2007
DOI: 10.1007/s00280-007-0582-9
|View full text |Cite
|
Sign up to set email alerts
|

Pharmacodynamic model for chemotherapy-induced anemia in rats

Abstract: Anticancer agents often cause bone marrow toxicity resulting in progressive anemia which may influence the therapeutic effects of erythropoietic-stimulating agents. The objective of this study was to develop a pharmacodynamic (PD) model to describe chemotherapy-induced anemia in rats. Anemia was induced in male Wistar rats with a single intravenous (i.v.) injection of 60 mg/kg carboplatin. Hematological responses including reticulocytes, red blood cells (RBC), hemoglobin, and endogenous rat erythropoietin (EPO… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

2
41
0

Year Published

2008
2008
2018
2018

Publication Types

Select...
8
1

Relationship

3
6

Authors

Journals

citations
Cited by 40 publications
(43 citation statements)
references
References 45 publications
(74 reference statements)
2
41
0
Order By: Relevance
“…[20][21][22][23][24] As monocytes are derived from the same granulocyte-macrophage progenitor cells as other leukocytes, PD models of leukocytopenia may be applicable to monocytopenia. A semiphysiological model proposed by Friberg et al 20,21 for chemotherapy-related myelosuppression was chosen as a standard model to describe monocytopenia after S-CKD602.…”
Section: Introductionmentioning
confidence: 99%
“…[20][21][22][23][24] As monocytes are derived from the same granulocyte-macrophage progenitor cells as other leukocytes, PD models of leukocytopenia may be applicable to monocytopenia. A semiphysiological model proposed by Friberg et al 20,21 for chemotherapy-related myelosuppression was chosen as a standard model to describe monocytopenia after S-CKD602.…”
Section: Introductionmentioning
confidence: 99%
“…Efficacy data are often limited in these studies due to inclusion of different tumour types and the advanced disease state of the patients [6]. Over the last years, the time course of neutropenia or other drug related haematological toxicities have been modelled linking the pharmacokinetic (PK) model with a model that describes the haematological toxicity [7][8][9][10][11]. Among these approaches, the model developed by Friberg et al [9] has been applied repeatedly to describe the time course of myelosuppression after administration of several cytotoxic anticancer drugs [12][13][14][15][16][17][18][19].…”
Section: Introductionmentioning
confidence: 99%
“…Other diseases have been described, including bacterial cell growth and irreversible loss after drug therapy, fasting plasma glucose in diabetes, and pain and bone mineral density progression in osteoarthritis (Jusko, 1971;Ravn et al, 1996;Meunier et al, 1999;Frey et al, 2003;Pillai et al, 2004;de Winter et al, 2006). Mechanism-based disease progression models are continually being derived because their insight into how various pathologies contribute to progression and how drugs exert their effects on specific processes is essential to optimizing therapy (Holford and Peace, 1992a,b;Nemeroff, 1994;Hoogendoorn et al, 2005;Holford et al, 2006;Meier et al, 2007;Woo et al, 2008). To date, there are limited mechanism-based models relevant to osteoarthritis and none specific to anti-inflammatory drug effects in rheumatoid arthritis (RA).…”
mentioning
confidence: 99%