PAROXETINE Drug Interactions
Also known as: Paroxetine
Paroxetine is a prescription medication used to help women manage moderate to severe hot flashes and night sweats (vasomotor symptoms) associated with menopause. While it belongs to a class of drugs that can affect brain chemicals, this specific formulation works differently and is not used to treat mental health conditions.PAROXETINE has 14 documented drug interactions in our database, including 0 contraindicated, 9 major, 2 moderate, and 3 minor interactions.
0
Contraindicated
9
Major
2
Moderate
3
Minor
Concurrent use of carvedilol and paroxetine can lead to significantly increased plasma concentrations of carvedilol. This elevation in carvedilol levels can result in enhanced beta-blocking effects, potentially causing severe bradycardia, hypotension, or heart block.
Mechanism
Paroxetine is a potent inhibitor of the cytochrome P450 2D6 (CYP2D6) enzyme. Carvedilol is primarily metabolized by CYP2D6, so paroxetine inhibits its metabolism, leading to reduced clearance and increased systemic exposure of carvedilol.
Clinical Management
Avoid co-administration if possible. If concomitant use is unavoidable, a significant reduction in carvedilol dosage (e.g., by 50% or more) should be considered, and the patient must be closely monitored for signs of bradycardia, hypotension, and heart block, especially during initiation or dose changes of paroxetine. Consider using an alternative antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram) or an alternative beta-blocker not primarily metabolized by CYP2D6 (e.g., atenolol).
The co-administration of paroxetine, a potent CYP2D6 inhibitor, with pindolol, a beta-blocker primarily metabolized by CYP2D6, can significantly increase pindolol plasma concentrations. This elevated exposure to pindolol may lead to enhanced beta-blockade effects, including severe bradycardia, hypotension, and heart block, particularly in susceptible patients.
Mechanism
Paroxetine potently inhibits the cytochrome P450 2D6 (CYP2D6) enzyme. Pindolol is primarily metabolized by CYP2D6, therefore, paroxetine reduces the metabolism and clearance of pindolol, leading to increased systemic exposure and pharmacodynamic effects.
Clinical Management
This combination should generally be avoided. If co-administration is unavoidable, a significant reduction in pindolol dosage (e.g., by 50% or more) is recommended, along with close and frequent monitoring of heart rate, blood pressure, and ECG for signs of excessive beta-blockade. Consider using an alternative beta-blocker that is not primarily metabolized by CYP2D6 (e.g., atenolol, nadolol, bisoprolol) or an antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram).
The co-administration of nebivolol and paroxetine can lead to significantly increased plasma concentrations of nebivolol. This can result in enhanced beta-blockade effects, including severe bradycardia, hypotension, and potential heart block, requiring close monitoring.
Mechanism
Paroxetine is a potent inhibitor of the cytochrome P450 2D6 (CYP2D6) enzyme. Nebivolol is primarily metabolized by CYP2D6, so paroxetine inhibits its metabolism, leading to reduced clearance and elevated systemic exposure.
Clinical Management
Avoid concurrent use if possible. If co-administration is necessary, a significant reduction in the nebivolol dose should be considered, along with frequent and close monitoring for signs of bradycardia, hypotension, and other symptoms of excessive beta-blockade. Consider alternative beta-blockers not metabolized by CYP2D6 (e.g., atenolol, bisoprolol, nadolol) or antidepressants with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram).
The coadministration of metoprolol and paroxetine can lead to a significant increase in metoprolol plasma concentrations. This interaction can result in enhanced beta-blockade effects, potentially causing severe bradycardia, hypotension, or heart block, which may be life-threatening.
Mechanism
Paroxetine is a potent inhibitor of the cytochrome P450 2D6 (CYP2D6) enzyme. Metoprolol is primarily metabolized by CYP2D6, so paroxetine inhibits its metabolism, leading to reduced clearance and increased systemic exposure of metoprolol.
Clinical Management
Avoid concurrent use if possible. If coadministration is necessary, closely monitor the patient for signs of bradycardia, hypotension, and heart block. A significant reduction in the metoprolol dose may be required, or consider switching to a beta-blocker not primarily metabolized by CYP2D6 (e.g., atenolol, bisoprolol, nadolol) or an antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram).
The co-administration of paroxetine with metoprolol can significantly increase metoprolol plasma concentrations, leading to enhanced beta-blockade effects. This interaction can result in severe bradycardia, hypotension, and heart block, posing a significant risk to the patient.
Mechanism
Paroxetine is a potent inhibitor of cytochrome P450 2D6 (CYP2D6), the primary enzyme responsible for the metabolism of metoprolol. Inhibition of CYP2D6 by paroxetine reduces metoprolol clearance, thereby increasing its systemic exposure and pharmacodynamic effects.
Clinical Management
Avoid concurrent use of paroxetine with metoprolol if possible. If co-administration is necessary, consider using an alternative beta-blocker that is not significantly metabolized by CYP2D6 (e.g., atenolol, bisoprolol) or an antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram). If the combination is unavoidable, initiate metoprolol at a much lower dose with careful titration, or significantly reduce the current metoprolol dose, and closely monitor the patient for signs of bradycardia, hypotension, and other symptoms of excessive beta-blockade.
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).
Paroxetine, a potent CYP2D6 inhibitor, can significantly increase systemic exposure to timolol, a beta-blocker primarily metabolized by CYP2D6. This interaction can lead to enhanced beta-blockade, manifesting as severe bradycardia, hypotension, and potentially heart block.
Mechanism
Paroxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is a primary metabolic pathway for timolol. This pharmacokinetic inhibition reduces timolol's clearance, leading to elevated plasma concentrations and prolonged pharmacological effects.
Clinical Management
Concomitant use should be approached with caution. If co-administration is necessary, consider using an alternative antidepressant with minimal CYP2D6 inhibitory effects (e.g., sertraline, escitalopram) or an alternative beta-blocker not significantly metabolized by CYP2D6 (e.g., atenolol, bisoprolol). If the combination is unavoidable, monitor the patient closely for signs of excessive beta-blockade such as bradycardia, hypotension, and dizziness, and be prepared to reduce the timolol dose.
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.
Combining escitalopram and paroxetine, both selective serotonin reuptake inhibitors (SSRIs), significantly increases the risk of serotonin syndrome and other serotonergic side effects such as nausea, dizziness, anxiety, and insomnia. This combination should generally be avoided due to the heightened risk of adverse effects without clear evidence of increased efficacy.
Mechanism
Both escitalopram and paroxetine inhibit the reuptake of serotonin into presynaptic neurons, leading to increased serotonin concentrations in the central nervous system. When used concurrently, their additive serotonergic effects can result in excessive serotonin activity.
Clinical Management
This combination is generally not recommended. If co-administration is deemed absolutely necessary, patients should be closely monitored for signs and symptoms of serotonin syndrome (e.g., agitation, confusion, diaphoresis, tremor, hyperreflexia). Consider alternative monotherapy or switching to a different antidepressant class if an SSRI is not sufficient.
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).
Combining fluoxetine and paroxetine, both selective serotonin reuptake inhibitors (SSRIs), can lead to an increased risk of serotonin syndrome and additive serotonergic side effects. Patients may experience symptoms such as agitation, confusion, sweating, tremor, and diarrhea.
Mechanism
Both fluoxetine and paroxetine increase serotonin levels in the central nervous system by inhibiting its reuptake. Concurrent use leads to an additive effect on serotonin concentrations, potentially causing excessive serotonergic activity.
Clinical Management
Coadministration of fluoxetine and paroxetine is generally not recommended due to the increased risk of serotonin syndrome and other adverse effects. If combination therapy is deemed necessary, close monitoring for signs and symptoms of serotonin syndrome is crucial, and dose adjustments of one or both agents may be required. Consider alternative antidepressant strategies if possible.
The interaction between atenolol and paroxetine is generally considered minor. While paroxetine is a potent CYP2D6 inhibitor, atenolol is primarily renally cleared and not significantly metabolized by CYP2D6, minimizing pharmacokinetic interaction risk. However, both drugs can independently cause bradycardia, so additive pharmacodynamic effects are theoretically possible, though less common with atenolol.
Mechanism
Paroxetine is a potent inhibitor of CYP2D6. However, atenolol is predominantly eliminated by renal excretion of unchanged drug, with minimal hepatic metabolism by CYP2D6. Therefore, paroxetine's CYP2D6 inhibition is unlikely to significantly alter atenolol plasma levels. Both drugs can independently cause bradycardia, suggesting a potential, albeit low, pharmacodynamic additive effect.
Clinical Management
Routine monitoring for signs of excessive beta-blockade (e.g., bradycardia, hypotension) is prudent, especially during initiation or dose changes of either medication, though significant interactions are rare. No specific dose adjustments are typically required for atenolol when co-administered with paroxetine. If excessive bradycardia or hypotension occurs, consider alternative beta-blockers that are also renally cleared or SSRIs with less CYP2D6 inhibition.
The interaction between nadolol and paroxetine is considered minor. Nadolol is primarily renally cleared, and its metabolism is minimally affected by CYP2D6 inhibition, which is the primary mechanism by which paroxetine interacts with other beta-blockers. While both drugs can independently cause bradycardia, an additive effect is unlikely to be clinically significant with nadolol.
Mechanism
Nadolol is predominantly eliminated by renal excretion with minimal hepatic metabolism, thus it is not significantly affected by paroxetine's potent CYP2D6 inhibitory activity. Although both drugs can independently cause bradycardia, a significant pharmacodynamic interaction leading to enhanced bradycardia is not expected given nadolol's clearance pathway.
Clinical Management
No specific dose adjustments are typically required for nadolol when co-administered with paroxetine. Standard monitoring for the individual effects of each drug, such as heart rate and blood pressure, is recommended. If bradycardia or hypotension occurs, consider other contributing factors or individual patient sensitivities rather than this specific interaction.
The interaction between bisoprolol and paroxetine is generally considered minor. While paroxetine is a potent CYP2D6 inhibitor, bisoprolol is primarily renally cleared and minimally metabolized by CYP2D6, reducing the likelihood of a significant pharmacokinetic interaction. However, both drugs can independently cause bradycardia, so additive effects on heart rate are theoretically possible.
Mechanism
Paroxetine is a potent inhibitor of CYP2D6. However, bisoprolol is predominantly eliminated by renal excretion with minimal hepatic metabolism, and CYP2D6 plays a negligible role in its clearance. Therefore, paroxetine's CYP2D6 inhibition is unlikely to significantly alter bisoprolol plasma levels. Both drugs can have bradycardic effects.
Clinical Management
Close monitoring for excessive bradycardia or hypotension is generally not required unless the patient has pre-existing cardiac conditions that predispose them to these effects. No routine dose adjustment for either medication is typically necessary. If symptoms of bradycardia occur, evaluate for other causes or consider dose adjustment if deemed clinically appropriate.
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