LABETALOL Drug Interactions
Also known as: Labetalol Hydrochloride
Labetalol is a medication used to treat high blood pressure (hypertension). It works by relaxing blood vessels and slowing the heart rate, which helps to lower your blood pressure. This can reduce the risk of complications like heart attack and stroke.LABETALOL has 7 documented drug interactions in our database, including 0 contraindicated, 0 major, 3 moderate, and 4 minor interactions.
0
Contraindicated
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Major
3
Moderate
4
Minor
Fluoxetine, a potent CYP2D6 inhibitor, can increase plasma concentrations of labetalol, which is partially metabolized by CYP2D6. This can lead to an increased risk of beta-blocker adverse effects such as bradycardia, hypotension, and heart block.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, reducing the metabolism of labetalol, a substrate for this enzyme. This pharmacokinetic interaction leads to higher systemic exposure to labetalol.
Clinical Management
Monitor patients closely for signs and symptoms of beta-blockade, including bradycardia, hypotension, and dizziness, especially when initiating or adjusting fluoxetine. Consider a lower starting dose of labetalol or a dose reduction if co-administered with fluoxetine. If possible, consider alternative beta-blockers that are not primarily metabolized by CYP2D6 (e.g., atenolol, nadolol, bisoprolol) or SSRIs with less CYP2D6 inhibition (e.g., sertraline, escitalopram).
Paroxetine, a potent CYP2D6 inhibitor, can increase plasma concentrations of labetalol, which is partially metabolized by CYP2D6. This interaction may lead to an increased risk of beta-blocker adverse effects such as bradycardia, hypotension, and heart block.
Mechanism
Paroxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is involved in the metabolism of labetalol. This pharmacokinetic interaction reduces labetalol clearance, leading to higher systemic exposure.
Clinical Management
Monitor patients closely for signs and symptoms of increased beta-blockade, including bradycardia, hypotension, and dizziness. A lower starting dose or dose reduction of labetalol may be necessary, or consider using an alternative antidepressant with less CYP2D6 inhibitory potential (e.g., sertraline, escitalopram).
Coadministration of labetalol and fluvoxamine may increase labetalol plasma concentrations, potentially leading to enhanced beta-blockade effects such as bradycardia and hypotension. Both drugs can independently cause bradycardia, leading to additive effects.
Mechanism
Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19. While labetalol is primarily metabolized by glucuronidation, it also undergoes some metabolism via CYP2D6, and to a lesser extent, CYP1A2 and CYP2C19. Inhibition of these CYP enzymes by fluvoxamine could reduce labetalol clearance.
Clinical Management
Monitor patients for signs and symptoms of increased beta-blockade, including bradycardia, hypotension, and dizziness. Consider using the lowest effective dose of labetalol or an alternative antidepressant with less CYP inhibition, such as sertraline or escitalopram, if close monitoring is not feasible. Dose adjustment of labetalol may be necessary.
The interaction between labetalol and sertraline is generally considered minimal. While both drugs can independently affect heart rate, sertraline has weak CYP2D6 inhibitory effects, leading to a low risk of clinically significant pharmacokinetic interaction with labetalol.
Mechanism
Sertraline is a weak inhibitor of CYP2D6, the enzyme primarily responsible for labetalol metabolism. Therefore, sertraline is unlikely to cause a significant increase in labetalol plasma concentrations. Additive pharmacodynamic effects on heart rate are theoretically possible but clinically rare given the weak nature of the interaction.
Clinical Management
Generally, no specific dose adjustment or enhanced monitoring is required for this combination. However, clinicians should remain vigilant for signs of excessive beta-blockade (e.g., bradycardia, hypotension) if patients are particularly sensitive or on high doses of labetalol, though this is uncommon.
Labetalol is primarily metabolized by CYP2D6, but it is not considered a potent substrate like metoprolol or propranolol. Fluoxetine is a potent CYP2D6 inhibitor, but the clinical significance of this interaction with labetalol is generally considered low.
Mechanism
Fluoxetine, a potent CYP2D6 inhibitor, can theoretically decrease the metabolism of labetalol, which is partially metabolized by CYP2D6. This could lead to increased labetalol plasma concentrations.
Clinical Management
Monitor for signs of increased beta-blockade, such as bradycardia or hypotension, especially when initiating or discontinuing fluoxetine in patients on labetalol. Dose adjustments of labetalol are usually not necessary, but clinical monitoring is prudent.
Labetalol is primarily metabolized by CYP2D6, while citalopram is a weak inhibitor of CYP2D6. This interaction is generally not considered clinically significant, but theoretically, it could lead to a slight increase in labetalol levels.
Mechanism
Citalopram is a weak inhibitor of CYP2D6, the primary enzyme responsible for labetalol metabolism. This could potentially reduce the clearance of labetalol, leading to increased plasma concentrations.
Clinical Management
Monitor patients for signs of increased beta-blocker effects, such as bradycardia or hypotension, especially when initiating or significantly increasing citalopram dose. No routine dose adjustment is typically required, but individual patient response should guide management.
The interaction between labetalol and escitalopram is generally considered to be of minor clinical significance. While both drugs can independently cause bradycardia, escitalopram is not a significant inhibitor of CYP2D6, the primary metabolic pathway for many beta-blockers, including labetalol.
Mechanism
Labetalol is metabolized primarily by CYP2D6. Escitalopram is a weak inhibitor of CYP2D6, meaning it is unlikely to significantly alter labetalol plasma concentrations. Both drugs can independently cause bradycardia, leading to a theoretical additive pharmacodynamic effect, though this is less common with escitalopram.
Clinical Management
Generally, no specific dose adjustments or enhanced monitoring are required for this combination. However, clinicians should remain aware of the potential for additive bradycardia, especially in patients with pre-existing cardiac conditions or those on other bradycardia-inducing medications. Monitor vital signs as clinically indicated, particularly heart rate.
For complete prescribing information:
View full LABETALOL monograph →Medical Disclaimer
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