Inhibition of metoprolol metabolism and potentiation of its effects by paroxetine in routinely treated patients with acute myocardial infarction (AMI)

Goryachkina, Ksenia; Бурбелло, А Т; Болдуева, С. А.; Babak, Svetlana; Bergman, Ulf; Bertilsson, Leif

doi:10.1007/s00228-007-0404-3

Cited by 40 publications

(46 citation statements)

References 38 publications

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“…Totalt ble åtte studier/rapporter som belyser interaksjonsrisiko mellom metoprolol og antidepressiver identifisert (4)(5)(6)(7)(8)(9)(10)(11). Tabell 1 oppsummerer hovedfunn fra disse publikasjonene.…”

Section: Resultaterunclassified

“…Blant annet ble treningsindusert pulsøkning redusert med 30-40 % i kombinasjon med paroksetin (4). Interaksjonen mellom metoprolol og paroksetin er senere blitt bekreftet i en studie på hjertepasienter, der plasmakonsentrasjonen av metoprolol økte drøyt fire ganger (5 (6). Denne studien viste at økningen i plasmakonsentrasjonen av metoprolol var noe mindre ved bruk av depotformulering sammenliknet med vanlig tablettformulering, men økningen var også kraftig med depotformuleringen -i stør-relsesorden 3-4 ganger (6).…”

Section: Resultaterunclassified

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Interaksjoner mellom metoprolol og antidepressive legemidler

Molden¹,

Spigset²

2011

Tidsskriftet

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Section: Resultaterunclassified

Interaksjoner mellom metoprolol og antidepressive legemidler

Molden¹,

Spigset²

2011

Tidsskriftet

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“…It was reported that concurrent use of CYP2D6 substrates or inhibitors could influence cardiovascular patients’ therapeutic responses, in some cases even result in adverse effects. For example, when acute myocardial infarction patients were treated with metoprolol (a substrate for CYP2D6) and co-treated with paroxetine (an inhibitor of CYP2D6), paroxetine inhibited the metabolism of metoprolol and increased its concentration maximum (Cmax), resulting in enhanced therapeutic effects and/or adverse effects, such as severe dizziness, fainting and heart failure [34]. In anti-cancer therapy, many studies have demonstrated that altered expression of DMEs can influence the sensitivity and toxicity of drugs in target cells, and the expression of DMEs plays a pivotal role in chemotherapy sensitivity, resistance, and/or carcinogenesis [35,36].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA hsa-miR-370-3p suppresses the expression and induction of CYP2D6 by facilitating mRNA degradation

Zeng

Chen

Wang

et al. 2017

Biochemical Pharmacology

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Cytochrome P450 2D6 (CYP2D6) participates in the metabolism of approximately 20–25% of prescribed drugs. Genetic polymorphisms influence the expression and/or activity of CYP2D6, and inter-individual differences in drug activation and elimination caused by CYP2D6 genetic variants were reported. However, little is known about the potential modulation of CYP2D6 expression by microRNAs (miRNAs). In the current study, by using in silico prediction of the stabilities of miRNA/mRNA complexes, we screened 38 miRNA candidates that may interact with the transcript of CYP2D6. An inverse correlation between the expression of miRNA hsa-miR-370-3p and the expression of CYP2D6 was observed in human liver tissue samples. Electrophoretic mobility shift assays confirmed that hsa-miR-370-3p was able to directly bind to its cognate target within the coding region of the CYP2D6 transcript. The transfection of hsa-miR-370-3p mimics into the HepG2CYP2D6 cell line, a genetically modified cell line that overexpresses exogenous CYP2D6, was able to suppress the expression of CYP2D6 significantly at both mRNA and protein levels. The transfection of hsa-miR-370-3p mimics was also able to inhibit endogenous mRNA expression and/or protein production of CYP2D6 in HepaRG cells. Furthermore, in HepaRG, HepG2, and Huh7 cells, dexamethasone-induced expression of CYP2D6 was inhibited by hsa-miR-370-3p mimics. To investigate whether the miRNA mediated suppression is caused by inhibiting protein translation or promoting mRNA degradation, an actinomycin D assay was used to measure the stability of CYP2D6 transcripts. The results indicated that hsa-miR-370-3p mimics facilitated significantly the degradation of CYP2D6 mRNA. In addition, proteomics analyses of proteins isolated from the miRNA/mRNA/protein complex suggested that a group of multifunctional proteins facilitated the interaction between hsa-miR-370-3p and CYP2D6, thereby promoting mRNA degradation.

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“…Most patients treated for depression in primary care are treated with antidepressants [43], and common side effects include diarrhea, dizziness, dry mouth, fatigue, headache, nausea, sexual dysfunction, excessive sweating, tremors and weight gain [44]. Less common but potentially more serious adverse effects, particularly for patients in primary care with heart disease, may include increased risk of bleeding and unwanted effects on blood pressure and heart rate [45-49], as well as drug-drug interactions with cardiac medications [50,51]. For patients with generally low levels of depression, who are most likely to be newly identified through screening, the side effect burden and potential risk profile of antidepressants need to be carefully considered, particularly given that screening has not been shown to reduce symptoms of depression.…”

Section: Discussionmentioning

confidence: 99%

There are no randomized controlled trials that support the United States Preventive Services Task Force guideline on screening for depression in primary care: a systematic review

Thombs

Ziegelstein

Roseman

et al. 2014

BMC Med

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BackgroundThe United States Preventive Services Task Force (USPSTF) recommends screening adults for depression in primary care settings when staff-assisted depression management programs are available. This recommendation, however, is based on evidence from depression management programs conducted with patients already identified as depressed, even though screening is intended to identify depressed patients not already recognized or treated. The objective of this systematic review was to evaluate whether there is evidence from randomized controlled trials (RCTs) that depression screening benefits patients in primary care, using an explicit definition of screening.MethodsWe re-evaluated RCTs included in the 2009 USPSTF evidence review on depression screening, including only trials that compared depression outcomes between screened and non-screened patients and met the following three criteria: determined patient eligibility and randomized prior to screening; excluded patients already diagnosed with a recent episode of depression or already being treated for depression; and provided the same level of depression treatment services to patients identified as depressed in the screening and non-screening trial arms. We also reviewed studies included in a recent Cochrane systematic review, but not the USPSTF review; conducted a focused search to update the USPSTF review; and reviewed trial registries.ResultsOf the nine RCTs included in the USPSTF review, four fulfilled none of three criteria for a test of depression screening, four fulfilled one of three criteria, and one fulfilled two of three criteria. There were two additional RCTs included only in the Cochrane review, and each fulfilled one of three criteria. No eligible RCTs were found via the updated review.ConclusionsThe USPSTF recommendation to screen adults for depression in primary care settings when staff-assisted depression management programs are available is not supported by evidence from any RCTs that are directly relevant to the recommendation. The USPSTF should re-evaluate this recommendation.Please see related article: http://www.biomedcentral.com/1741-7015/12/14RegistrationPROSPERO (#CRD42013004276)

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Inhibition of metoprolol metabolism and potentiation of its effects by paroxetine in routinely treated patients with acute myocardial infarction (AMI)

Abstract: A pronounced inhibition of metoprolol metabolism by paroxetine was observed in AMI patients, but without serious adverse effects. We suggest, however, that the metoprolol dose is controlled upon initiation and withdrawal of paroxetine.

Cited by 40 publications

References 38 publications

Interaksjoner mellom metoprolol og antidepressive legemidler

Interaksjoner mellom metoprolol og antidepressive legemidler

MicroRNA hsa-miR-370-3p suppresses the expression and induction of CYP2D6 by facilitating mRNA degradation

There are no randomized controlled trials that support the United States Preventive Services Task Force guideline on screening for depression in primary care: a systematic review

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