CITALOPRAM Drug Interactions
Also known as: Citalopram
Citalopram is a medication called a selective serotonin reuptake inhibitor (SSRI) used to treat major depressive disorder in adults. It works by helping to restore the balance of a natural substance called serotonin in the brain, which can improve mood and feelings of well-being.CITALOPRAM has 13 documented drug interactions in our database, including 1 contraindicated, 0 major, 7 moderate, and 5 minor interactions.
1
Contraindicated
0
Major
7
Moderate
5
Minor
Combining escitalopram and citalopram is pharmacologically redundant and doubles the QT-prolongation risk.
Mechanism
Both drugs are the same pharmacological entity (escitalopram is the active S-enantiomer of citalopram). Concurrent use doubles the dose and QTc-prolonging effect.
Clinical Management
Contraindicated. Never prescribe together.
Citalopram is a moderate inhibitor of CYP2D6, which is the primary enzyme responsible for the metabolism of carvedilol. This interaction can lead to increased plasma concentrations of carvedilol, potentially enhancing its beta-blocking effects and increasing the risk of bradycardia, hypotension, or heart block.
Mechanism
Citalopram inhibits the cytochrome P450 2D6 (CYP2D6) enzyme. Carvedilol is extensively metabolized by CYP2D6, so inhibition of this enzyme by citalopram reduces carvedilol clearance, leading to elevated systemic exposure.
Clinical Management
Monitor patients closely for signs and symptoms of increased beta-blockade, such as bradycardia, hypotension, dizziness, or fatigue, when citalopram is initiated or its dose is changed. A carvedilol dose reduction may be necessary, or consider using an alternative antidepressant with minimal CYP2D6 inhibitory activity, such as escitalopram or sertraline.
The combination of pindolol and citalopram may lead to an increased risk of bradycardia and hypotension due to additive pharmacodynamic effects. While citalopram is not a strong CYP2D6 inhibitor, pindolol is metabolized by CYP2D6, so a pharmacokinetic interaction is possible, though less pronounced than with other SSRIs.
Mechanism
Both pindolol (a beta-blocker) and citalopram (an SSRI) can independently cause bradycardia, leading to an additive pharmacodynamic effect. Additionally, pindolol is metabolized by CYP2D6, and citalopram is a weak inhibitor of CYP2D6, which could potentially increase pindolol plasma concentrations.
Clinical Management
Monitor patients closely for signs and symptoms of bradycardia, hypotension, and other beta-blocker-related adverse effects, especially when initiating or adjusting doses of either medication. Consider using the lowest effective doses of both drugs. If adverse effects occur, dose reduction or switching to an alternative antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram) or a beta-blocker primarily cleared renally (e.g., atenolol, nadolol) may be necessary.
Citalopram is a weak inhibitor of CYP2D6, which is the primary enzyme responsible for nebivolol's metabolism. This interaction can lead to increased plasma concentrations of nebivolol, potentially enhancing its beta-blocking effects such as bradycardia, hypotension, and heart block.
Mechanism
Citalopram weakly inhibits cytochrome P450 2D6 (CYP2D6). Nebivolol is primarily metabolized by CYP2D6, so inhibition of this enzyme can reduce nebivolol clearance, increasing its systemic exposure.
Clinical Management
Monitor patients for signs and symptoms of increased beta-blockade, including bradycardia, hypotension, and dizziness, especially when initiating or adjusting citalopram or nebivolol. Consider using the lowest effective dose of nebivolol or selecting an alternative antidepressant with minimal CYP2D6 inhibition if close monitoring is not feasible.
Citalopram is a weak inhibitor of CYP2D6, which is the primary enzyme metabolizing metoprolol. This interaction can lead to increased plasma concentrations of metoprolol, potentially enhancing its beta-blocking effects and increasing the risk of bradycardia and hypotension.
Mechanism
Citalopram weakly inhibits cytochrome P450 2D6 (CYP2D6). Metoprolol is extensively metabolized by CYP2D6, so citalopram can decrease metoprolol's metabolic clearance, leading to elevated systemic exposure.
Clinical Management
Monitor patients for signs and symptoms of excessive beta-blockade, such as bradycardia, hypotension, and dizziness, especially when initiating or adjusting citalopram dose. A metoprolol dose reduction may be necessary if adverse effects occur. Consider using an alternative antidepressant with negligible CYP2D6 inhibition if close monitoring is not feasible.
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.
Citalopram can inhibit the metabolism of timolol, potentially increasing timolol plasma concentrations and enhancing its beta-blocking effects. This can lead to an increased risk of bradycardia, hypotension, and other systemic beta-blocker adverse effects, especially given timolol's systemic absorption even from ophthalmic administration.
Mechanism
Citalopram is a moderate inhibitor of CYP2D6, which is involved in the metabolism of timolol. Inhibition of timolol's metabolism by citalopram can lead to elevated plasma levels of timolol. Additionally, both drugs can independently cause bradycardia, leading to an additive pharmacodynamic effect.
Clinical Management
Monitor patients closely for signs and symptoms of excessive beta-blockade, such as bradycardia, hypotension, and fatigue. Consider using a beta-blocker less dependent on CYP2D6 metabolism (e.g., atenolol, bisoprolol) or an antidepressant with less CYP2D6 inhibition (e.g., sertraline, escitalopram) if an interaction is suspected or clinical concerns arise. Dose reduction of timolol may be necessary.
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).
Atenolol and citalopram are unlikely to have a significant pharmacokinetic interaction because atenolol is primarily renally cleared and citalopram has minimal CYP2D6 inhibition. However, both drugs can independently cause bradycardia, so an additive pharmacodynamic effect resulting in mild bradycardia is theoretically possible.
Mechanism
Atenolol is predominantly eliminated renally, bypassing hepatic cytochrome P450 metabolism. Citalopram is a weak inhibitor of CYP2D6, but this is largely irrelevant for atenolol's disposition. Both agents can cause a reduction in heart rate, leading to a potential additive pharmacodynamic effect.
Clinical Management
Generally, no specific dose adjustments are required for this combination. Monitor patients for signs of excessive bradycardia, especially if they have pre-existing cardiac conditions or are on other bradycardia-inducing medications. If bradycardia occurs, consider dose reduction of either agent or alternative therapies.
A clinically significant pharmacokinetic interaction between nadolol and citalopram is unlikely due to nadolol's primary renal clearance and citalopram's minimal inhibition of relevant CYP enzymes. However, both drugs can independently affect heart rate, and an additive pharmacodynamic effect resulting in bradycardia is theoretically possible, though rarely clinically significant.
Mechanism
Nadolol is primarily eliminated renally, with minimal involvement of CYP450 enzymes. Citalopram is a weak inhibitor of CYP2D6 and other CYP enzymes, which are not primary metabolic pathways for nadolol. Therefore, a pharmacokinetic interaction is not expected. A minor pharmacodynamic interaction is possible due to the additive potential for bradycardia.
Clinical Management
Generally, no specific dose adjustments or enhanced monitoring are required for this combination. Monitor patients for signs of excessive bradycardia or hypotension, especially if they have pre-existing cardiac conditions or are on other bradycardia-inducing medications. If severe bradycardia occurs, consider dose reduction of one or both agents.
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.
Citalopram is not a significant inhibitor of CYP2D6, the primary enzyme metabolizing metoprolol. Therefore, a clinically significant pharmacokinetic interaction leading to increased metoprolol levels is unlikely. However, both drugs can independently cause bradycardia, so additive pharmacodynamic effects are theoretically possible, though rarely clinically significant.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Citalopram is a weak or negligible inhibitor of CYP2D6, minimizing pharmacokinetic interaction. Both metoprolol (beta-blocker) and citalopram (SSRI) can cause bradycardia, suggesting a potential additive pharmacodynamic effect.
Clinical Management
Generally, no specific dose adjustment or enhanced monitoring is required for this combination due to the low interaction potential. However, clinicians should remain vigilant for signs of excessive bradycardia, especially in patients with pre-existing cardiac conditions or those on higher doses of metoprolol. If bradycardia occurs, consider assessing contributing factors.
Bisoprolol and citalopram are generally considered safe to use together. While both drugs can independently affect heart rate, the risk of a significant interaction leading to severe bradycardia or other adverse cardiac events is low, especially given bisoprolol's renal clearance.
Mechanism
Citalopram is a weak inhibitor of CYP2D6, but bisoprolol is primarily eliminated renally with minimal CYP2D6 involvement, thus pharmacokinetic interaction is unlikely. A theoretical additive pharmacodynamic effect on heart rate is possible, but not clinically significant for this combination.
Clinical Management
No specific dose adjustments are typically required for this combination. Monitor patients for expected therapeutic effects and any signs of excessive bradycardia or hypotension, especially at treatment initiation or dose changes, as with any beta-blocker therapy.
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