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 levosulpiride. 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 levosulpiride (100%). We do not expect any change in exposure for levosulpiride, 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, half-life, and volume of distribution of levosulpiride are unknown to us.
|Serotonergic Effects a||0||Ø||Ø|
Rating: According to our knowledge, neither abarelix nor levosulpiride increase serotonergic activity.
|Kiesel & Durán b||0||Ø||Ø|
Rating: According to our knowledge, neither abarelix nor levosulpiride increase anticholinergic activity.
QT time prolongation
Rating: In combination, abarelix and levosulpiride can potentially trigger ventricular arrhythmias of the torsades de pointes type.
General adverse effects
|Side effects||∑ frequency||aba||lev|
|Ventricular arrhythmia||0.0 %||n.a.||0.0|
|Neuroleptic malignant syndrome||0.0 %||n.a.||0.0|
|Thromboembolic disorder||0.0 %||n.a.||0.0|
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: We report the case of an 89-year-old female patient who presented to the emergency department after out-of-hospital cardiac arrest due to polymorphic ventricular tachycardia treated by public access defibrillation. The admission electrocardiogram (ECG) showed extreme QT prolongation (650 milliseconds) with recurrent episodes of nonsustained polymorphic ventricular tachycardia. Intravenous magnesium sulfate therapy was instituted. After history taking, it was found that the patient was on citalopram and that, 2 days prior to admission, she had begun treatment with levosulpiride. This drug combination resulted in marked prolongation of the QT interval that triggered the electrical storm.