ACEBUTOLOL HYDROCHLORIDE Drug Interactions
Also known as: Acebutolol Hydrochloride
Acebutolol Hydrochloride is a type of medicine called a beta-blocker, primarily used to treat high blood pressure (hypertension) and certain irregular heartbeats (ventricular arrhythmias). It works by relaxing blood vessels and slowing down the heart rate, which helps the heart beat more regularly and reduces the force of blood pumping through your arteries.ACEBUTOLOL HYDROCHLORIDE has 7 documented drug interactions in our database, including 0 contraindicated, 1 major, 4 moderate, and 2 minor interactions.
0
Contraindicated
1
Major
4
Moderate
2
Minor
The coadministration of acebutolol and paroxetine can lead to significantly increased plasma concentrations of acebutolol, potentially resulting in enhanced beta-blocker effects. This interaction can manifest as severe bradycardia, hypotension, and heart block, increasing the risk of adverse cardiovascular events.
Mechanism
Paroxetine is a potent inhibitor of cytochrome P450 2D6 (CYP2D6). Acebutolol is metabolized by CYP2D6 to its active metabolite diacetolol, and its clearance can be significantly reduced by CYP2D6 inhibition, leading to higher systemic exposure.
Clinical Management
Avoid concurrent use if possible. If coadministration is necessary, a significant reduction in acebutolol dosage (e.g., by 50% or more) should be considered, along with close monitoring of heart rate, blood pressure, and cardiac rhythm, especially during initiation or dose changes of paroxetine. Consider an alternative beta-blocker not primarily metabolized by CYP2D6, such as atenolol or bisoprolol, or an antidepressant with minimal CYP2D6 inhibition.
Fluoxetine, a potent CYP2D6 inhibitor, can increase plasma concentrations of acebutolol, which is partially metabolized by CYP2D6. This interaction may enhance the pharmacologic effects of acebutolol, potentially leading to increased risk of bradycardia, hypotension, or heart block.
Mechanism
Fluoxetine inhibits cytochrome P450 2D6 (CYP2D6), an enzyme involved in the metabolism of acebutolol. This inhibition reduces acebutolol clearance, leading to higher systemic exposure.
Clinical Management
Monitor patients closely for signs and symptoms of beta-blockade, such as bradycardia, hypotension, and dizziness, especially when initiating or adjusting fluoxetine. Consider using an alternative antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram) or a beta-blocker primarily cleared renally (e.g., atenolol, nadolol) if close monitoring is not feasible or if adverse effects occur.
The co-administration of acebutolol and citalopram may lead to an increased risk of bradycardia and hypotension. Citalopram is a weak inhibitor of CYP2D6, which is involved in the metabolism of acebutolol, potentially increasing acebutolol plasma concentrations. Both drugs can also independently cause bradycardia.
Mechanism
Acebutolol is metabolized by CYP2D6. Citalopram is a weak inhibitor of CYP2D6, which may reduce the metabolism of acebutolol, leading to increased acebutolol plasma levels and enhanced beta-blocking effects. Additionally, both acebutolol and citalopram can independently cause bradycardia, leading to an additive pharmacodynamic effect.
Clinical Management
Monitor patients for signs and symptoms of bradycardia and hypotension, especially when initiating or adjusting doses of either medication. If adverse effects occur, consider reducing the acebutolol dose or using an alternative antidepressant with less CYP2D6 inhibition or a beta-blocker with minimal CYP2D6 metabolism (e.g., atenolol, bisoprolol).
Fluoxetine is a potent CYP2D6 inhibitor, which can increase plasma concentrations of acebutolol. This interaction may lead to enhanced beta-blockade effects such as bradycardia, hypotension, and heart block, particularly in susceptible patients.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is involved in the metabolism of acebutolol. This inhibition reduces acebutolol clearance, leading to elevated systemic exposure.
Clinical Management
Monitor patients closely for signs and symptoms of excessive beta-blockade, including bradycardia, hypotension, and dizziness. Consider using alternative SSRIs with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram) or an alternative beta-blocker not primarily metabolized by CYP2D6 (e.g., atenolol, nadolol). If co-administration is necessary, a lower dose of acebutolol may be required.
The co-administration of acebutolol and fluvoxamine may lead to an increased risk of bradycardia and hypotension. While acebutolol is primarily metabolized by CYP2D6, fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, and a moderate inhibitor of CYP2D6, which could potentially increase acebutolol plasma concentrations.
Mechanism
Fluvoxamine is a moderate inhibitor of CYP2D6, the primary enzyme responsible for acebutolol's metabolism to diacetolol. This inhibition could decrease acebutolol clearance, leading to elevated systemic exposure and enhanced beta-adrenergic blockade.
Clinical Management
Monitor patients closely for signs and symptoms of bradycardia and hypotension, especially when initiating or adjusting fluvoxamine dose. Consider using a lower starting dose of acebutolol or an alternative antidepressant with less CYP2D6 inhibitory potential if clinically appropriate. Regular blood pressure and heart rate monitoring are recommended.
The interaction between acebutolol and sertraline is generally considered minor. While both drugs can independently cause bradycardia, sertraline has minimal CYP2D6 inhibitory activity, reducing the risk of pharmacokinetic interaction with acebutolol, which is partially metabolized by CYP2D6.
Mechanism
Sertraline is a weak inhibitor of CYP2D6, which is involved in the metabolism of acebutolol (and its active metabolite diacetolol). Therefore, sertraline is unlikely to significantly increase acebutolol plasma concentrations. Additive pharmacodynamic effects on heart rate are theoretically possible but generally not clinically significant with this combination.
Clinical Management
No specific dose adjustments are typically required for acebutolol or sertraline when co-administered. Monitor for signs of excessive bradycardia, hypotension, or other beta-blocker side effects, especially in patients sensitive to these effects. Routine monitoring of vital signs is generally sufficient.
The interaction between acebutolol and escitalopram is generally considered minor. Escitalopram has minimal CYP2D6 inhibitory activity, therefore, it is unlikely to significantly alter acebutolol plasma levels. However, both drugs can independently cause bradycardia, and an additive pharmacodynamic effect is theoretically possible.
Mechanism
Escitalopram is a weak inhibitor of CYP2D6, the enzyme responsible for the metabolism of some beta-blockers. Acebutolol is partially metabolized by CYP2D6, but escitalopram's weak inhibition is unlikely to cause a clinically significant pharmacokinetic interaction. A theoretical additive pharmacodynamic effect on heart rate is possible due to both drugs' potential to induce bradycardia.
Clinical Management
No specific dose adjustments are typically required for this combination. Monitor patients for signs of excessive bradycardia (e.g., heart rate <50 bpm, dizziness, fatigue), especially at the initiation of escitalopram or after dose increases. If significant bradycardia occurs, consider dose reduction of acebutolol or an alternative antidepressant with no cardiac effects.
For complete prescribing information:
View full ACEBUTOLOL HYDROCHLORIDE monograph →Medical Disclaimer
The information on RxGuide is intended for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician, pharmacist, or other qualified health provider with any questions you may have regarding a medical condition or medication. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.