The Influence of Smoking on the Serum Level of Duloxetine

Fric, Mirijam; Pfuhlmann, Bruno; Laux, Gerd; Riederer, P.; Distler, G. I.; Artmann, S.; Wohlschläger, M.; Liebmann, Moritz; Deckert, J

doi:10.1055/s-2008-1073173

Cited by 39 publications

(25 citation statements)

References 18 publications

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“…46,47 Serum levels of duloxetine were found to be significantly lower among smokers, and it was suggested to occur by CYP1A2 induction by the polycylic hydrocarbons found in cigarettes. 48 See Table 2 for a summary of CYP enzyme inducers and inhibitors relevant to pregnancy.…”

Section: Sri-drug Interactionsmentioning

confidence: 99%

Fetal Serotonin Reuptake Inhibitor Antidepressant Exposure: Maternal and Fetal Factors

2012

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Prenatal serotonin reuptake inhibitor exposure is common and neonatal outcomes vary greatly, often leading to confusion about whether to use or even continue antenatal use of these antidepressants. Importantly, some but not all infants are affected, which raises questions about how maternal drug metabolism contributes to fetal drug exposure. To address this key question, our paper reviews the role of key maternal, fetal, and placental pharmacokinetic, metabolic, and genetic factors that affect the extent of fetal drug exposure. Considering the role of these factors may further our understanding of variables that may assist in optimizing maternal psychopharmacotherapy during pregnancy and neonatal outcomes. W W WL'exposition prénatale à un inhibiteur du recaptage de la sérotonine est fréquente et les impacts néonataux varient grandement, ce qui provoque souvent la confusion lorsqu'il s'agit d'utiliser ou même de continuer l'usage prénatal de ces antidépresseurs. D'abord et avant tout, certains bébés, mais pas tous, sont affectés, ce qui soulève des questions sur la façon dont le métabolisme maternel des médicaments contribue à l'exposition foetale aux médicaments. Pour aborder cette importante question, notre article examine le rôle des principaux facteurs maternels, foetaux, pharmacocinétiques placentaires, métaboliques, et génétiques qui affectent la portée de l'exposition foetale aux médicaments. Examiner le rôle de ces facteurs approfondira notre compréhension des variables qui peuvent aider à optimiser la psychopharmacothérapie maternelle durant la grossesse et les résultats néonataux.consider the impact of physiological factors of the pregnancy itself and SRI-related pharmacological factors that influence maternal drug metabolism and, by extension, fetal exposure. Further, neonatal outcomes following in utero SRI exposure depends largely on the extent of fetal drug exposure, and thus understanding factors that affect fetal drug pharmacology also offers important clues to developmental risks associated with prenatal drug exposure. Our paper will review key maternal, placental, and fetal metabolic and genetic factors that influence SRI pharmacology and fetal drug exposure. Both SSRIs (for example, citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline) and SNRIs (for example, duloxetine and venlafaxine) are increasingly used to manage antenatal mood disturbances 8 and will be referred to as SRIs (meaning, SRI ADs). This review is offered as a way to further our understanding of variables that may account for the variations in maternal perinatal SRI pharmacology and neonatal outcomes, and thereby contribute to assessing the benefits and risks associated with SRI use in this setting. E ach year in North America, 15% to 20% of women experience mood disorders (for example, depression) during their pregnancy, leading to one-third of these women being treated with an SRI AD; however, up to 50% stop medication within the first 60 days of pregnancy.

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Section: Sri-drug Interactionsmentioning

confidence: 99%

Fetal Serotonin Reuptake Inhibitor Antidepressant Exposure: Maternal and Fetal Factors

2012

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“…Low-dose treatment with the slowly reversible acetylcholinesterase inhibitor rivastigmine was chosen since we observed moderate but distracting nausea at comparatively low doses of the rapidly reversible acetylcholinesterase inhibitor galantamine in our earlier studies [8] . Rivastigmine is not noted to have pharmacokinetic interactions with other drugs or nicotine, resulting in a change of plasma concentrations, as it has been shown in smokers for several other drugs such as antipsychotics [5] and antidepressants [12] . Baseline conditions for tobacco consumption and tobacco craving were assessed two times on visit 1 and again on visit 2, at the end of the 4-weeks baseline period immediately before starting the intervention.…”

Section: Procedures and Measurementsmentioning

confidence: 96%

Rivastigmine Reduces Tobacco Craving in Alcohol-dependent Smokers

Diehl

Nakovics²,

Mutschler³

et al. 2009

Pharmacopsychiatry

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“…In fact, plasma levels of psychotropic drugs may differ from one subject to another due to interindividual variability [10]. Other factors, such as polypharmacy [7] or smoking, have been demonstrated to alter DLX pharmacokinetics; a study reported that smokers tend to show remarkably lower serum drug levels, and this has been correlated to induction of CYP1A2 by polycyclic hydrocarbons contained in tobacco smoke [11].…”

Section: Introductionmentioning

confidence: 98%