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 the the health Sciences, 4301 Jones bridge Road, Bethesda, MD 20814, USA

2Department of inner Medicine, Tripler military Medical Center, 1 Jarrett White Road, Honolulu, hi 96859-5000, USA

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

4Department that Pharmacy, Tripler military Medical Center, 1 Jarrett White Road, Honolulu, hello 96859-5000, USA


Abstract

The aim of this document is come report the an initial case that atomoxetine leading to false-positive urine medicine screen. An otherwise healthy 27-year-old female through a history of fist deficit hyperactivity disorder (ADHD) treated v atomoxetine had an acute start tonic-clonic seizure. On come to the hospital, a pee toxicological drug screen with immunochemical copy enzyme donor immunoassay (CEDIA) to be performed. Results were hopeful for amphetamines; however, the visibility of these substances might not be shown with to pee gas chromatography-mass spectrometry (GC-MS). She denied any type of illicit medicine use, herbal medications, or supplements, and also her various other prescription medications have not been previously known to cause a false-positive result for amphetamines. If stimulant therapies for ADHD might certainly an outcome in a positive an outcome on urine screen for amphetamines, there have actually been no reports that false-positive outcomes for amphetamines secondary to patients utilizing atomoxetine. Us implicate atomoxetine, and/or that is metabolites, together a link or link which might interfere through urine drug immunoassays resulting in false-positive results for amphetamines CEDIA assays.

1. Introduction

Atomoxetine is classified together a selective norepinephrine reuptake inhibitor and is typically prescribed together a nonstimulant treatment for the administration of ADHD in children and also adults. The drug acts at presynaptic norepinephrine transporters in neurons blocking removed of norepinephrine indigenous the synaptic cleft v a mechanism that is not completely understood <1>. The major oxidative metabolite that atomoxetine is 4-hydroxyatomoxetine (active metabolite but present in a much reduced concentration compared to the parental drug) i m sorry is consequently conjugated come 4-hydroxyatomoxetine--glucoronide via the cytochrome P450 CYP2D6 pathway <1–3>. To a lesser extent, atomoxetine is demethylated to -desmethylatomoxetine, which is considerably less active compared come the parental drug.

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Structurally, atomoxetine <-methyl-3-(2-methylphenoxy)-3-phenylpropan-1-amine> bears part similarities come amphetamine <1-phenylpropan-2-amine> (Figure 1) <1, 3>. Current research additionally suggests that atomoxetine block -methyl--aspartate (NMDA) receptors altering glutaminergic transmission, and also this device may contribute to its efficacy together a therapy for ADHD <4>.