ArticleJournal of pharmacokinetics and pharmacodynamics2012
Multi-response model for rheumatoid arthritis based on delay differential equations in collagen-induced arthritic mice treated with an anti-GM-CSF antibody.
Article in Journal of pharmacokinetics and pharmacodynamics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Computing optimal drug dosing with OptiDose: implementation in NONMEM.Journal of pharmacokinetics and pharmacodynamics · 2023Article
- Systemic Administration of Neutral Electrolyzed Saline as a Novel Treatment for Rheumatoid Arthritis Reduces Mechanical and Inflammatory Damage to the Joints: Preclinical Evaluation in Mice.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Delay differential equations based models in NONMEM.Journal of pharmacokinetics and pharmacodynamics · 2021Article
- Cathelicidin and Calprotectin Are Disparately Altered in Murine Models of Inflammatory Arthritis and Airway Inflammation.Frontiers in immunology · 2020Article
- Role of the Gut Microbiome in Modulating Arthritis Progression in Mice.Scientific reports · 2016Article
- Modeling of delays in PKPD: classical approaches and a tutorial for delay differential equations.Journal of pharmacokinetics and pharmacodynamics · 2014Article
- General relationship between transit compartments and lifespan models.Journal of pharmacokinetics and pharmacodynamics · 2012Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collagen-induced arthritis (CIA) in mice is an experimental model for rheumatoid arthritis, a human chronic inflammatory destructive disease. The therapeutic effect of neutralizing the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) by an antibody was examined in the mouse disease in a view of deriving a pharmacokinetic/pharmacodynamic (PKPD) model. In CIA mice the development of disease is measured by a total arthritic score (TAS) and an ankylosis score (AKS). We present a multi-response PKPD model which describes the time course of the unperturbed and perturbed TAS and AKS. The antibody acts directly on GM-CSF by binding to it. Therefore, a compartment for the cytokine GM-CSF is an essential component of the mathematical model. This compartment drives the disease development in the PKPD model. Different known properties of arthritis development in the CIA model are included in the PKPD model. Firstly, the inflammation, driven by GM-CSF, dominates at the beginning of the disease and decreases after some time. Secondly, a destructive (ankylosis) part evolves in the TAS that is delayed in time. In order to model these two properties a delay differential equation was used. The PKPD model was applied to different experiments with doses ranging from 0.1 to 100 mg/kg. The influence of the drug was modeled by a non-linear approach. The final mathematical model consists of three differential equations representing the compartments for GM-CSF, inflammation and destruction. Our mathematical model described well all available dosing schedules by a simultaneous fit. We also present an equivalent and easy reformulation as ordinary differential equation which grants the use of standard PKPD software.
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