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3. Developmental pharmacokinetics of indomethacin in preterm neonates: Severely decreased drug clearance in the first week of life.

Author

Krzyzanski, Wojciech, Stockard, Bradley, Gaedigk, Andrea, Scott, Allison, Nolte, Whitney, Gibson, Kim, Leeder, J. Steven, and Lewis, Tamorah

Subjects
*NEONATAL intensive care units, *INDOMETHACIN, *NEWBORN infants, *PHARMACOKINETICS, *INTRACRANIAL hemorrhage
Abstract

Indomethacin is used commonly in preterm neonates for the prevention of intracranial hemorrhage and closure of an abnormally open cardiac vessel. Due to biomedical advances, the infants who receive this drug in the neonatal intensive care unit setting have become younger, smaller, and less mature (more preterm) at the time of treatment. To develop a pharmacokinetics (PK) model to aid future dosing, we designed a prospective cohort study to characterize indomethacin PK in a dynamically changing patient population. A population PK base model was created using NONMEM, and a covariate model was developed in a primary development cohort and subsequently was tested for accuracy in a validation cohort. Postnatal age was a significant covariate for hepatic clearance (CLH) and renal clearance (CLR). The typical value of the total clearance (CL, the sum of CLR and CLH) was 3.09 ml/h and expressed as CL/WTmedian = 3.96 ml/h/kg, where WTmedian is the median body weight. The intersubject variability of CLR and CLH were 61% and 207%, respectively. The typical value of the volume of distribution Vp = 366 ml (Vp/WTmedian = 470 ml/kg), and its intersubject variability was 38.8%. Half‐life was 82.1 h. Compared with more mature and older preterm populations studied previously, indomethacin CL is considerably lower in this contemporary population. Model‐informed precision dosing incorporating important covariates other than weight alone offers an opportunity to individualize dosing in a susceptible patient undergoing rapid change. [ABSTRACT FROM AUTHOR]

Published
2023
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7. Genome Wide Association Study Identifies the HMGCS2 Locus to be Associated With Chlorthalidone Induced Glucose Increase in Hypertensive Patients

Author

Singh, Sonal, primary, McDonough, Caitrin W., additional, Gong, Yan, additional, Alghamdi, Wael A., additional, Arwood, Meghan J., additional, Bargal, Salma A., additional, Dumeny, Leanne, additional, Li, Wen‐Yi, additional, Mehanna, Mai, additional, Stockard, Bradley, additional, Yang, Guang, additional, de Oliveira, Felipe A., additional, Fredette, Natalie C., additional, Shahin, Mohamed H., additional, Bailey, Kent R., additional, Beitelshees, Amber L., additional, Boerwinkle, Eric, additional, Chapman, Arlene B., additional, Gums, John G., additional, Turner, Stephen T., additional, Cooper‐DeHoff, Rhonda M., additional, and Johnson, Julie A., additional

Published
2018
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10. Genome Wide Association Study Identifies the Locus to be Associated With Chlorthalidone Induced Glucose Increase in Hypertensive Patients.

Author

Singh, Sonal, McDonough, Caitrin W., Yan Gong, Alghamdi, Wael A., Arwood, Meghan J., Bargal, Salma A., Dumeny, Leanne, Wen-Yi Li, Mehanna, Mai, Stockard, Bradley, Guang Yang, de Oliveira, Felipe A., Fredette, Natalie C., Shahin, Mohamed H., Bailey, Kent R., Beitelshees, Amber L., Boerwinkle, Eric, Chapman, Arlene B., Gums, John G., and Turner, Stephen T.

Published
2018
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11. Global and Targeted Metabolic Profiling Identifies Metabolic Markers for FLT3-ITD in Pediatric AML Patients

Author

Stockard, Bradley, Guingab, Joy, Garrett, Timothy, Pounds, Stanley, Rubnitz, Jeffrey E, and Lamba, Jatinder

Abstract

Acute myeloid leukemia (AML) is a clinically challenging disease with high interpatient variability in response to chemotherapy. Despite continuing advances in treatment options, current 5-year survival rates for pediatric AML are suboptimal at ~60%. Variability in treatment response and survival outcomes are due in part to the heterogeneous nature of AML, with many genetic lesions and cytogenetic features contributing to disease progression. One of the most well known genetic lesions associated with AML involves Fms-Like Tyrosine Kinase-3 (FLT3), a receptor tyrosine kinase expressed in hematopoietic stem cells. Internal tandem duplication of the juxtamembrane domain coding sequence of FLT3 (FLT3/ITD) causes autonomous cellular proliferations leading to disease progression. Previous metabolomics studies have successfully identified significant metabolic alterations in hematological malignancies. However, no metabolomics studies on pediatric AML have been reported at this time. In this study, we propose to use global and targeted metabolomics to identify differential metabolite abundance associated with FLT3-ITD status in pediatric AML patients treated in the St Jude AML02 clinical trial.

Published
2017
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