PROPRANOLOL HYDROCHLORIDE Drug Interactions
Also known as: propranolol hydrochloride
Propranolol hydrochloride is a medication that helps manage conditions like high blood pressure, chest pain (angina), and prevents migraine headaches. It works by affecting certain signals in the body, which helps to slow the heart rate and relax blood vessels, making it easier for the heart to pump blood.PROPRANOLOL HYDROCHLORIDE has 7 documented drug interactions in our database, including 0 contraindicated, 4 major, 1 moderate, and 2 minor interactions.
0
Contraindicated
4
Major
1
Moderate
2
Minor
Fluoxetine, a potent CYP2D6 inhibitor, can significantly increase plasma concentrations of propranolol, a beta-blocker primarily metabolized by CYP2D6. This interaction can lead to enhanced beta-blockade effects, manifesting as severe bradycardia, hypotension, or heart block.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is a major metabolic pathway for propranolol. This inhibition reduces the clearance of propranolol, leading to elevated systemic exposure and increased pharmacodynamic effects.
Clinical Management
If co-administration is necessary, a significant reduction in propranolol dosage may be required, along with close monitoring of heart rate, blood pressure, and cardiac rhythm for signs of excessive beta-blockade. Consider using an alternative antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram) or a beta-blocker primarily cleared renally (e.g., atenolol, nadolol) to avoid this interaction.
Fluoxetine, a potent CYP2D6 inhibitor, can significantly increase plasma concentrations of propranolol, a beta-blocker primarily metabolized by CYP2D6. This interaction can lead to profound bradycardia, hypotension, and other symptoms of beta-blockade.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is a primary metabolic pathway for propranolol. This pharmacokinetic interaction reduces propranolol clearance, leading to elevated systemic exposure.
Clinical Management
If co-administration is necessary, close monitoring for signs of excessive beta-blockade (e.g., bradycardia, hypotension, fatigue) is essential. A lower starting dose of propranolol may be required, and dose adjustments should be made cautiously based on clinical response and tolerability. Consider using an alternative beta-blocker less dependent on CYP2D6 metabolism (e.g., atenolol, nadolol) or an antidepressant with less CYP2D6 inhibitory potential (e.g., sertraline).
Paroxetine, a potent CYP2D6 inhibitor, can significantly increase plasma concentrations of propranolol, a beta-blocker primarily metabolized by CYP2D6. This elevated propranolol level can lead to enhanced beta-blockade effects, potentially causing severe bradycardia, hypotension, and heart block.
Mechanism
Paroxetine potently inhibits the cytochrome P450 2D6 (CYP2D6) enzyme. Propranolol is a substrate of CYP2D6, so its metabolism is reduced, leading to decreased clearance and increased systemic exposure.
Clinical Management
Concomitant use should be approached with caution or avoided if possible. If co-administration is necessary, a significant reduction in propranolol dosage may be required, along with close monitoring for signs of excessive beta-blockade (e.g., bradycardia, hypotension, fatigue). Consider alternative beta-blockers primarily cleared renally (e.g., atenolol, nadolol) or SSRIs with minimal CYP2D6 inhibition (e.g., escitalopram, sertraline).
Coadministration of fluvoxamine with propranolol can significantly increase propranolol plasma concentrations, leading to enhanced beta-blockade effects. This can manifest as severe bradycardia, hypotension, and potentially heart block, increasing the risk of adverse cardiovascular events.
Mechanism
Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, both of which are involved in the metabolism of propranolol. Inhibition of these enzymes reduces propranolol clearance, leading to elevated systemic exposure.
Clinical Management
Avoid concurrent use if possible. If coadministration is necessary, initiate propranolol at a lower dose and monitor the patient closely for signs of bradycardia, hypotension, and other symptoms of excessive beta-blockade. Consider therapeutic drug monitoring for propranolol or using an alternative beta-blocker that is not metabolized by CYP1A2 or CYP2C19.
Citalopram is a weak inhibitor of CYP2D6, which is one of the primary enzymes responsible for the metabolism of propranolol. This interaction can lead to increased plasma concentrations of propranolol, potentially enhancing its beta-blocking effects such as bradycardia and hypotension.
Mechanism
Citalopram weakly inhibits cytochrome P450 2D6 (CYP2D6). Propranolol is extensively metabolized by CYP2D6, leading to reduced clearance and elevated systemic exposure of propranolol when co-administered with citalopram.
Clinical Management
Monitor patients for signs and symptoms of enhanced beta-blockade, including bradycardia, hypotension, and fatigue. While the interaction is generally less severe than with potent CYP2D6 inhibitors like fluoxetine or paroxetine, dose adjustments of propranolol may be necessary if adverse effects occur. Consider using a beta-blocker primarily cleared renally (e.g., atenolol) or an antidepressant with minimal CYP inhibition if concerns persist.
The interaction between propranolol and sertraline is generally considered minor. While both drugs can independently cause bradycardia, sertraline has minimal CYP2D6 inhibitory effects, leading to a low likelihood of significantly increasing propranolol plasma levels.
Mechanism
Propranolol is metabolized by CYP2D6. Sertraline is a weak inhibitor of CYP2D6, therefore it is unlikely to cause a clinically significant increase in propranolol concentrations through pharmacokinetic inhibition. Both drugs can independently cause bradycardia, leading to a potential, albeit low, additive pharmacodynamic effect.
Clinical Management
Routine monitoring for signs of excessive beta-blockade (e.g., bradycardia, hypotension) is advisable, especially when initiating or adjusting sertraline dose in patients on propranolol. However, dose adjustments are typically not required. Prescribers should be aware of the potential for additive bradycardia, particularly in susceptible patients.
The interaction between propranolol and escitalopram is generally considered minor. While both drugs can independently cause bradycardia, escitalopram has minimal CYP2D6 inhibitory effects, thus not significantly altering propranolol's metabolism.
Mechanism
Escitalopram is a weak inhibitor of CYP2D6, the primary enzyme responsible for the metabolism of propranolol. Therefore, escitalopram is unlikely to cause a clinically significant increase in propranolol plasma concentrations. Both drugs can independently cause bradycardia, leading to a potential additive pharmacodynamic effect.
Clinical Management
Generally, no special precautions or dose adjustments are required when co-administering propranolol and escitalopram. However, clinicians should monitor for signs of excessive bradycardia, especially in sensitive patients or those with pre-existing cardiac conditions. If bradycardia occurs, consider dose reduction of either agent or alternative therapies.
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