Esidep Drug Interactions

Serotonergic Drugs: Based on the mechanism of action of SNRIs and SSRIs including escitalopram, and the potential for serotonin syndrome, caution is advised when escitalopram is co-administered with other drugs that may affect the serotonergic neurotransmitter systems, such as triptans, linezolid (an antibiotic which is a reversible non-selective MAOI), lithium, tramadol, or St. John's Wort (see Precautions). The concomitant use of escitalopram with other SSRIs, SNRIs or tryptophan is not recommended.
Triptans: There have been rare postmarketing reports of serotonin syndrome with use of an SSRI and a triptan. If concomitant treatment of escitalopram with a triptan is clinically warranted, careful observation of the patient is advised, particularly during treatment initiation and dose increases (see Precautions).
CNS Drugs: Given the primary CNS effects of escitalopram, caution should be used when it is taken in combination with other centrally acting drugs.
Alcohol: Although escitalopram did not potentiate the cognitive and motor effects of alcohol in a clinical trial, as with other psychotropic medications, the use of alcohol by patients taking escitalopram is not recommended.
Monoamine Oxidase Inhibitors (MAOIs): (see Contraindications and Precautions).
Drugs that Interfere with Hemostasis (NSAIDs, Aspirin, Warfarin, etc.): Serotonin release by platelets plays an important role in hemostasis. An association between use of psychotropic drugs that interfere with serotonin reuptake and the occurrence of upper gastrointestinal bleeding has also shown that concurrent use of an NSAID or aspirin may potentiate the risk of bleeding. Altered anticoagulant effects, including increased bleeding, have been reported when SSRIs and SNRIs are co-administered with warfarin. Patients receiving warfarin therapy should be carefully monitored when escitalopram is initiated or discontinued.
Cimetidine: An increase in citalopram AUC and Cmax of 43% and 39%, respectively, have been reported in patients who had received 21 days of 40 mg/day racemic citalopram and 400 mg/day cimetidine for 8 day. The clinical significance of these findings is unknown.
Digoxin: No significant affect on the pharmacokinetics of either citalopram or digoxin has been reported with combined administration of citalopram (40 mg/day for 21 day) and digoxin (single dose 1 mg).
Lithium: Co-administration of racemic citalopram (40 mg/day for 10 days) and lithium (30 mmol/day for 5 days) had no significant effect on the pharmacokinetics of citalopram or lithium. Nevertheless, plasma lithium levels should be monitored with appropriate adjustment to the lithium dose in accordance with standard clinical practice. Because lithium may enhance the serotonergic effects of escitalopram, caution should be exercised when escitalopram and lithium are co-administered.
Pimozide: Increased QTc intervals have been reported when pimozide and racemic citalopram have been concurrently administered. Effects on escitalopram have not been evaluated. Pharmacokinetics of racemic citalopram (AUC and peak plasma concentrations) was not affected by pimozide. Concomitant use of pimozide with escitalopram is contraindicated.
Sumatriptan: There have been rare postmarketing reports describing patients with weakness, hyperreflexia, and incoordination following the use of an SSRI and sumatriptan. If concomitant treatment with sumatriptan and an SSRI (e.g., fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, escitalopram) is clinically warranted, appropriate observation of the patient is advised.
Theophylline: Combined administration of racemic citalopram (40 mg/day for 21 days) and the CYP1A2 substrate theophylline (single dose of 300 mg) did not affect the pharmacokinetics of theophylline. The effect of theophylline on the pharmacokinetics of citalopram was not evaluated.
Warfarin: Administration of 40 mg/day racemic citalopram for 21 days did not affect the pharmacokinetics of warfarin, a CYP3A4 substrate. Prothrombin time was increased by 5%, the clinical significance of which is unknown.
Carbamazepine: Combined administration of racemic citalopram (40 mg/day for 14 days) and carbamazepine (titrated to 400 mg/day for 35 days) did not significantly affect the pharmacokinetics of carbamazepine, a CYP3A4 substrate. Although trough citalopram plasma levels were unaffected, given the enzyme-inducing properties of carbamazepine, the possibility that carbamazepine might increase the clearance of escitalopram should be considered if the two drugs are coadministered.
Triazolam: Combined administration of racemic citalopram (titrated to 40 mg/day for 28 days) and the CYP3A4 substrate triazolam (single dose of 0.25 mg) did not significantly affect the pharmacokinetics of either citalopram or triazolam.
Ketoconazole: Combined administration of racemic citalopram (40 mg) and ketoconazole (200 mg), a potent CYP3A4 inhibitor, decreased the C_max and AUC of ketoconazole by 21% and 10%, respectively, and did not significantly affect the pharmacokinetics of citalopram.
Ritonavir: Combined administration of a single dose of ritonavir (600 mg), both a CYP3A4 substrate and a potent inhibitor of CYP3A4, and escitalopram (20 mg) did not affect the pharmacokinetics of either ritonavir or escitalopram.
CYP3A4 and -2C19 Inhibitors: It has been reported that CYP3A4 and -2C19 are the primary enzymes involved in the metabolism of escitalopram. However, co-administration of escitalopram (20 mg) and ritonavir (600 mg), a potent inhibitor of CYP3A4, did not significantly affect the pharmacokinetics of escitalopram. Because escitalopram is metabolized by multiple enzyme systems, inhibition of a single enzyme may not appreciably decrease escitalopram clearance.
Drugs Metabolized by Cytochrome P4502D6: An inhibitory effect of escitalopram on CYP2D6 is not known. In addition, steady state levels of racemic citalopram were not significantly different in poor metabolizers and extensive CYP2D6 metabolizers after multiple-dose administration of citalopram, suggesting that co-administration, with escitalopram, of a drug that inhibits CYP2D6, is unlikely to have clinically significant effects on escitalopram metabolism. However, there are limited in vivo information suggesting a modest CYP2D6 inhibitory effect for escitalopram, i.e., co-administration of escitalopram (20 mg/day for 21 days) with the tricyclic antidepressant desipramine (single dose of 50 mg), a substrate for CYP2D6, resulted in a 40% increase in C_max and a 100% increase in AUC of desipramine. The clinical significance of this finding is unknown. Nevertheless, caution is indicated in the co-administration of escitalopram and drugs metabolized by CYP2D6.
Metoprolol: A 50% increase in C_max and 82% increase in AUC of the beta-adrenergic blocker metoprolol (single dose of 100 mg) has been reported after co-administration of 20 mg/day escitalopram for 21 days. Increased metoprolol plasma levels have been associated with decreased cardioselectivity. Co-administration of escitalopram and metoprolol had no clinically significant effects on blood pressure or heart rate.
Electroconvulsive Therapy (ECT): There are no clinical studies of the combined use of ECT and escitalopram.