyword(s):  
Erythropoietin Receptor ◽  
Colony Stimulating Factor ◽  
Erythroid Progenitors ◽  
Erythroid Progenitor ◽  
Gm Csf ◽  
Proliferation And Differentiation ◽  
Macrophage Colony Stimulating Factor ◽  
Α Chain ◽  
Macrophage Colony ◽  
Stimulating Factor

The cytokine Granulocyte–Macrophage Colony-Stimulating Factor (GM-CSF) regulates proliferation, differentiation, and apoptosis during myelopoiesis and erythropoiesis. Structure–function relationships of GM-CSF interactions with its receptor (GM-R), the biochemistry of GM-R signal transduction, and GM-CSF action in vivo are relatively well understood. Much less is known, however, about GM-R function in primary hematopoietic cells. In this paper we show that expression of the human GM-R in a heterologous cell system (primary avian erythroid and myeloid cells) confirms respective results in murine or human cell lines, but also provides new insights how the GM-R regulates progenitor proliferation and differentiation. As expected, the hGM-CSF stimulated myeloid progenitor proliferation and differentiation and enhanced erythroid progenitor proliferation during terminal differentiation. In the latter cells, however, the hGM-R only partially substituted for the activities of the erythropoietin receptor (EpoR). It failed to replace the EpoR in its cooperation with c-Kit to induce long-term proliferation of erythroid progenitors. Furthermore, the hGM-R α chain specifically interfered with EpoR signaling, an activity neither seen for the βc subunit of the receptor complex alone, nor for the α chain of the closely related Interleukin-3 receptor. These results point to a novel role of the GM-R α chain in defining cell type–specific functions of the GM-R.

Use of Cytokines in Clozapine-Induced Agranulocytosis

1996 ◽  
Vol 41 (5) ◽  
pp. 280-284 ◽  
Author(s):  
Ian Chin-Yee ◽  
Kalyna Bezchlibnyk-Butler ◽  
Lillian Wong
Keyword(s):  
Case Report ◽  
High Risk ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Review Of Literature ◽  
Gm Csf ◽  
Prolonged Duration ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Objective: To report and review the use of cytokines for the treatment of clozapine-induced neutropenia. Method: Case report and review of literature. Results: Cytokines, granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), appear to shorten the duration of clozapine-induced neutropenia. Conclusions: G-CSF or GM-CSF therapy should be considered in patients with profound neutropenia of prolonged duration (high-risk neutropenia).

Recombinant granulocyte macrophage colony stimulating factor (rhu-GM-CSF) in the treatment of extensive leg ulcers: A case report

Surgery ◽  
2000 ◽  
Vol 127 (5) ◽  
pp. 589-592 ◽  
Author(s):  
Furqan H. Siddiqui ◽  
Joseph J. Biundo ◽  
Cleveland Moore ◽  
Maria Luisa Ermitaño ◽  
Alejandro P. Ortigas ◽  
...  
Keyword(s):  
Case Report ◽  
Leg Ulcers ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

scholarly journals Effect of priming polymorphonuclear leukocytes with cytokines (granulocyte-macrophage colony-stimulating factor [GM-CSF] and G-CSF) on the host resistance to Streptococcus pneumoniae in chinchillas infected with influenza A virus

Blood ◽  
1994 ◽  
Vol 83 (7) ◽  
pp. 1929-1934 ◽  
Author(s):  
JS Abramson ◽  
HR Hudnor
Keyword(s):  
Streptococcus Pneumoniae ◽  
Influenza A Virus ◽  
Influenza A ◽  
Pneumococcal Disease ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Increased Risk ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract Patients infected with influenza A virus (IAV) are at increased risk for bacterial superinfections, and this occurs in association with depressed polymorphonuclear leukocyte (PMNL) function. Recently, we reported that in vitro exposure of human PMNL to granulocyte-macrophage colony-stimulating factor (GM-CSF) reverses IAV-induced cell dysfunction. The present study used an established animal model of IAV infection to examine whether G-CSF and/or GM-CSF can overcome IAV- induced PMNL dysfunction and thereby prevent secondary infections. Preliminary studies determined a dosing schedule of these cytokines that caused significant priming of chinchilla PMNL. In subsequent studies, animals were inoculated intranasally with IAV (day 1) followed 3 days later by Streptococcus pneumoniae, and administered daily intraperitoneal injections with a cytokine or placebo on days 3 through 9. Animals had blood obtained on multiple occasions for PMNL studies, and were followed-up for evidence of pneumococcal disease. Both cytokines caused significant priming of the PMNL chemiluminescence response and this was associated with reversal of the IAV-induced PMNL dysfunction. However, neither cytokine decreased the incidence of pneumococcal disease.

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