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Pharmaceutics
Special Issues
Pharmacokinetics of Drugs in Pregnancy and Lactation
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Pharmacokinetics of Drugs in Pregnancy and Lactation

A special issue of Pharmaceutics (ISSN 1999-4923). This special issue belongs to the section "Pharmacokinetics and Pharmacodynamics".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 1266

Special Issue Editors

Dr. Paola Mian

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Guest Editor
Department of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Interests: perinatal pharmacology; paediatric pharmacology; pharmacometrics
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Daniel J. Touw

E-Mail Website
Guest Editor
Department of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Interests: analytical method development; pharmacokinetics; therapeutic drug monitoring; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pregnancy and the postpartum period are associated with several anatomical and physiological changes that can alter the pharmacokinetics (PK) and pharmacodynamics (PD) of many drugs. For certain drugs, dosing changes may be required during pregnancy and postpartum to achieve drug exposures comparable to what is observed in non-pregnant populations. Currently, there is a lack in data on fetal drug exposure during pregnancy, and neonatal exposure through transfer of drugs via human milk during breastfeeding. The reason for this is that these populations are considerably underrepresented in clinical trials, and thereby crucial information on PK/PD is widely lacking. Over the past several years, there has been an increase in the application of modeling and simulation approaches such as population PK (PopPK) and physiologically based PK (PBPK) modelling, in combination with in vitro and ex vivo experiments, to provide guidance on drug dosing in these special patient populations. This Special Issue focuses on the current status of the application of pharmacokinetic techniques (e.g., population PK modelling, PBPK modelling) or in vitro (e.g., organ-on-a-chip) and ex vivo (placenta perfusion experiments) techniques to predict maternal and fetal exposure of drugs, and thereby guide drug therapy, during pregnancy, postpartum period and/or lactation.

Dr. Paola Mian
Prof. Dr. Daniel J. Touw
Guest Editors

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Keywords

  • pharmacokinetics
  • pregnancy
  • lactation
  • model-informed precision dosing

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Published Papers (1 paper)

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Research

16 pages, 6726 KiB  
Article
Maternal MitoQ Treatment Is Protective Against Programmed Alterations in CYP Activity Due to Antenatal Dexamethasone
by Millicent G. A. Bennett, Ashley S. Meakin, Kimberley J. Botting-Lawford, Youguo Niu, Sage G. Ford, Michael P. Murphy, Michael D. Wiese, Dino A. Giussani and Janna L. Morrison
Pharmaceutics 2025, 17(3), 285; https://doi.org/10.3390/pharmaceutics17030285 - 22 Feb 2025
Viewed by 828
Abstract
Background/Objectives: In pregnancy threatened by preterm birth, antenatal corticosteroids (ACS) are administered to accelerate fetal lung maturation. However, they have side effects, including the production of reactive oxygen species that can impact cytochrome P450 (CYP) activity. We hypothesised that antioxidants could protect [...] Read more.
Background/Objectives: In pregnancy threatened by preterm birth, antenatal corticosteroids (ACS) are administered to accelerate fetal lung maturation. However, they have side effects, including the production of reactive oxygen species that can impact cytochrome P450 (CYP) activity. We hypothesised that antioxidants could protect a fetus treated with ACS during gestation and prevent the programming of altered hepatic CYP activity in the offspring. The primary outcome of our study was the impact of different maternal treatments on the activity of hepatic drug-metabolising enzymes in offspring. Methods: At 100 ± 1 days gestational age (dGA, term = 147 dGA), 73 ewes were randomly allocated to the following: saline (5 mL IV daily 105–137 ± 2 dGA, n = 17), ACS (Dexamethasone (Dex); 12 mg IM at 115 and 116 dGA; n = 25), MitoQ (6 mg/kg MS010 IV, daily bolus 105–137 ± 2 dGA; n = 17) or Dex and MitoQ (Dex+MitoQ; n = 14). CYP activity and protein abundance were assessed using functional assays and Western blot. Results: Dex decreased the hepatic activity of fetal CYP3A (−56%, PDex = 0.0322), and 9 mo lamb CYP1A2 (−22%, PDex = 0.0003), CYP2B6 (−36%, PDex = 0.0234), CYP2C8 (−34%, PDex = 0.0493) and CYP2E1 (−57%, PDex = 0.0009). For all, except CYP1A2, activity returned to control levels with Dex+MitoQ in 9 mo lambs. In 9 mo lambs, MitoQ alone increased activity of CYP2B6 (+16%, PMitoQ = 0.0011) and CYP3A (midazolam, +25%, PMitoQ = 0.0162) and increased CAT expression (PMitoQ = 0.0171). Dex+MitoQ increased CYP3A4/5 activity (testosterone, +65%, PIntx < 0.0003), decreased CYP1A2 activity (−14%, PIntx = 0.0036) and decreased mitochondrial abundance (PIntx = 0.0051). All treatments decreased fetal hepatic DRP1, a regulator of mitochondrial fission (PDex = 0.0055, PMitoQ = 0.0006 and PIntx = 0.0034). Conclusions: Antenatal Dex reduced activity of only one CYP in the fetus but programmed the reduced activity of several hepatic CYPs in young adult offspring, and this effect was ameliorated by combination with MitoQ. Full article
(This article belongs to the Special Issue Pharmacokinetics of Drugs in Pregnancy and Lactation)
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