QT time prolongation
Adverse drug events
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Explanations of the substances for patients
We have no additional warnings for the combination of abarelix and dexmedetomidine. Please also consult the relevant specialist information.
The reported changes in exposure correspond to the changes in the plasma concentration-time curve [ AUC ]. We do not expect any change in exposure for abarelix, when combined with dexmedetomidine (100%). We do not expect any change in exposure for dexmedetomidine, when combined with abarelix (100%).
The pharmacokinetic parameters of the average population are used as the starting point for calculating the individual changes in exposure due to the interactions.
The bioavailability of abarelix is unknown. The terminal half-life [ t12 ] is rather long at 316.8 hours and constant plasma levels [ Css ] are only reached after more than 1267.2 hours. The protein binding [ Pb ] is 97.5% strong. The metabolism via cytochromes is currently still being worked on.
The bioavailability of dexmedetomidine is unknown. The terminal half-life [ t12 ] is rather short at 2 hours and constant plasma levels [ Css ] are reached quickly. The protein binding [ Pb ] is moderately strong at 94%. The metabolism does not take place via the common cytochromes.
|Serotonergic Effects a||0||Ø||Ø|
Rating: According to our knowledge, neither abarelix nor dexmedetomidine increase serotonergic activity.
|Kiesel & Durán b||0||Ø||Ø|
Rating: According to our knowledge, neither abarelix nor dexmedetomidine increase anticholinergic activity.
QT time prolongation
Rating: In combination, abarelix and dexmedetomidine can potentially trigger ventricular arrhythmias of the torsades de pointes type.
General adverse effects
|Side effects||∑ frequency||aba||dex|
|Respiratory depression||37.0 %||n.a.||37.0|
|Atrial fibrillation||4.0 %||n.a.||4.0|
Anemia (3%): dexmedetomidine
Hypoxia (3%): dexmedetomidine
Pulmonary edema: dexmedetomidine
Ventricular tachycardia: dexmedetomidine
Based on your answers and scientific information, we assess the individual risk of undesirable side effects. These recommendations are intended to advise professionals and are not a substitute for consultation with a doctor. In the restricted test version (alpha), the risk of all substances has not yet been conclusively assessed.
Abstract: Dexmedetomidine is a selective alpha-2 adrenergic agonist that is used frequently for short-term sedation in children. It has been noted to cause hypertension, hypotension, bradycardia, and sinus pauses; however, QTc prolongation has not been reported with dexmedetomidine administration. We describe a case of marked QT prolongation with use of dexmedetomidine in a pediatric critical care setting. Clinicians should be vigilant about potential QT prolongation in patients on dexmedetomidine, particularly in those receiving multiple other medications.
Abstract: BACKGROUND: Clinical indications for the perioperative use of dexmedetomidine in pediatric anesthesia are accumulating. However, in 2013, dexmedetomidine was added to the list of medications with possible risk of prolonging the QT interval and/or inducing Torsades de Pointes. Unfortunately, current evidence for dexmedetomidine-induced QT prolongation is sparse and somewhat contradictory. OBJECTIVE: The purpose of this study was to evaluate temporal changes in corrected QT interval (QTc) after a rapid bolus administration of dexmedetomidine under total intravenous anesthesia (TIVA) with a standardized propofol and remifentanil administration. METHODS: Electrocardiography (ECG) and corresponding trend data were extracted from automated electronic data capture of physiological monitoring. Ten-second epochs of ECG data were extracted in 1-min intervals for 12 min, starting 1 min before dexmedetomidine bolus administration, and ending 10 min after. QT intervals were extracted using an automated routine in MATLAB, and corrected for heart rate (HR) using Bazett's (QTcB) and Fridericia's formulas (QTcF). QTcB and QTcF were compared using Wilcoxon signed-rank test between baseline measurements and the subsequent four interval values. RESULTS: Data from 21 subjects (17 male) with median (range) age 7.1 (5.4-9.5) yr, weight 23.6 (16.2-36.7) kg, and height 121 (103-140) cm were analyzed. Bolus administration of dexmedetomidine reduced HR in all subjects (median 22%), and caused transient reduction of QT interval, with its peak at 1-min postbolus administration: QTcB (median reduction 30.7 ms, P < 0.001) or QTcF (median reduction 15.4 ms, P = 0.001); QT shortening became statistically insignificant 4 min following dexmedetomidine bolus administration for QTcB and 2 min for QTcF. CONCLUSION: In this study, a rapid bolus of dexmedetomidine transiently shortened corrected QT intervals. However, these effects are confounded by dexmedetomidine-induced bradycardia. These findings should be confirmed in pediatric studies without concomitant TIVA administration and with optimized correction of baseline HR.