Joshua L. Fenderson
*
,1 Amy N. Stratton
*
,2 Jennifer S. Domingo,3 Gerald O. Matthews
*
,3 and Christopher D. Tan4


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1Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA

2Department of Internal Medicine, Tripler Army Medical Center, 1 Jarrett White Road, Honolulu, HI 96859-5000, USA

3Department of Psychiatry, Tripler Army Medical Center, 1 Jarrett White Road, Honolulu, HI 96859-5000, USA

4Department of Pharmacy, Tripler Army Medical Center, 1 Jarrett White Road, Honolulu, HI 96859-5000, USA


Abstract

The aim of this paper is to report the first case of atomoxetine leading to false-positive urine drug screen. An otherwise healthy 27-year-old female with a history of attention deficit hyperactivity disorder (ADHD) treated with atomoxetine had an acute onset tonic-clonic seizure. On arrival to the hospital, a urine toxicological drug screen with immunochemical cloned enzyme donor immunoassay (CEDIA) was performed. Results were positive for amphetamines; however, the presence of these substances could not be confirmed with urine gas chromatography-mass spectrometry (GC-MS). She denied any illicit drug use, herbal medications, or supplements, and her other prescription medications have not been previously known to cause a false-positive result for amphetamines. While stimulant treatments for ADHD could certainly result in a positive result on urine screen for amphetamines, there have been no reports of false-positive results for amphetamines secondary to patients using atomoxetine. We implicate atomoxetine, and/or its metabolites, as a compound or compounds which may interfere with urine drug immunoassays leading to false-positive results for amphetamines CEDIA assays.

1. Introduction

Atomoxetine is classified as a selective norepinephrine reuptake inhibitor and is commonly prescribed as a nonstimulant treatment for the management of ADHD in children and adults. The drug acts at presynaptic norepinephrine transporters in neurons blocking removal of norepinephrine from the synaptic cleft through a mechanism that is not fully understood <1>. The primary oxidative metabolite of atomoxetine is 4-hydroxyatomoxetine (active metabolite but present in a much lower concentration compared to the parent drug) which is subsequently conjugated to 4-hydroxyatomoxetine--glucoronide via the cytochrome P450 CYP2D6 pathway <1–3>. To a lesser extent, atomoxetine is demethylated to -desmethylatomoxetine, which is substantially less active compared to the parent drug.

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Structurally, atomoxetine <-methyl-3-(2-methylphenoxy)-3-phenylpropan-1-amine> bears some similarities to amphetamine <1-phenylpropan-2-amine> (Figure 1) <1, 3>. Recent research also suggests that atomoxetine blocks -methyl--aspartate (NMDA) receptors altering glutaminergic transmission, and this mechanism may contribute to its efficacy as a treatment for ADHD <4>.