ArticleBritish journal of clinical pharmacology2000
CYP2D6 and CYP2C19 genotypes of patients with terodiline cardiotoxicity identified through the yellow card system.
Article in British journal of clinical pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- SLCO1B1 genetic variant associated with statin-induced myopathy: a proof-of-concept study using the clinical practice research datalink.Clinical pharmacology and therapeutics · 2013Pooled it
- Cardiovascular adverse effects of common non-oncologic medications: from mechanisms to clinical management.European heart journal. Cardiovascular pharmacotherapy · 2026Review
- The Therapeutic Potential of Carnosine as an Antidote against Drug-Induced Cardiotoxicity and Neurotoxicity: Focus on Nrf2 Pathway.Molecules (Basel, Switzerland) · 2022Review
- Toward a broader view of mechanisms of drug cardiotoxicity.Cell reports. Medicine · 2021Review
- Mechanisms Underlying the Actions of Antidepressant and Antipsychotic Drugs That Cause Sudden Cardiac Arrest.Arrhythmia & electrophysiology review · 2018Review
- Pharmacogenetics of Drug-Induced QT Interval Prolongation: An Update.Drug safety · 2015Review
- Pharmacological and electrophysiological characterization of nine, single nucleotide polymorphisms of the hERG-encoded potassium channel.British journal of pharmacology · 2010Article
- Sudden cardiac death secondary to antidepressant and antipsychotic drugs.Expert opinion on drug safety · 2008Review
- Drug-induced spatial dispersion of repolarization.Cardiology journal · 2008Review
- Pharmacogenetic aspects of drug-induced torsade de pointes: potential tool for improving clinical drug development and prescribing.Drug safety · 2004Review
- Safety of non-antiarrhythmic drugs that prolong the QT interval or induce torsade de pointes: an overview.Drug safety · 2002Review
- Clinical significance of the cytochrome P450 2C19 genetic polymorphism.Clinical pharmacokinetics · 2002Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTerodiline has concentration dependent QT prolonging effects and thus the potential for cardiotoxicity. Pharmacogenetic variation in terodiline metabolism could be responsible for cardiotoxicity. We sought to determine whether CYP2D6 (debrisoquine hydroxylase) or CYP2C19 (S-mephenytoin hydroxylase) status is a risk factor for terodiline cardiotoxicity.
methodsUsing the UK Yellow Card scheme to identify patients, blood samples were obtained from eight patients who survived ventricular tachycardia or torsades de pointes suspected to be due to terodiline, for determination of CYP2D6 and CYP2C19 genotypes. Genotype prevalence was compared with that in published general population groups.
resultsOne patient was a CYP2D6 poor metaboliser (CYP2D6*4 homozygous) and a second was heterozygous for CYP2D6*4, a slightly lower frequency for these genotypes compared with the general population (P = 0.31). In the case of CYP2C19, one patient was a poor metaboliser and four were heterozygous for the variant CYP2C19*2 allele, compared with general population frequencies of 2% and 23%, respectively (P = 0.035).
conclusionsThese findings suggest that debrisoquine poor metaboliser status is not primarily responsible for terodiline cardiotoxicity. However, possession of the CYP2C19*2 allele appears to contribute to adverse cardiac reactions to terodiline. The present study demonstrates the feasibility of using spontaneous adverse drug reaction reporting schemes to determine the contribution of genotype for metabolizing enzymes to uncommon adverse drug reactions.
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