SERTRALINE Drug Interactions
Also known as: Sertraline
Sertraline (brand name: Sertraline) is a medication known as a selective serotonin reuptake inhibitor (SSRI). It is used to treat various mental health conditions, including depression, obsessive-compulsive disorder, panic disorder, post-traumatic stress disorder, social anxiety disorder, and premenstrual dysphoric disorder. Sertraline works by helping to restore the balance of a natural substance in the brain called serotonin, which can improve mood and reduce anxiety.SERTRALINE has 13 documented drug interactions in our database, including 0 contraindicated, 0 major, 2 moderate, and 11 minor interactions.
0
Contraindicated
0
Major
2
Moderate
11
Minor
SSRIs can increase metoprolol plasma levels by inhibiting CYP2D6, potentially causing excessive beta-blockade.
Mechanism
Sertraline moderately inhibits CYP2D6, which is the primary metabolic pathway for metoprolol, increasing metoprolol AUC by 30–100%.
Clinical Management
Monitor for signs of excessive beta-blockade (bradycardia, fatigue, dizziness). Consider dose reduction of metoprolol.
Combining sertraline and fluoxetine, both selective serotonin reuptake inhibitors (SSRIs), significantly increases the risk of serotonin syndrome. Patients may experience symptoms such as agitation, confusion, sweating, tremor, and hyperreflexia, which can range from mild to life-threatening.
Mechanism
Both sertraline and fluoxetine increase synaptic serotonin concentrations by inhibiting serotonin reuptake in the central nervous system. When used concurrently, their additive serotonergic effects can lead to excessive stimulation of serotonin receptors.
Clinical Management
Concurrent use should generally be avoided due to the increased risk of serotonin syndrome. If co-administration is deemed necessary, close monitoring for signs and symptoms of serotonin syndrome is crucial, and lower doses of one or both agents may be considered. Patients should be educated on the symptoms of serotonin syndrome and advised to seek immediate medical attention if they occur.
Sertraline is a weak inhibitor of CYP2D6, the primary enzyme metabolizing carvedilol. While a theoretical increase in carvedilol plasma concentrations is possible, it is generally not considered clinically significant for most patients.
Mechanism
Carvedilol is primarily metabolized by CYP2D6. Sertraline is a weak inhibitor of CYP2D6, which could potentially reduce the metabolism of carvedilol and increase its systemic exposure.
Clinical Management
Routine co-administration of carvedilol and sertraline typically does not require specific dose adjustments or enhanced monitoring. However, clinicians should be aware of the potential for increased carvedilol effects (e.g., bradycardia, hypotension) in sensitive individuals, especially if sertraline dosage is high or if other CYP2D6 inhibitors are present.
Atenolol and sertraline are generally considered safe to co-administer with a low risk of significant interaction. While both drugs can independently cause bradycardia, atenolol's renal clearance and sertraline's minimal CYP2D6 inhibition suggest a low pharmacokinetic interaction potential.
Mechanism
Atenolol is primarily renally cleared, not significantly metabolized by CYP450 enzymes, thus avoiding pharmacokinetic interaction with sertraline, which has minimal CYP2D6 inhibition. A theoretical additive pharmacodynamic effect leading to bradycardia is possible but generally not clinically significant.
Clinical Management
Routine monitoring for vital signs, especially heart rate, is advisable, particularly when initiating or adjusting doses in sensitive patients. No specific dose adjustments are typically required for either medication due to this combination. If symptomatic bradycardia occurs, consider alternative agents or dose reduction.
The interaction between nadolol and sertraline is considered minor. While both drugs can independently cause bradycardia, sertraline has minimal CYP2D6 inhibition, and nadolol is primarily renally cleared, reducing the likelihood of a significant pharmacokinetic interaction.
Mechanism
Nadolol is primarily cleared renally, and its metabolism is not significantly affected by CYP2D6 inhibition. Sertraline is a weak inhibitor of CYP2D6, therefore, it is unlikely to significantly alter nadolol plasma levels. Both drugs can have bradycardic effects, leading to a theoretical additive pharmacodynamic effect.
Clinical Management
Generally, no specific dose adjustments are required when co-administering nadolol and sertraline. However, clinicians should monitor patients for signs of excessive bradycardia or hypotension, especially during initiation or dose changes of either medication. If such symptoms occur, consider reducing the dose of one or both drugs.
The interaction between pindolol and sertraline is generally considered minor. Sertraline has minimal CYP2D6 inhibitory effects, which is the primary metabolic pathway for some beta-blockers, but pindolol is not extensively metabolized by CYP2D6. Both drugs can independently cause bradycardia, but additive effects are unlikely to be clinically significant with typical doses.
Mechanism
Sertraline is a weak inhibitor of CYP2D6. While some beta-blockers are extensively metabolized by CYP2D6, pindolol is primarily metabolized by CYP2D9 and to a lesser extent CYP2D6, with significant renal excretion of unchanged drug. Therefore, sertraline's weak CYP2D6 inhibition is unlikely to significantly alter pindolol plasma concentrations.
Clinical Management
No specific dose adjustments are usually required for pindolol or sertraline when co-administered. Monitor patients for signs of excessive beta-blockade (e.g., bradycardia, hypotension), especially if they are sensitive to beta-blockers or have underlying cardiac conditions. If concerns arise, consider alternative SSRIs with even lower CYP2D6 inhibition potential.
The interaction between nebivolol and sertraline is generally considered to be of minor clinical significance. While both drugs can independently cause bradycardia, sertraline has minimal CYP2D6 inhibitory effects, thus unlikely to significantly alter nebivolol's plasma concentrations.
Mechanism
Nebivolol is metabolized by CYP2D6. Sertraline is a weak inhibitor of CYP2D6. Although both drugs can cause bradycardia, the pharmacokinetic interaction is minimal, and additive pharmacodynamic effects are generally not clinically significant.
Clinical Management
Routine monitoring for vital signs, including heart rate, is advisable, especially when initiating or adjusting either medication. No specific dose adjustments are typically required for either drug due to this interaction. Patients should be advised to report symptoms of excessive bradycardia or hypotension.
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.
Sertraline is a weak inhibitor of CYP2D6, the primary enzyme metabolizing metoprolol. While a theoretical increase in metoprolol levels is possible, it is generally not considered clinically significant.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Sertraline has minimal inhibitory effects on CYP2D6, leading to a small potential for reduced metoprolol metabolism and increased plasma concentrations.
Clinical Management
Generally, no specific dose adjustments are required when co-administering metoprolol and sertraline. Monitor patients for expected therapeutic effects of metoprolol and for signs of excessive beta-blockade (e.g., bradycardia, hypotension), especially if initiating sertraline or increasing its dose in a patient already on metoprolol.
The interaction between bisoprolol and sertraline is generally considered minor. While both drugs can independently cause bradycardia, sertraline has minimal impact on the metabolism of bisoprolol, which is primarily renally cleared.
Mechanism
Bisoprolol is primarily eliminated via renal excretion, with minimal involvement of CYP2D6. Sertraline is a weak inhibitor of CYP2D6, and therefore, it is not expected to significantly alter bisoprolol plasma concentrations.
Clinical Management
No specific dose adjustments are typically required for bisoprolol or sertraline when co-administered. However, clinicians should monitor patients for additive pharmacodynamic effects such as bradycardia, especially in sensitive individuals. Routine monitoring of heart rate and blood pressure is advisable.
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 timolol and sertraline is generally considered minor due to sertraline's minimal CYP2D6 inhibition. While both drugs can independently cause bradycardia, the risk of a significant pharmacokinetic interaction leading to increased timolol levels is low.
Mechanism
Timolol is metabolized by CYP2D6, but sertraline is a weak inhibitor of this enzyme. Therefore, significant inhibition of timolol metabolism by sertraline is unlikely, though additive pharmacodynamic effects on heart rate are theoretically possible.
Clinical Management
No specific dose adjustments are typically required. Monitor patients for signs of excessive beta-blockade, such as bradycardia or hypotension, especially if they are sensitive to beta-blockers or have underlying cardiac conditions. If such symptoms occur, consider reducing the timolol dose.
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.
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