Publications by authors named "Lillian S Ting"

Clostridium difficile infection causes diarrheal disease with potentially fatal complications. Although treatments are available, including vancomycin, metronidazole, and fidaxomicin, the recurrence of disease after therapy remains a problem. LFF571 is a novel thiopeptide antibacterial that shows in vitro potency against C.

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We evaluated the drug-drug interaction between pasireotide SC and verapamil, a known P-glycoprotein inhibitor. Subjects received pasireotide SC (single dose, 600 μg) on day 1, and samples for pharmacokinetics evaluation were collected from days 1 to 8. Subjects received an oral dose of verapamil 240 mg/d for 10 days (days 15-24).

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Clostridium difficile is the leading cause of hospital-acquired infectious diarrhea. LFF571 is a novel inhibitor of the prokaryotic translation elongation factor Tu and is active against a range of bacterial species, including C. difficile.

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Study Objective: To assess the contribution of polymorphisms in the uridine diphosphate glucuronosyltransferase gene (UGT) and the multidrug resistance-associated protein 2 gene (ABCC2) to mycophenolic acid (MPA) pharmacokinetics and clinical outcomes in thoracic transplant recipients.

Design: Open-label, cross-sectional study.

Setting: Transplant clinic in Vancouver, British Columbia, Canada.

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Given the paucity of data on pharmacokinetics of mycophenolic acid (MPA) in islet transplant, the aim of this study was to characterize pharmacokinetic parameters of MPA and its 2 glucuronidated metabolites in stable islet transplant recipients. Sixteen subjects were entered into this open-label study after written informed consent. Upon administration of a steady-state morning mycophenolate mofetil dose, 12-hour serial concentrations of MPA and its phenolic glucuronide (MPAG) and acyl-glucuronide (AcMPAG) were measured by a validated high-performance liquid chromatography method and pharmacokinetic parameters analyzed by noncompartmental modeling.

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Background: Mycophenolate mofetil is widely used in islet transplant recipients and its active metabolite, mycophenolic acid (MPA), exhibits wide pharmacokinetic variability. However, to our knowledge, no limited sampling strategy (LSS) exists for monitoring MPA in this subpopulation.

Objective: To define optimal LSSs for MPA monitoring and to test their predictive performance in islet transplant recipients.

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Objective: To review the current clinical evidence on the effects of corticosteroid interactions with the immunosuppressive drugs cyclosporine, tacrolimus, mycophenolate, and sirolimus.

Data Sources: Articles were retrieved through MEDLINE (1966-February 2008) using the terms corticosteroids, glucocorticoids, immunosuppressants, cyclosporine, tacrolimus, mycophenolate, sirolimus, drug interactions, CYP3A4, P-glycoprotein, and UDP-glucuronosyltransferases. Bibliographies were manually searched for additional relevant articles.

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Mycophenolate mofetil is an immunosuppressant commonly used in solid organ transplantation. Its active metabolite, mycophenolic acid (MPA), is metabolized to the inactive 7-O-mycophenolic acid glucuronide (MPAG) and the active acyl glucuronide (AcMPAG). Most pharmacokinetic (PK) studies have been focused on MPA, but not its metabolites, in kidney transplant recipients.

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Background And Methods: Eight limited sampling strategies (LSSs) for estimating mycophenolic acid area under the concentration-time curve (4 developed from lung transplant recipients at our center, 4 developed for heart transplant recipients from other research groups) were evaluated in 27 heart or heart-kidney transplant patients.

Results: The LSSs from our lung transplant patients performed well when applied to the heart transplant population, with percent bias and percent precision within the acceptable limit of +/-15%.

Conclusions: The LSSs developed at our center are robust enough to be applied to both lung and heart transplant populations.

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Despite evidence in the literature suggesting that a strong correlation exists between the pharmacokinetic parameters and pharmacodynamic effect of anticancer agents, many of these agents are still dosed by body surface area. Therapeutic drug monitoring with the aim of pharmacokinetic-guided dosing would not only maintain target concentrations associated with efficacy but may potentially minimise the likelihood of dose-related systemic toxicities. The pharmacokinetic parameter that displays the best correlation with the pharmacodynamics of anticancer drugs is the area under the plasma concentration-time curve (AUC).

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Study Objective: To develop limited sampling strategies for estimation of mycophenolic acid exposure (by determining area under the concentration-time curve [AUC]) in lung transplant recipients by using sampling times within 2 hours after drug administration and a maximum of three plasma samples.

Design: Prospective, open-label clinical study.

Setting: Lung transplant clinic in Vancouver, British Columbia, Canada.

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Background: Mycophenolic acid (MPA) is the active metabolite of mycophenolate mofetil, an immunosuppressive agent commonly used in solid organ transplantation. MPA is metabolized to the inactive metabolite 7-O-mycophenolic acid glucuronide (MPAG) and the active metabolite acyl glucuronide (AcMPAG). Pharmacokinetic profiling of MPA by determining AUC is a tool for determining drug exposure.

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Therapeutic drug monitoring has gained much attention in the management of immunosuppressive therapy. Area under the plasma drug concentration-time curve (AUC) is the pharmacokinetic (PK) parameter most commonly used to assess total exposure to a drug. However, estimation of AUC requires multiple blood samples throughout the dosing period, which is often inconvenient and expensive.

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This study was designed to examine the relationship between untimed antiretroviral concentrations measured in plasma samples collected for virus-load testing and response to highly active antiretroviral therapy. Plasma nonnucleoside reverse-transcriptase-inhibitor and protease-inhibitor concentrations were retrospectively measured in all virus-load plasma samples collected during the first year of therapy, for 122 patients in British Columbia, Canada, who initiated therapy between August 1996 and September 1999 and who had CD4 counts <50 cells/micro L. Drug levels were designated a priori as "low" if the concentrations were below the published Ctrough-SD.

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