Cisapride-induced dysrhythmia in a pediatric patient receiving extracorporeal life support

Pettignano, Robert; Cr, Chambliss; Darsey, Edress; Heard, Micheal; Clark, Reese H.

doi:10.1097/00003246-199607000-00035

Cited by 34 publications

(14 citation statements)

References 14 publications

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“…Cisapride has been associated with QT interval prolongation [2][3][4][5], which in turn could lead to life-threatening arrhythmias, such as torsades de pointe [6,7]. Most reported cardiac adverse events occurred at high doses of cisapride [8][9][10], in patients acutely ill [11], or in patients receiving medications known to increase cisapride levels (i.e. imidazoles, macrolides) or to cause QT interval prolongation [7].…”

Section: Introductionmentioning

confidence: 99%

Effects of Cisapride on Ventricular Depolarization-Repolarization and Arrhythmia Markers in Infants

Zamora¹,

Belli²,

Ferrazzini³

et al. 2001

Neonatology

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To study prospectively the effects of cisapride on ventricular repolarization, depolarization, and arrhythmia markers in neonates, we determined before and three days after starting cisapride (1 mg/kg/day): corrected QT interval (QTc) and QT dispersion (QTd) on standard ECGs, and duration of filtered QRS (fQRS) and of low amplitude (<40 µV) terminal signals (LAS40, ms) and root mean square of the last 40 ms (RMS40, µV) using high-gain signal-averaged ECG (SAECG). Twenty-four term and 11 preterm infants (gestational age 23–35 weeks) were studied at a median chronological age of 32 days. QTc and QTd were not different between term and preterm infants. Cisapride lengthened QTc (mean ± SD; ms: 396.6 ± 24.8 before vs. 417.0 ± 35.2 after, p < 0.001). Three term and two preterm infants (5/35 = 14%; 95% CI: 5–30%) had a QTc >450 ms after cisapride. QTd after cisapride increased significantly in all infants with prolonged QTc. Filtered QRS, LAS40, and RMS40 before and after cisapride were within our normal values. We conclude that cisapride prolongs ventricular repolarization in neonates and infants without altering depolarization. Although no clinical arrhythmias were observed the dose of 0.8 mg/kg/day should not be exceeded.

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Section: Introductionmentioning

confidence: 99%

Effects of Cisapride on Ventricular Depolarization-Repolarization and Arrhythmia Markers in Infants

Zamora¹,

Belli²,

Ferrazzini³

et al. 2001

Neonatology

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“…3 However, inappropriate lengthening of the QT interval and induction of major cardiac rhythm disturbances, such as polymorphic ventricular tachycardia (torsades de pointes), have been observed in some patients. [4][5][6][7][8][9] Although some of these episodes have occurred at high doses of cisapride, several cases of torsades de pointes and sudden deaths have been seen unexpectedly in patients, including children, receiving clinically recommended doses of the drug. 5,7 The study of the electrophysiological mechanism(s) responsible for the development of torsades de pointes is an area of extensive investigation.…”

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confidence: 99%

Block of the Rapid Component of the Delayed Rectifier Potassium Current by the Prokinetic Agent Cisapride Underlies Drug-Related Lengthening of the QT Interval

et al. 1998

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“…1,8 Excessive doses of cisapride, a prokinetic drug used in gastroesophageal reflux disease, and its administration with drugs inhibiting its metabolism may lead to serious cardiac arrhythmias, occasionally resulting in death. 148,149 CYP3A4 is the principal enzyme responsible for biotransformation of cisapride to norcisapride, 3-fluoro-2-hydroxycisapride and 4-fluoro-2-hydroxycisapride. 150 Although norcisapride elicits 15% of cisapride prokinetic action, it has no activity regarding myocardial conduction.…”

Section: Gastroesophageal Refluxmentioning

confidence: 99%

Advances of Molecular Clinical Pharmacology in Gastroenterology and Hepatology

Prandota¹

2010

American Journal of Therapeutics

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During developmental age, differences in pharmacodynamic reactions to several drugs may reflect polymorphisms of genes encoding drug-transporting proteins, receptors, drug targets, and gene products, whose disturbed activity sometimes plays an important role in certain diseases. Administration of drugs with a narrow therapeutic index may quite easily be associated with changes in pharmacokinetics and development of adverse drug reactions, which occasionally may cause fatalities. In such cases, polypragmasy and resulting drug interactions may enhance effects of changes in drug-metabolizing enzymes' activities. Phenotyping and genotyping of patients slowly are finding their place in some therapeutic regimens used in clinical gastroenterology and hepatology. At present, some assays to measure, for example, thiopurine S-methyltransferase activity are already commercially available. Polymorphisms of CYP450 enzymes, interleukins, and altered gene expression play an important role in some patients' various gastrointestinal tract and liver diseases. Herbal drugs also affect proinflammatory and antiinflammatory cytokine and nitric oxide balance in the body. Therapeutic use of recombined proteins, such as infliximab, natalizumab, onercept, humanized antibody to integrin α-4 β-7, or IFN-β in some large-bowel diseases increased therapeutic efficacy. IFN-α used in the patients with chronic hepatitis C improved cellular immunity in these subjects and exerted antiviral activity. Practical application of progress in pharmacogenetics, pharmacokinetics, pharmacodynamics, and use of bioproducts in novel therapeutic regimens has opened therapeutic frontiers and increased clinical safety.

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Cisapride-induced dysrhythmia in a pediatric patient receiving extracorporeal life support

Cited by 34 publications

References 14 publications

Effects of Cisapride on Ventricular Depolarization-Repolarization and Arrhythmia Markers in Infants

Effects of Cisapride on Ventricular Depolarization-Repolarization and Arrhythmia Markers in Infants

Block of the Rapid Component of the Delayed Rectifier Potassium Current by the Prokinetic Agent Cisapride Underlies Drug-Related Lengthening of the QT Interval

Advances of Molecular Clinical Pharmacology in Gastroenterology and Hepatology

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