5 HT3-receptor antagonists and cardiac repolarization time in patients expressing a novel genetic target associated with baseline QTc interval abnormalities

Quraishi, Sadeq A.; Schuler, Gregg H.; Janicki, Piotr K.

doi:10.1016/j.jclinane.2010.11.003

Cited by 6 publications

(3 citation statements)

References 45 publications

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“…Up to 10%-30% of asymptomatic individuals may have a prolonged QTc at baseline. 20 Likewise, administration of dolasetron in patients known to be predisposed to unstable tachyarrhythmias should also be avoided. However, when choosing a replacement antiemetic, it should be noted that ondansetron has also been shown to induce arrhythmia and prolong QTc, though to a lesser extent than dolasetron.…”

Section: Patient Considerations Regarding Dolasetronmentioning

confidence: 99%

“…10 Recent genetic data has also identified a single nucleotide polymorphism within the NOS1AP gene that may place patients at increased risk for developing prolonged QTc after 5-HT 3 receptor antagonist administration. 20 Further investigation into these polymorphisms may allow clinicians to individualize therapeutic regimens more precisely and to treat their patients more effectively. However, dose adjustments for dolasetron are currently unnecessary based on readily available information (age, renal function, and hepatic function).…”

Section: Patient Considerations Regarding Dolasetronmentioning

confidence: 99%

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Reappraisal of the role of dolasetron in prevention and treatment of nausea and vomiting associated with surgery or chemotherapy

Roberts

Bezinover²,

Janicki³

2012

CMAR

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Chemotherapy-induced nausea and vomiting and postoperative nausea and vomiting are one of the most frequent but also very concerning consequences for patients undergoing chemotherapy or surgical procedures under general anesthesia. There are a variety of mechanisms involved in the activation of nausea and vomiting. Serotonin, a ubiquitous central and peripheral neurotransmitter, is thought to be the predominant mediator of the perception of nausea and triggering of the vomiting response in both the brain and the periphery via the 5-hydroxytryptamine type 3 (5-HT3) receptor pathways. 5-HT3 receptor antagonists disrupt this pathway, largely at the level of the vagal afferent pathways, to decrease nausea and vomiting. This review will focus on dolasetron, an older but sill commonly used 5-HT3 receptor antagonist and its multimodal mechanism of action, safety and tolerability, patient considerations, and a review of the current literature on its use to combat both chemotherapy-induced and postoperative nausea and vomiting in these two important patient populations.

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Section: Patient Considerations Regarding Dolasetronmentioning

confidence: 99%

Section: Patient Considerations Regarding Dolasetronmentioning

confidence: 99%

Reappraisal of the role of dolasetron in prevention and treatment of nausea and vomiting associated with surgery or chemotherapy

Roberts

Bezinover²,

Janicki³

2012

CMAR

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“…NOS1AP has also been associated with antipsychotic-induced QT prolongation [ 48 ] and drug-induced torsade de pointes [ 56 ]. Heterozygous and homozygous major allele carriers of the rs10494366 variant had an increased risk of a prolonged QT interval following granisetron or dolasetron administration in the perioperative setting, compared with homozygous minor allele carriers [ 72 ].…”

Section: Pharmacodynamic Genetic Susceptibilitymentioning

confidence: 99%

Pharmacogenetics of Drug-Induced QT Interval Prolongation: An Update

et al. 2015

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A prolonged QT interval is an important risk factor for ventricular arrhythmias and sudden cardiac death. QT prolongation can be caused by drugs. There are multiple risk factors for drug-induced QT prolongation, including genetic variation. QT prolongation is one of the most common reasons for withdrawal of drugs from the market, despite the fact that these drugs may be beneficial for certain patients and not harmful in every patient. Identifying genetic variants associated with drug-induced QT prolongation might add to tailored pharmacotherapy and prevent beneficial drugs from being withdrawn unnecessarily. In this review, our objective was to provide an overview of the genetic background of drug-induced QT prolongation, distinguishing pharmacokinetic and pharmacodynamic pathways. Pharmacokinetic-mediated genetic susceptibility is mainly characterized by variation in genes encoding drug-metabolizing cytochrome P450 enzymes or drug transporters. For instance, the P-glycoprotein drug transporter plays a role in the pharmacokinetic susceptibility of drug-induced QT prolongation. The pharmacodynamic component of genetic susceptibility is mainly characterized by genes known to be associated with QT interval duration in the general population and genes in which the causal mutations of congenital long QT syndromes are located. Ethnicity influences susceptibility to drug-induced QT interval prolongation, with Caucasians being more sensitive than other ethnicities. Research on the association between pharmacogenetic interactions and clinical endpoints such as sudden cardiac death is still limited. Future studies in this area could enable us to determine the risk of arrhythmias more adequately in clinical practice.

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Local-anesthetic like inhibition of the cardiac sodium channel Nav1.5 α-subunit by 5-HT 3 receptor antagonists

Klooster

Foadi

Hage

et al. 2016

European Journal of Pharmacology

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5 HT3-receptor antagonists and cardiac repolarization time in patients expressing a novel genetic target associated with baseline QTc interval abnormalities

Cited by 6 publications

References 45 publications

Reappraisal of the role of dolasetron in prevention and treatment of nausea and vomiting associated with surgery or chemotherapy

Reappraisal of the role of dolasetron in prevention and treatment of nausea and vomiting associated with surgery or chemotherapy

Pharmacogenetics of Drug-Induced QT Interval Prolongation: An Update

Local-anesthetic like inhibition of the cardiac sodium channel Nav1.5 α-subunit by 5-HT 3 receptor antagonists

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