Tobakksrøyking og interaksjoner med legemidler

Molden, Espen; Spigset, Olav

doi:10.4045/tidsskr.08.0122

Cited by 5 publications

(2 citation statements)

References 10 publications

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“…Det er denne oppfatningen som har tvunget vårt eget tidsskrift til å sette inn den samme meningsløse setningen i hver bidige oversiktsartikkel: «Artikkelen bygger på forfatterens erfaringer kombinert med et usystematisk søk i PubMed og referanser fra forfatterens eget arkiv.» Selvfølgelig! Hvis jeg leser en oversiktsartikkel av Karl O. Nakken om epilepsi (10), en av Bjørn Bjorvatn om søvnfor-styrrelser (11) eller en av Espen Molden om medikamentelle interaksjoner (12), da leser jeg den nettopp fordi jeg vil vite hva akkurat Karl O. Nakken, Bjørn Bjorvatn eller Espen Molden mener og hvordan de fortolker forskningen, fordi jeg anser dem som saerlig kompetente innen sine respektive felter. Men for at ikke vi andre skal tro at de selv tror de er noe, så tvinges de alle til å utføre den samme botsøvelsen: Å innrømme at dette er nok ikke ordentlig kunnskap, det bare noe de mener etter å ha jobbet 20-30-40 år i feltet.…”

Section: åRsaker Til Vulgaercochranismens Fremvekstunclassified

Evidensbasert medisin eller vulgærcochranisme?

Wyller¹

2011

Tidsskriftet

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Evidensbasert medisin eller vulgaercochranisme?1 Evidensbasert medisin har med sine randomiserte studier og metaanalyser hatt enorm betydning for klinisk medisin. Vi har nå langt sikrere kunnskap om hva som virker og hva som ikke virker -og om hva som til og med kan vaere skadelig. Men evidensbasert medisin er dessverre blitt vulgarisert til bare å handle om evidens og til systematisk nedvurdering av erfaringsbasert kunnskap.

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Section: åRsaker Til Vulgaercochranismens Fremvekstunclassified

Evidensbasert medisin eller vulgærcochranisme?

Wyller¹

2011

Tidsskriftet

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“…Nicotine, from TS and e-cigs, has been associated with the development of a number of potential toxic mechanisms inflicted on the brain, including increased oxidative stress (Bernard et al, 2019;Kuntic et al, 2020), neuroinflammation (Stamatovic et al, 2011;Li et al, 2019), cerebral thrombosis (Kaisar et al, 2017;Qasim et al, 2018), changes in BBB-related protein function or expression (Wang et al, 1994;Abbruscato et al, 2004;Kaisar et al, 2018), BBB permeability (Abbruscato et al, 2002;Hawkins et al, 2004;Kaisar et al, 2017), and cerebral blood flow (Hans et al, 1993;Zubieta et al, 2001). Furthermore, nicotine and chemical constituents of both TS and e-cigs have been reported to interact with the liver cytochrome P450 (CYP-P450) enzymes and affect plasma drug levels of certain central nervous system (CNS) drugs (Zevin and Benowitz 1999;Molden and Spigset 2009;Ellingrod 2013). Also, it has also been reported that CNS drugs utilize similar nicotine transport systems at the BBB interface, and in the presence of nicotine, their transport to the brain can be directly affected (Tega et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Effects of Nicotine Exposure From Tobacco Products and Electronic Cigarettes on the Pathogenesis of Neurological Diseases: Impact on CNS Drug Delivery

Sharma

Kanchanwala

Mimun

et al. 2022

Front. Drug. Deliv.

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Nicotine, the major component of tobacco smoke (TS) and electronic cigarette (e-cig) vape, has been reported in some cases to be prodromal to cerebrovascular toxicity as well as a promoting factor for the onset of various neurological diseases. In some conditions, pre-exposure to nicotine can lead to a state of compromised blood-brain barrier (BBB) integrity, including altered BBB-related protein expression, BBB leakage, and defective ion and glucose homeostasis within the brain. Moreover, drugs used to treat central nervous system disorders (CNS) have been reported to interact with nicotine and other components of TS/e-cig through both transporter and enzyme-based mechanisms. Herein we discuss nicotine’s potential toxicity at the brain cerebrovasculature and explain how nicotine (from smoking/vaping) may interfere with the uptake of CNS drugs through a CNS drug interaction perspective.

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In Vivo Assessment of the Effect of CYP1A2 Inhibition and Induction on Pomalidomide Pharmacokinetics in Healthy Subjects

Li¹,

Liu²,

Wang³

et al. 2018

The Journal of Clinical Pharma

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Pomalidomide is an immunomodulatory drug, and the dosage of 4 mg per day taken orally on days 1‐21 of repeated 28‐day cycles has been approved in the European Union and the United States to treat patients with relapsed/refractory multiple myeloma. In vitro data showed that pomalidomide is a substrate of multiple cytochrome P450 (CYP) isozymes and that its oxidative metabolism is mediated primarily by CYP1A2 and CYP3A4, with minor contributions from CYP2C19 and CYP2D6. The effect of CYP1A2 inhibition by fluvoxamine (a strong CYP1A2 inhibitor) and CYP1A2 induction by smoking on pomalidomide pharmacokinetics in healthy subjects has been assessed in 2 separate phase 1 open‐label, single‐dose studies. Following administration of a single oral dose of 4 mg pomalidomide, the plasma exposure when coadministered with fluvoxamine was 225.1% and 123.7% of that when administered alone for the total plasma exposure (AUC0‐inf) and the plasma peak exposure (Cmax), respectively. In smokers with elevated CYP1A2 activity demonstrated by high caffeine clearance (a marker of CYP1A2 induction), the AUC0‐inf was 32.3% lower, whereas the Cmax was 14.4% higher than that in nonsmokers. In addition, pomalidomide was safe and well tolerated as a single oral dose of 4 mg in healthy male smokers and nonsmokers ≥ 40 to ≤ 80 years old, and a single oral dose of 4 mg pomalidomide coadministered with multiple oral 50‐mg doses of the CYP1A2 inhibitor fluvoxamine compared with pomalidomide alone was safe and well tolerated by the healthy male subjects.

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Tobakksrøyking og interaksjoner med legemidler

Cited by 5 publications

References 10 publications

Evidensbasert medisin eller vulgærcochranisme?

Evidensbasert medisin eller vulgærcochranisme?

Effects of Nicotine Exposure From Tobacco Products and Electronic Cigarettes on the Pathogenesis of Neurological Diseases: Impact on CNS Drug Delivery

In Vivo Assessment of the Effect of CYP1A2 Inhibition and Induction on Pomalidomide Pharmacokinetics in Healthy Subjects

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