Lexapro withdrawal. Lexapro withdrawal side effects, Lexapro withdrawal solutions.

Below is a list of Lexapro withdrawal side effects. These Lexapro side effects can occur while taking the Lexapro before withdrawal or may become apparent once Lexapro withdrawal begins. It is imperative you use a Lexapro withdrawal plan designed to eliminate or reduce Lexapro withdrawal side effects. Once Lexapro withdrawal side effects begin, they are more difficult to get rid of.

8. Lexapro withdrawal - Bundle Branch Block Right – These are specialized cells in the upper right heart chamber and are the heart’s pacemaker. They send electrical signals to the heart that keeps it beating or contracting regularly. Normally the signal goes to the lower heart chambers at the same time through the bundle of His (hiss) on both the left and right sides of the heart, so the lower chambers contract at the same time. When the bundle is damaged on the right side, the signal does not fire at the same time as the left, which changes the pace of blood flow. This can lead to a person fainting.

Triglycerides are three fatty acids bound together in one molecule stored by the body and available to create high levels of energy when used.

To read more about Lexapro from the FDA, click here and type Lexapro in search box.

Study Of Drug Therapy For Compulsive Buying Yields A Puzzle

Science Daily — Researchers at the Stanford University School of Medicine say they are puzzled by findings from their new study indicating that an antidepressant, which previously showed promise in treating a behavioral disorder known as compulsive buying, did not result in a sustained benefit for the patients who took it.

The medication is escitalopram, a commonly prescribed antidepressant sold under the brand name Lexapro. In the study, researchers found no difference in the relapse rate of people with compulsive-buying disorder when they continued to take escitalopram compared with those who had been switched to a placebo. Those results are perplexing to lead author Lorrin Koran, MD, professor of psychiatry and behavioral sciences emeritus, because he had done a similar study in 2003 that found compulsive-buying patients improved stably after taking another antidepressant medication, citalopram, in which escitalopram is the active ingredient.

"It was a shock that, when we did the trial again with the active ingredient, it didn't work exactly the same way. It should have," said Koran, who also led the 2003 study. The results of the latest double-blind, placebo-controlled trial will be published in the April issue of the Journal of Clinical Psychopharmacology.

Koran said the unexpected result from the new study may in part be due to the small number of participants in the double-blind phase of the trial, which involved just 17 subjects whose buying behavior had markedly improved in the initial stage of the trial when they were all taking escitalopram. Of the nine randomly assigned to take a placebo in the later part of the trial, six relapsed, while five of eight continuing on escitalopram relapsed.

But the study size is likely not the only factor influencing the outcome of the trial.

"I don't think we're dealing with one pure biological disorder," said Koran. "We're dealing with a behavior that has different biological roots in different people and therefore we may have had very different groups of people in the two studies."

In the 2003 study, 24 patients were all initially given citalopram for the open-label portion of the study, during which they all knew they were taking citalopram. Fifteen of those patients reported marked improvements in their buying behaviors. For the second portion of that trial, these 15 patients were randomly assigned to take either citalopram or a placebo without knowing which one they were taking. Of seven patients who continued taking the medication, all seven maintained their improvement, while five of the eight patients receiving a placebo relapsed.

People suffering from compulsive buying disorder are preoccupied with shopping for unneeded items and are frequently unable to resist purchasing them. The problem is not a simple lack of willpower, said Koran, who described it as being as real a disorder as other impulsive behaviors such as alcoholism and pathological gambling. Sufferers of the disorder commonly wind up with closets or rooms filled with unwanted purchases, amassing thousands of dollars of debt in the process and often damaging their relationships by lying to loved ones about their purchases.

A recent nationwide, random-sample telephone survey conducted by Koran and his colleagues indicated that compulsive buying appeared to affect nearly 6 percent of the U.S. population, with nearly equal proportions of men and women affected.

Koran said a larger double-blind, placebo-controlled clinical trial is needed to reach a conclusive result regarding the effectiveness of escitalopram in treating patients with compulsive buying disorder.

He suggested future clinical trials might be able to yield more information if they were combined with imaging studies of the patients' brains. He cited recent work by Brian Knutson, PhD, assistant professor of psychology and neuroscience, whose recent imaging studies suggest that scientists might be able to directly visualize brain activity related to compulsive purchases.

"We would look for a difference in the brain activation patterns of those who respond to the drug vs. those who don't," said Koran.

The inconclusive nature of the results from the latest trial of escitalopram should not discourage anyone suffering from compulsive buying from seeking treatment, since several types of treatment seem to be helpful, Koran emphasized.

Other co-authors include Hugh Brent Solvason, MD, PhD, assistant professor of psychiatry and behavioral sciences; Nona Gamel, clinical research manager; and Emily Smith, clinical research coordinator.

Note: This story has been adapted from a news release issued by Stanford University Medical Center.

Following a single oral dose (20 mg tablet or solution) of Lexapro, peak blood levels occur at about 5 hours. Absorption of Lexapro
is not affected by food.

The absolute bioavailability of citalopram is about 80% relative to an intravenous dose, and the volume of distribution of citalopram is about 12 L/kg. Data specific on Lexapro are unavailable.

The binding of Lexapro to human plasma proteins is approximately 56%.

Metabolism and Elimination

Following oral administrations of Lexapro, the fraction of drug recovered in the urine as Lexapro and S - demethylcitalopram (S-DCT) is about 8% and 10%, respectively. The oral clearance of Lexapro is 600 mL/min, with approximately 7% of that due to renal clearance.

Lexapro is metabolized to S-DCT and S-didemethylcitalopram (S-DDCT). In humans, unchanged Lexapro is the predominant compound in plasma. At steady state, the concentration of the Lexapro metabolite S-DCT in plasma is approximately one-third that of Lexapro. The level of S-DDCT was not detectable in most subjects. In vitro studies show that Lexapro
is at least 7 and 27 times more potent than S - DCT and S-DDCT, respectively, in the inhibition of serotonin reuptake, suggesting that the metabolites of Lexapro do not contribute significantly to the antidepressant actions of Lexapro. S-DCT and S-DDCT also have no or very low affinity for serotonergic _(5-HT1-7)or other receptors including alpha- and beta-adrenergic, dopamine _(D1-5),^histamine_(H1-3),^muscarinic_(M1-5),and benzodiazepine receptors. S-DCT and S-DDCT also do not bind to various ion channels including Na⁺, K+, Cl^-, and Ca⁺⁺ channels.

In vitro studies using human liver microsomes indicated that CYP3A4 and CYP2C19 are the primary isozymes involved in the N-demethylation of Lexapro.

Population Subgroups

Age - Lexapro pharmacokinetics in subjects t 65 years of age were compared to younger subjects in a single-dose and a multiple-dose study. Lexapro AUC and half-life were increased by approximately 50% in elderly subjects, and _Cmaxwas unchanged. 10 mg is the recommended dose for elderly patients (see DOSAGE AND ADMINISTRATION).

Gender - In a multiple-dose study of Lexapro (10 mg/day for 3 weeks) in 18 male (9 elderly and 9 young) and 18 female (9 elderly and 9 young) subjects, there were no differences in AUC, _Cmax,and half-life between the male and female subjects. No adjustment of dosage on the basis of gender is needed.

Reduced hepatic function - Citalopram oral clearance was reduced by 37% and half-life was doubled in patients with reduced hepatic function compared to normal subjects. 10 mg is the recommended dose of Lexapro for most hepatically impaired patients (see DOSAGE AND ADMINISTRATION).

Reduced renal function - In patients with mild to moderate renal function impairment, oral clearance of citalopram was reduced by 17% compared to normal subjects. No adjustment of dosage for such patients is recommended. No information is available about the pharmacokinetics of Lexapro in patients with severely reduced renal function (creatinine clearance < 20 mL/min).

Drug-Drug Interactions

In vitro enzyme inhibition data did not reveal an inhibitory effect of Lexapro on CYP3A4, -1A2, -2C9, -2C19, and -2E1. Based on in vitro data, Lexapro would be expected to have little inhibitory effect on in vivo metabolism mediated by these cytochromes. While in vivo data to address this question are limited, results from drug interaction studies suggest that Lexapro, at a dose of 20 mg, has no 3A4 inhibitory effect and a modest 2D6 inhibitory effect. See Drug Interactions under PRECAUTIONS for more detailed information on available drug interaction data.

Clinical Efficacy Trials

Major Depressive Disorder

The efficacy of LEXAPRO as a treatment for major depressive disorder was established in three, 8-week, placebo-controlled studies conducted in outpatients between 18 and 65 years of age who met DSM-IV criteria for major depressive disorder. The primary outcome in all three studies was change from baseline to endpoint in the Montgomery Asberg Depression Rating Scale (MADRS).

A fixed-dose study compared 10 mg/day LEXAPRO and 20 mg/day LEXAPRO to placebo and 40 mg/day citalopram. The 10 mg/day and 20 mg/day LEXAPRO treatment groups showed significantly greater mean improvement compared to placebo on the MADRS. The 10 mg and 20 mg LEXAPRO groups were similar on this outcome measure.

In a second fixed-dose study of 10 mg/day LEXAPRO and placebo, the 10 mg/day LEXAPRO treatment group showed significantly greater mean improvement compared to placebo on the MADRS.

In a flexible-dose study, comparing LEXAPRO, titrated between 10 and 20 mg/day, to placebo and citalopram, titrated between 20 and 40 mg/day, the LEXAPRO treatment group showed significantly greater mean improvement compared to placebo on the MADRS.

Analyses of the relationship between treatment outcome and age, gender, and race did not suggest any differential responsiveness on the basis of these patient characteristics.

In a longer-term trial, 274 patients meeting (DSM-IV) criteria for major depressive disorder, who had responded during an initial 8-week, open-label treatment phase with LEXAPRO 10 or 20 mg/day, were randomized to continuation of LEXAPRO at their same dose, or to placebo, for up to 36 weeks of observation for relapse. Response during the open-label phase was defined by having a decrease of the MADRS total score to d 12. Relapse during the double-blind phase was defined as an increase of the MADRS total score to t 22, or discontinuation due to insufficient clinical response. Patients receiving continued LEXAPRO experienced a significantly longer time to relapse over the subsequent 36 weeks compared to those receiving placebo.

Generalized Anxiety Disorder

The efficacy of LEXAPRO in the treatment of Generalized Anxiety Disorder (GAD) was demonstrated in three, 8-week, multicenter, flexible-dose, placebo-controlled studies that compared LEXAPRO 10-20 mg/day to placebo in outpatients between 18 and 80 years of age who met DSM-IV criteria for GAD. In all three studies, LEXAPRO showed significantly greater mean improvement compared to placebo on the Hamilton Anxiety Scale (HAM-A).

There were too few patients in differing ethnic and age groups to adequately assess whether or not LEXAPRO has differential effects in these groups. There was no difference in response to LEXAPRO between men and women.

INDICATIONS AND USAGE

Major Depressive Disorder

LEXAPRO is indicated for the treatment of major depressive disorder.

The efficacy of LEXAPRO in the treatment of major depressive disorder was established in three, 8-week, placebo-controlled trials of outpatients whose diagnoses corresponded most closely to the DSM-IV category of major depressive disorder (see CLINICAL PHARMACOLOGY).

A major depressive episode (DSM-IV) implies a prominent and relatively persistent (nearly every day for at least 2 weeks) depressed or dysphoric mood that usually interferes with daily functioning, and includes at least five of the following nine symptoms: depressed mood, loss of interest in usual activities, significant change in weight and/or appetite, insomnia or hypersomnia, psychomotor agitation or retardation, increased fatigue, feelings of guilt or worthlessness, slowed thinking or impaired concentration, a suicide attempt or suicidal ideation.

The efficacy of LEXAPRO in hospitalized patients with major depressive disorders has not been adequately studied.

The efficacy of LEXAPRO in maintaining a response, in patients with major depressive disorder who responded during an 8-week, acute-treatment phase while taking LEXAPRO and were then observed for relapse during a period of up to 36 weeks, was demonstrated in a placebo-controlled trial (see Clinical Efficacy Trials under CLINICAL PHARMACOLOGY). Nevertheless, the physician who elects to use LEXAPRO for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient (see DOSAGE AND ADMINISTRATION).

Generalized Anxiety Disorder

LEXAPRO is indicated for the treatment of Generalized Anxiety Disorder (GAD).

The efficacy of LEXAPRO was established in three, 8-week, placebo-controlled trials in patients with GAD (see CLINICAL PHARMACOLOGY).

Generalized Anxiety Disorder (DSM-IV) is characterized by excessive anxiety and worry (apprehensive expectation) that is persistent for at least 6 months and which the person finds difficult to control. It must be associated with at least 3 of the following symptoms: restlessness or feeling keyed up or on edge, being easily fatigued, difficulty concentrating or mind going blank, irritability, muscle tension, and sleep disturbance.

The efficacy of LEXAPRO in the long-term treatment of GAD, that is, for more than 8 weeks, has not been systematically evaluated in controlled trials. The physician who elects to use LEXAPRO for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient.

CONTRAINDICATIONS

Concomitant use in patients taking monoamine oxidase inhibitors (MAOIs) is contraindicated (see WARNINGS).

LEXAPRO is contraindicated in patients with a hypersensitivity to Lexapro
or citalopram or any of the inactive ingredients in LEXAPRO. WARNINGS

Potential for Interaction with Monoamine Oxidase Inhibitors

In patients receiving serotonin reuptake inhibitor drugs in combination with a monoamine oxidase inhibitor (MAOI), there have been reports of serious, sometimes fatal, reactions including hyperthermia, rigidity, myoclonus, autonomic instability with possible rapid fluctuations of vital signs, and mental status changes that include extreme agitation progressing to delirium and coma. These reactions have also been reported in patients who have recently discontinued SSRI treatment and have been started on an MAOI. Some cases presented with features resembling neuroleptic malignant syndrome. Furthermore, limited animal data on the effects of combined use of SSRIs and MAOIs suggest that these drugs may act synergistically to elevate blood pressure and evoke behavioral excitation. Therefore, it is recommended that LEXAPRO should not be used in combination with an MAOI, or within 14 days of discontinuing treatment with an MAOI. Similarly, at least 14 days should be allowed after stopping LEXAPRO before starting an MAOI.

Serotonin syndrome has been reported in two patients who were concomitantly receiving linezolid, an antibiotic which is a reversible non-selective MAOI.

Clinical Worsening and Suicide Risk

Patients with major depressive disorder, both adult and pediatric, may experience worsening of their depression and/or the emergence of suicidal ideation and behavior (suicidality), whether or not they are taking antidepressant medications, and this risk may persist until significant remission occurs. Although there has been a long-standing concern that antidepressants may have a role in inducing worsening of depression and the emergence of suicidality in certain patients, a causal role for antidepressants in inducing such behaviors has not been established. Nevertheless, patients being treated with antidepressants should be observed closely for clinical worsening and suicidality, especially at the beginning of a course of drug therapy, or at the time of dose changes, either increases or decreases. Consideration should be given to changing the therapeutic regimen, including possibly discontinuing the medication, in patients whose depression is persistently worse or whose emergent suicidality is severe, abrupt in onset, or was not part of the patient’s presenting symptoms.

Because of the possibility of co-morbidity between major depressive disorder and other psychiatric and nonpsychiatric disorders, the same precautions observed when treating patients with major depressive disorder should be observed when treating patients with other psychiatric and nonpsychiatric disorders.

The following symptoms, anxiety, agitation, panic attacks, insomnia, irritability, hostility (aggressiveness), impulsivity, akathisia (psychomotor restlessness), hypomania, and mania, have been reported in adult and pediatric patients being treated with antidepressants for major depressive disorder as well as for other indications, both psychiatric and nonpsychiatric. Although a causal link between the emergence of such symptoms and either the worsening of depression and/or the emergence of suicidal impulses has not been established, consideration should be given to changing the therapeutic regimen, including possibly discontinuing the medication, in patients for whom such symptoms are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

Families and caregivers of patients being treated with antidepressants for major depressive disorder or other indications, both psychiatric and nonpsychiatric, should be alerted about the need to monitor patients for the emergence of agitation, irritability, and the other symptoms described above, as well as the emergence of suicidality, and to report such symptoms immediately to health-care providers. Prescriptions for LEXAPRO should be written for the smallest quantity of tablets consistent with good patient management, in order to reduce the risk of overdose.

If the decision has been made to discontinue treatment, medication should be tapered, as rapidly as is feasible, but with recognition that abrupt discontinuation can be associated with certain symptoms (see PRECAUTIONS and DOSAGE AND ADMINISTRATION, Discontinuation of Treatment with LEXAPRO, for a description of the risks of discontinuation of LEXAPRO).

It should be noted that LEXAPRO is not approved for use in treating any indications in the pediatric population.

A major depressive episode may be the initial presentation of bipolar disorder. It is generally believed (though not established in controlled trials) that treating such an episode with an antidepressant alone may increase the likelihood of precipitation of a mixed/manic episode in patients at risk for bipolar disorder. Whether any of the symptoms described above represent such a conversion is unknown. However, prior to initiating treatment with an antidepressant, patients should be adequately screened to determine if they are at risk for bipolar disorder; such screening should include a detailed psychiatric history, including a family history of suicide, bipolar disorder, and depression. It should be noted that LEXAPRO is not approved for use in treating bipolar depression.

PRECAUTIONS

General

Discontinuation of Treatment with LEXAPRO

During marketing of Lexapro and other SSRIs and SNRIs (serotonin and norepinephrine reuptake inhibitors), there have been spontaneous reports of adverse events occurring upon discontinuation of these drugs, particularly when abrupt, including the following: dysphoric mood, irritability, agitation, dizziness, sensory disturbances (e.g., paresthesias such as electric shock sensations), anxiety, confusion, headache, lethargy, emotional lability, insomnia, and hypomania. While these events are generally self-limiting, there have been reports of serious discontinuation symptoms.

Patients should be monitored for these symptoms when discontinuing treatment with LEXAPRO. A gradual reduction in the dose rather than abrupt cessation is recommended whenever possible. If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose may be considered. Subsequently, the physician may continue decreasing the dose but at a more gradual rate (see DOSAGE AND ADMINISTRATION).

Abnormal Bleeding

Published case reports have documented the occurrence of bleeding episodes in patients treated with psychotropic drugs that interfere with serotonin reuptake. Subsequent epidemiological studies, both of the case-control and cohort design, have demonstrated an association between use of psychotropic drugs that interfere with serotonin reuptake and the occurrence of upper gastrointestinal bleeding. In two studies, concurrent use of a nonsteroidal anti-inflammatory drug (NSAID) or aspirin potentiated the risk of bleeding (see Drug Interactions). Although these studies focused on upper gastrointestinal bleeding, there is reason to believe that bleeding at other sites may be similarly potentiated. Patients should be cautioned regarding the risk of bleeding associated with the concomitant use of LEXAPRO with NSAIDs, aspirin, or other drugs that affect coagulation.

Hyponatremia

One case of hyponatremia has been reported in association with LEXAPRO treatment. Several cases of hyponatremia or SIADH (syndrome of inappropriate antidiuretic hormone secretion) have been reported in association with racemic citalopram. All patients with these events have recovered with discontinuation of Lexapro
or citalopram and/or medical intervention. Hyponatremia and SIADH have also been reported in association with other marketed drugs effective in the treatment of major depressive disorder.

Activation of Mania/Hypomania

In placebo-controlled trials of LEXAPRO in major depressive disorder, activation of mania/hypomania was reported in one (0.1%) of 715 patients treated with LEXAPRO and in none of the 592 patients treated with placebo. One additional case of hypomania has been reported in association with LEXAPRO treatment. Activation of mania/hypomania has also been reported in a small proportion of patients with major affective disorders treated with racemic citalopram and other marketed drugs effective in the treatment of major depressive disorder. As with all drugs effective in the treatment of major depressive disorder, LEXAPRO should be used cautiously in patients with a history of mania.

Seizures

Although anticonvulsant effects of racemic citalopram have been observed in animal studies, LEXAPRO has not been systematically evaluated in patients with a seizure disorder. These patients were excluded from clinical studies during the product's premarketing testing. In clinical trials of LEXAPRO, cases of convulsion have been reported in association with LEXAPRO treatment. Like other drugs effective in the treatment of major depressive disorder, LEXAPRO should be introduced with care in patients with a history of seizure disorder.

Interference with Cognitive and Motor Performance

In a study in normal volunteers, LEXAPRO 10 mg/day did not produce impairment of intellectual function or psychomotor performance. Because any psychoactive drug may impair judgment, thinking, or motor skills, however, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that LEXAPRO therapy does not affect their ability to engage in such activities.

Use in Patients with Concomitant Illness

LEXAPRO has not been systematically evaluated in patients with a recent history of myocardial infarction or unstable heart disease. Patients with these diagnoses were generally excluded from clinical studies during the product's premarketing testing.

In subjects with hepatic impairment, clearance of racemic citalopram was decreased and plasma concentrations were increased. The recommended dose of LEXAPRO in hepatically impaired patients is 10 mg/day (see DOSAGE AND ADMINISTRATION).

Because Lexapro
is extensively metabolized, excretion of unchanged drug in urine is a minor route of elimination. Until adequate numbers of patients with severe renal impairment have been evaluated during chronic treatment with LEXAPRO, however, it should be used with caution in such patients (see DOSAGE AND ADMINISTRATION).

Information for Patients

Physicians are advised to discuss the following issues with patients for whom they prescribe LEXAPRO.

In a study in normal volunteers, LEXAPRO 10 mg/day did not impair psychomotor performance. The effect of LEXAPRO on psychomotor coordination, judgment, or thinking has not been systematically examined in controlled studies. Because psychoactive drugs may impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that LEXAPRO therapy does not affect their ability to engage in such activities.

Patients should be told that, although LEXAPRO has not been shown in experiments with normal subjects to increase the mental and motor skill impairments caused by alcohol, the concomitant use of LEXAPRO and alcohol in depressed patients is not advised.

Patients should be made aware that Lexapro
is the active isomer of Celexa (citalopram hydrobromide) and that the two medications should not be taken concomitantly.

Patients should be advised to inform their physician if they are taking, or plan to take, any prescription or over-the-counter drugs, as there is a potential for interactions.

Patients should be cautioned about the concomitant use of LEXAPRO and NSAIDs, aspirin, or other drugs that affect coagulation since the combined use of psychotropic drugs that interfere with serotonin reuptake and these agents has been associated with an increased risk of bleeding.

Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy.

Patients should be advised to notify their physician if they are breastfeeding an infant.

While patients may notice improvement with LEXAPRO therapy in 1 to 4 weeks, they should be advised to continue therapy as directed.

Patients and their families should be encouraged to be alert to the emergence of anxiety, agitation, panic attacks, insomnia, irritability, hostility, impulsivity, akathisia, hypomania, mania, worsening of depression, and suicidal ideation, especially early during antidepressant treatment. Such symptoms should be reported to the patient’s physician, especially if they are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

Laboratory Tests

There are no specific laboratory tests recommended.

Citalopram - Since Lexapro s the active isomer of racemic citalopram (Celexa), the two agents should not be coadministered.

CNS Drugs - Given the primary CNS effects of Lexapr, caution should be used when it is taken in combination with other centrally acting drugs.

Alcohol - Although LEXAPRO 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 LEXAPRO is not recommended. Monoamine Oxidase Inhibitors (MAOIs) - See CONTRAINDICATIONS and WARNINGS.

Serotonin release by platelets plays an important role in hemostasis. Epidemiological studies of the case-control and cohort design that have demonstrated an association between use of psychotropic drugs that interfere with serotonin reuptake and the occurrence of upper gastrointestinal bleeding have also shown that concurrent use of an NSAID or aspirin potentiated the risk of bleeding. Thus, patients should be cautioned about the use of such drugs concurrently with LEXAPRO.

Cimetidine - In subjects who had received 21 days of 40 mg/day racemic citalopram, combined administration of 400 mg/day cimetidine for 8 days resulted in an increase in citalopram AUC and _Cmaxof 43% and 39%, respectively. The clinical significance of these findings is unknown.

Digoxin - In subjects who had received 21 days of 40 mg/day racemic citalopram, combined administration of citalopram and digoxin (single dose of 1 mg) did not significantly affect the pharmacokinetics of either citalopram or digoxin.

Lithium - Coadministration 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 Lexapro, caution should be exercised when LEXAPRO and lithium are coadministered.

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, Lexapro) 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 Lexapro
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 _Cmaxand 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 Lexapro
(20 mg) did not affect the pharmacokinetics of either ritonavir or Lexapro.

CYP3A4 and -2C19 Inhibitors - In vitro studies indicated that CYP3A4 and -2C19 are the primary enzymes involved in the metabolism of Lexapro. However, coadministration of Lexapro
(20 mg) and ritonavir (600 mg), a potent inhibitor of CYP3A4, did not significantly affect the pharmacokinetics of Lexapro.

Because Lexapro is metabolized by multiple enzyme systems, inhibition of a single enzyme may not appreciably decrease Lexapro
clearance.

Drugs Metabolized by Cytochrome P4502D6 - In vitro studies did not reveal an inhibitory effect of Lexapro on CYP2D6. 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 coadministration, with Lexapro, of a drug that inhibits CYP2D6, is unlikely to have clinically significant effects on Lexapro metabolism. However, there are limited in vivo data suggesting a modest CYP2D6 inhibitory effect for Lexapro, i.e., coadministration of Lexapro (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 _Cmaxand a 100% increase in AUC of desipramine. The clinical significance of this finding is unknown. Nevertheless, caution is indicated in the coadministration of Lexapro and drugs metabolized by CYP2D6.

Metoprolol - Administration of 20 mg/day LEXAPRO for 21 days in healthy volunteers resulted in a 50% increase in _Cmax and 82% increase in AUC of the beta-adrenergic blocker metoprolol (given in a single dose of 100 mg). Increased metoprolol plasma levels have been associated with decreased cardioselectivity. Coadministration of LEXAPRO 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 Lexapro.

Racemic citalopram was administered in the diet to NMRI/BOM strain mice and COBS WI strain rats for 18 and 24 months, respectively. There was no evidence for carcinogenicity of racemic citalopram in mice receiving up to 240 mg/kg/day. There was an increased incidence of small intestine carcinoma in rats receiving 8 or 24 mg/kg/day racemic citalopram. A no-effect dose for this finding was not established. The relevance of these findings to humans is unknown.

Racemic citalopram was mutagenic in the in vitro bacterial reverse mutation assay (Ames test) in 2 of 5 bacterial strains (Salmonella TA98 and TA1 537) in the absence of metabolic activation. It was clastogenic in the in vitro Chinese hamster lung cell assay for chromosomal aberrations in the presence and absence of metabolic activation. Racemic citalopram was not mutagenic in the in vitro mammalian forward gene mutation assay (HPRT) in mouse lymphoma cells or in a coupled in vitro/in vivo unscheduled DNA synthesis (UDS) assay in rat liver. It was not clastogenic in the in vitro chromosomal aberration assay in human lymphocytes or in two in vivo mouse micronucleus assays.

When racemic citalopram was administered orally to 16 male and 24 female rats prior to and throughout mating and gestation at doses of 32, 48, and 72 mg/kg/day, mating was decreased at all doses, and fertility was decreased at doses t 32 mg/kg/day. Gestation duration was increased at 48 mg/kg/day.

In a rat embryo/fetal development study, oral administration of Lexapro (56, 112, or 150 mg/kg/day) to pregnant animals during the period of organogenesis resulted in decreased fetal body weight and associated delays in ossification at the two higher doses (approximately t 56 times the maximum recommended human dose [MRHD] of 20 mg/day on a body surface area [mg/m²] basis). Maternal toxicity (clinical signs and decreased body weight gain and food consumption), mild at 56 mg/kg/day, was present at all dose levels. The developmental no-effect dose of 56 mg/kg/day is approximately 28 times the MRHD on a mg/m² basis. No teratogenicity was observed at any of the doses tested (as high as 75 times the MRHD on a mg/m² basis).

When female rats were treated with Lexapro (6, 12, 24, or 48 mg/kg/day) during pregnancy and through weaning, slightly increased offspring mortality and growth retardation were noted at 48 mg/kg/day which is approximately 24 times the MRHD on a mg/m² basis. Slight maternal toxicity (clinical signs and decreased body weight gain and food consumption) was seen at this dose. Slightly increased offspring mortality was seen at 24 mg/kg/day. The no-effect dose was 12 mg/kg/day which is approximately 6 times the MRHD on a mg/m² basis.

In animal reproduction studies, racemic citalopram has been shown to have adverse effects on embryo/fetal and postnatal development, including teratogenic effects, when administered at doses greater than human therapeutic doses.

In two rat embryo/fetal development studies, oral administration of racemic citalopram (32, 56, or 112 mg/kg/day) to pregnant animals during the period of organogenesis resulted in decreased embryo/fetal growth and survival and

an increased incidence of fetal abnormalities (including cardiovascular and skeletal defects) at the high dose. This dose was also associated with maternal toxicity (clinical signs, decreased body weight gain). The developmental no-effect dose was 56 mg/kg/day. In a rabbit study, no adverse effects on embryo/fetal development were observed at doses of racemic citalopram of up to 16 mg/kg/day. Thus, teratogenic effects of racemic citalopram were observed at a maternally toxic dose in the rat and were not observed in the rabbit.

When female rats were treated with racemic citalopram (4.8, 12.8, or 32 mg/kg/day) from late gestation through weaning, increased offspring mortality during the first 4 days after birth and persistent offspring growth retardation were observed at the highest dose. The no-effect dose was 12.8 mg/kg/day. Similar effects on offspring mortality and growth were seen when dams were treated throughout gestation and early lactation at doses t 24 mg/kg/day. A no-effect dose was not determined in that study.

There are no adequate and well-controlled studies in pregnant women; therefore, Lexapro should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Neonates exposed to LEXAPRO and other SSRIs or SNRIs, late in the third trimester, have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding. Such complications can arise immediately upon delivery. Reported clinical findings have included respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hypertonia, hyperreflexia, tremor, jitteriness, irritability, and constant crying. These features are consistent with either a direct toxic effect of SSRIs and SNRIs or, possibly, a drug discontinuation syndrome. It should be noted that, in some cases, the clinical picture is consistent with serotonin syndrome (see WARNINGS).

When treating a pregnant woman with LEXAPRO during the third trimester, the physician should carefully consider the potential risks and benefits of treatment (see DOSAGE AND ADMINISTRATION).

Racemic citalopram, like many other drugs, is excreted in human breast milk. There have been two reports of infants experiencing excessive somnolence, decreased feeding, and weight loss in association with breastfeeding from a citalopram-treated mother; in one case, the infant was reported to recover completely upon discontinuation of citalopram by its mother and, in the second case, no follow-up information was available. The decision whether to continue or discontinue either nursing or LEXAPRO therapy should take into account the risks of citalopram exposure for the infant and the benefits of LEXAPRO treatment for the mother.

Safety and effectiveness in pediatric patients have not been established (see WARNINGS-Clinical Worsening and Suicide Risk.

Approximately 6% of the 1144 patients receiving Lexapro in controlled trials of LEXAPRO in major depressive disorder and GAD were 60 years of age or older; elderly patients in these trials received daily doses of LEXAPRO between 10 and 20 mg. The number of elderly patients in these trials was insufficient to adequately assess for possible differential efficacy and safety measures on the basis of age. Nevertheless, greater sensitivity of some elderly individuals to effects of LEXAPRO cannot be ruled out.

In two pharmacokinetic studies, Lexapro half-life was increased by approximately 50% in elderly subjects as compared to young subjects and _Cmaxwas unchanged (see CLINICAL PHARMACOLOGY). 10 mg/day is the recommended dose for elderly patients (see DOSAGE AND ADMINISTRATION).

Of 4422 patients in clinical studies of racemic citalopram, 1357 were 60 and over, 1034 were 65 and over, and 457 were 75 and over. No overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but again, greater sensitivity of some elderly individuals cannot be ruled out.

Adverse event information for LEXAPRO was collected from 715 patients with major depressive disorder who were exposed to Lexapro and from 592 patients who were exposed to placebo in double-blind, placebo-controlled trials. An additional 284 patients with major depressive disorder were newly exposed to Lexapro
in open-label trials. The adverse event information for LEXAPRO in patients with GAD was collected from 429 patients exposed to Lexapro and from 427 patients exposed to placebo in double-blind, placebo-controlled trials.

Adverse events during exposure were obtained primarily by general inquiry and recorded by clinical investigators using terminology of their own choosing. Consequently, it is not possible to provide a meaningful estimate of the proportion of individuals experiencing adverse events without first grouping similar types of events into a smaller number of standardized event categories. In the tables and tabulations that follow, standard World Health Organization (WHO) terminology has been used to classify reported adverse events.

The stated frequencies of adverse events represent the proportion of individuals who experienced, at least once, a treatment-emergent adverse event of the type listed. An event was considered treatment-emergent if it occurred for the first time or worsened while receiving therapy following baseline evaluation.

Among the 715 depressed patients who received LEXAPRO in placebo-controlled trials, 6% discontinued treatment due to an adverse event, as compared to 2% of 592 patients receiving placebo. In two fixed-dose studies, the rate of discontinuation for adverse events in patients receiving 10 mg/day LEXAPRO was not significantly different from the rate of discontinuation for adverse events in patients receiving placebo. The rate of discontinuation for adverse events in patients assigned to a fixed dose of 20 mg/day LEXAPRO was 10%, which was significantly different from the rate of discontinuation for adverse events in patients receiving 10 mg/day LEXAPRO (4%) and placebo (3%). Adverse events that were associated with the discontinuation of at least 1% of patients treated with LEXAPRO, and for which the rate was at least twice that of placebo, were nausea (2%) and ejaculation disorder (2% of male patients).

Among the 429 GAD patients who received LEXAPRO 10-20 mg/day in placebo-controlled trials, 8% discontinued treatment due to an adverse event, as compared to 4% of 427 patients receiving placebo. Adverse events that were associated with the discontinuation of at least 1% of patients treated with LEXAPRO, and for which the rate was at least twice the placebo rate, were nausea (2%), insomnia (1%), and fatigue (1%).

Table 1 enumerates the incidence, rounded to the nearest percent, of treatment-emergent adverse events that occurred among 715 depressed patients who received LEXAPRO at doses ranging from 10 to 20 mg/day in placebo-controlled trials. Events included are those occurring in 2% or more of patients treated with LEXAPRO and for which the incidence in patients treated with LEXAPRO was greater than the incidence in placebo-treated patients.

The prescriber should be aware that these figures can not be used to predict the incidence of adverse events in the course of usual medical practice where patient characteristics and other factors differ from those which prevailed in the clinical trials. Similarly, the cited frequencies cannot be compared with figures obtained from other clinical investigations involving different treatments, uses, and investigators. The cited figures, however, do provide the prescribing physician with some basis for estimating the relative contribution of drug and non-drug factors to the adverse event incidence rate in the population studied.

The most commonly observed adverse events in LEXAPRO patients (incidence of approximately 5% or greater and approximately twice the incidence in placebo patients) were insomnia, ejaculation disorder (primarily ejaculatory delay), nausea, sweating increased, fatigue, and somnolence (see TABLE 1).

*Events reported by at least 2% of patients treated with LEXAPRO are reported, except for the following events which had an incidence on placebo t LEXAPRO: headache, upper respiratory tract infection, back pain, pharyngitis, inflicted injury, anxiety.

Table 2 enumerates the incidence, rounded to the nearest percent of treatment-emergent adverse events that occurred among 429 GAD patients who received LEXAPRO 10 to 20 mg/day in placebo-controlled trials. Events included are those occurring in 2% or more of patients treated with LEXAPRO and for which the incidence in patients treated with LEXAPRO was greater than the incidence in placebo-treated patients.

The most commonly observed adverse events in LEXAPRO patients (incidence of approximately 5% or greater and approximately twice the incidence in placebo patients) were nausea, ejaculation disorder (primarily ejaculatory delay), insomnia, fatigue, decreased libido, and anorgasmia (see TABLE 2).

*Events reported by at least 2% of patients treated with LEXAPRO are reported, except for the following events which had an incidence on placebo t LEXAPRO: inflicted injury, dizziness, back pain, upper respiratory tract infection, rhinitis, pharyngitis.

The potential dose dependency of common adverse events (defined as an incidence rate of t5% in either the 10 mg or 20 mg LEXAPRO groups) was examined on the basis of the combined incidence of adverse events in two fixed-dose trials. The overall incidence rates of adverse events in 10 mg LEXAPRO-treated patients (66%) was similar to that of the placebo-treated patients (6 1%), while the incidence rate in 20 mg/day LEXAPRO-treated patients was greater (86%). Table 3 shows common adverse events that occurred in the 20 mg/day LEXAPRO group with an incidence that was approximately twice that of the 10 mg/day LEXAPRO group and approximately twice that of the placebo group.

TABLE 3
Incidence of Common Adverse Events* in Patients with Major
Depressive Disorder Receiving Placebo, 10 mg/day LEXAPRO, or
20 mg/day LEXAPRO

Although changes in sexual desire, sexual performance, and sexual satisfaction often occur as manifestations of a psychiatric disorder, they may also be a consequence of pharmacologic treatment. In particular, some evidence suggests that SSRIs can cause such untoward sexual experiences.

Reliable estimates of the incidence and severity of untoward experiences involving sexual desire, performance, and satisfaction are difficult to obtain, however, in part because patients and physicians may be reluctant to discuss them. Accordingly, estimates of the incidence of untoward sexual experience and performance cited in product labeling are likely to underestimate their actual incidence.

Table 4 shows the incidence rates of sexual side effects in patients with major depressive disorder and GAD in placebo-controlled trials.

There are no adequately designed studies examining sexual dysfunction with Lexapro
treatment. Priapism has been reported with all SSRIs.

While it is difficult to know the precise risk of sexual dysfunction associated with the use of SSRIs, physicians should routinely inquire about such possible side effects.

LEXAPRO and placebo groups were compared with respect to (1) mean change from baseline in vital signs (pulse, systolic blood pressure, and diastolic blood pressure) and (2) the incidence of patients meeting criteria for potentially clinically significant changes from baseline in these variables. These analyses did not reveal any clinically important changes in vital signs associated with LEXAPRO treatment. In addition, a comparison of supine and standing vital sign measures in subjects receiving LEXAPRO indicated that LEXAPRO treatment is not associated with orthostatic changes.

Patients treated with LEXAPRO in controlled trials did not differ from placebo-treated patients with regard to clinically important change in body weight.

LEXAPRO and placebo groups were compared with respect to (1) mean change from baseline in various serum

chemistry, hematology, and urinalysis variables, and (2) the incidence of patients meeting criteria for potentially clinically significant changes from baseline in these variables. These analyses revealed no clinically important changes in laboratory test parameters associated with LEXAPRO treatment.

Electrocardiograms from LEXAPRO (N=625), racemic citalopram (N=351), and placebo (N=527) groups were compared with respect to (1) mean change from baseline in various ECG parameters and (2) the incidence of patients meeting criteria for potentially clinically significant changes from baseline in these variables. These analyses revealed (1) a decrease in heart rate of 2.2 bpm for LEXAPRO and 2.7 bpm for racemic citalopram, compared to an increase of 0.3 bpm for placebo and (2) an increase in QTc interval of 3.9 msec for LEXAPRO and 3.7 msec for racemic citalopram, compared to 0.5 msec for placebo. Neither LEXAPRO nor racemic citalopram were associated with the development of clinically significant ECG abnormalities.

Following is a list of WHO terms that reflect treatment-emergent adverse events, as defined in the introduction to the ADVERSE REACTIONS section, reported by the 1428 patients treated with LEXAPRO for periods of up to one year in double-blind or open-label clinical trials during its premarketing evaluation. All reported events are included except those already listed in Tables 1 & 2, those occurring in only one patient, event terms that are so general as to be uninformative, and those that are unlikely to be drug related. It is important to emphasize that, although the events reported occurred during treatment with LEXAPRO, they were not necessarily caused by it.

Events are further categorized by body system and listed in order of decreasing frequency according to the following definitions: frequent adverse events are those occurring on one or more occasions in at least 1/100 patients; infrequent adverse events are those occurring in less than 1/100 patients but at least 1/1 000 patients. Cardiovascular - Frequent: palpitation, hypertension. Infrequent: bradycardia, tachycardia, ECG abnormal, flushing, varicose vein.

Central and Peripheral Nervous System Disorders - Frequent: light-headed feeling, migraine. Infrequent: tremor, vertigo, restless legs, shaking, twitching, dysequilibrium, tics, carpal tunnel syndrome, muscle contractions involuntary, sluggishness, coordination abnormal, faintness, hyperreflexia, muscular tone increased. Gastrointestinal Disorders - Frequent: heartburn, abdominal cramp, gastroenteritis. Infrequent: gastroesophageal reflux, bloating, abdominal discomfort, dyspepsia, increased stool frequency, belching, gastritis, hemorrhoids, gagging, polyposis gastric, swallowing difficult.

General - Frequent: allergy, pain in limb, fever, hot flushes, chest pain. Infrequent: edema of extremities, chills, tightness of chest, leg pain, asthenia, syncope, malaise, anaphylaxis, fall.

Hemic and Lymphatic Disorders - Infrequent: bruise, anemia, nosebleed, hematoma, lymphadenopathy cervical. Metabolic and Nutritional Disorders - Frequent: increased weight. Infrequent: decreased weight, hyperglycemia, thirst, bilirubin increased, hepatic enzymes increased, gout, hypercholesterolemia.

Musculoskeletal System Disorders - Frequent: arthralgia, myalgia. Infrequent: jaw stiffness, muscle cramp, muscle stiffness, arthritis, muscle weakness, back discomfort, arthropathy, jaw pain, joint stiffness. Psychiatric Disorders - Frequent: appetite increased, lethargy, irritability, concentration impaired. Infrequent: jitteriness, panic reaction, agitation, apathy, forgetfulness, depression aggravated, nervousness, restlessness aggravated, suicide attempt, amnesia, anxiety attack, bruxism, carbohydrate craving, confusion, depersonalization, disorientation, emotional lability, feeling unreal, tremulousness nervous, crying abnormal, depression, excitability, auditory hallucination, suicidal tendency.

Reproductive Disorders/Female* - Frequent: menstrual cramps, menstrual disorder. Infrequent: menorrhagia, breast neoplasm, pelvic inflammation, premenstrual syndrome, spotting between menses.

Respiratory System Disorders - Frequent: bronchitis, sinus congestion, coughing, nasal congestion, sinus headache. Infrequent: asthma, breath shortness, laryngitis, pneumonia, tracheitis.

Skin and Appendages Disorders - Frequent: rash. Infrequent: pruritus, acne, alopecia, eczema, dermatitis, dry skin, folliculitis, lipoma, furunculosis, dry lips, skin nodule.

Special Senses - Frequent: vision blurred, tinnitus. Infrequent: taste alteration, earache, conjunctivitis, vision abnormal, dry eyes, eye irritation, visual disturbance, eye infection, pupils dilated, metallic taste. Urinary System Disorders - Frequent: urinary frequency, urinary tract infection. Infrequent: urinary urgency, kidney stone, dysuria, blood in urine.

Events Reported Subsequent to the Marketing of Racemic Citalopram and Lexapro

Although no causal relationship to racemic citalopram or Lexapro treatment has been found, the following adverse events have been reported to have occurred in patients and to be temporally associated with racemic citalopram treatment and with Lexapro
treatment during postmarketing experience and were not observed during the premarketing evaluation of citalopram or Lexapro: acute renal failure, angioedema, toxic epidermal necrolysis, gastrointestinal hemorrhage, grand mal seizures (or convulsions), neuroleptic malignant syndrome, pancreatitis, QT prolongation, rhabdomyolysis, serotonin syndrome, thrombocytopenia, torsades de pointes.

Events Reported Subsequent to the Marketing of Racemic Citalopram (not observed during the postmarketing experience with Lexapro)

Although no causal relationship to racemic citalopram treatment has been found, the following adverse events have been reported to have occurred in patients and to be temporally associated with racemic citalopram treatment and were not observed during the premarketing evaluation of citalopram: akathisia, allergic reaction, anaphylaxis, choreoathetosis, delirium, dyskinesia, ecchymosis, erythema multiforme, hemolytic anemia, hepatic necrosis, myoclonus, nystagmus, priapism, prolactinemia, prothrombin decreased, spontaneous abortion, thrombosis, and ventricular arrhythmia.

Events Reported Subsequent to the Marketing of Lexapro (not observed during the postmarketing experience with citalopram)

Although no causal relationship to Lexapro treatment has been found, the following adverse events have been reported to have occurred in patients and to be temporally associated with Lexapro treatment and were not observed during the premarketing evaluation of Lexapro: aggression, atrial fibrillation, seizures, diplopia, dystonia, extrapyramidal disorders, abnormal gait, visual hallucinations, hepatitis, hypotension, myocardial infarction, orthostatic hypotension, pulmonary embolism, SIADH, ventricular tachycardia.

Animal studies suggest that the abuse liability of racemic citalopram is low. LEXAPRO has not been systematically studied in humans for its potential for abuse, tolerance, or physical dependence. The premarketing clinical experience with LEXAPRO did not reveal any drug-seeking behavior. However, these observations were not systematic and it is not possible to predict on the basis of this limited experience the extent to which a CNS-active drug will be misused, diverted, and/or abused once marketed. Consequently, physicians should carefully evaluate LEXAPRO patients for history of drug abuse and follow such patients closely, observing them for signs of misuse or abuse (e.g., development of tolerance, incrementations of dose, drug-seeking behavior).

There have been reports of LEXAPRO overdose involving doses of up to 600 mg. All patients recovered and no symptoms associated with the overdoses were reported. In clinical trials of racemic citalopram, there were no reports of fatal citalopram overdose involving overdoses of up to 2000 mg. During the postmarketing evaluation of citalopram, like other SSRIs, a fatal outcome in a patient who has taken an overdose of citalopram has been rarely reported.

Postmarketing reports of drug overdoses involving citalopram have included 12 fatalities, 10 in combination with other drugs and/or alcohol and 2 with citalopram alone (3920 mg and 2800 mg), as well as non-fatal overdoses of up to 6000 mg. Symptoms most often accompanying citalopram overdose, alone or in combination with other drugs and/or alcohol, included dizziness, sweating, nausea, vomiting, tremor, somnolence, sinus tachycardia, and convulsions. In more rare cases, observed symptoms included amnesia, confusion, coma, hyperventilation, cyanosis, rhabdomyolysis, and ECG changes (including QTc prolongation, nodal rhythm, ventricular arrhythmia, and one possible case of torsades de pointes).

Establish and maintain an airway to ensure adequate ventilation and oxygenation. Gastric evacuation by lavage and use of activated charcoal should be considered. Careful observation and cardiac and vital sign monitoring are recommended, along with general symptomatic and supportive care. Due to the large volume of distribution of Lexapro
, forced diuresis, dialysis, hemoperfusion, and exchange transfusion are unlikely to be of benefit. There are no specific antidotes for LEXAPRO.

In managing overdosage, consider the possibility of multiple-drug involvement. The physician should consider contacting a poison control center for additional information on the treatment of any overdose.

The recommended dose of LEXAPRO is 10 mg once daily. A fixed-dose trial of LEXAPRO demonstrated the effectiveness of both 10 mg and 20 mg of LEXAPRO, but failed to demonstrate a greater benefit of 20 mg over 10 mg (see Clinical Efficacy Trials under CLINICAL PHARMACOLOGY). If the dose is increased to 20 mg, this should occur after a minimum of one week.

LEXAPRO should be administered once daily, in the morning or evening, with or without food. Special Populations

10 mg/day is the recommended dose for most elderly patients and patients with hepatic impairment.

No dosage adjustment is necessary for patients with mild or moderate renal impairment. LEXAPRO should be used with caution in patients with severe renal impairment.

Neonates exposed to LEXAPRO and other SSRIs or SNRIs, late in the third trimester, have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding (see PRECAUTIONS). When treating pregnant women with LEXAPRO during the third trimester, the physician should carefully consider the potential risks and benefits of treatment. The physician may consider tapering LEXAPRO in the third trimester.

It is generally agreed that acute episodes of major depressive disorder require several months or longer of sustained pharmacological therapy beyond response to the acute episode. Systematic evaluation of continuing LEXAPRO 10 or 20 mg/day for periods of up to 36 weeks in patients with major depressive disorder who responded while taking LEXAPRO during an 8-week, acute-treatment phase demonstrated a benefit of such maintenance treatment (see Clinical Efficacy Trials under CLINICAL PHARMACOLOGY). Nevertheless, patients should be periodically reassessed to determine the need for maintenance treatment.

The recommended starting dose of LEXAPRO is 10 mg once daily. If the dose is increased to 20 mg, this should occur after a minimum of one week.

LEXAPRO should be administered once daily, in the morning or evening, with or without food.

Generalized anxiety disorder is recognized as a chronic condition. The efficacy of LEXAPRO in the treatment of GAD beyond 8 weeks has not been systematically studied. The physician who elects to use LEXAPRO for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient.

Symptoms associated with discontinuation of LEXAPRO and other SSRIs and SNRIs have been reported (see PRECAUTIONS). Patients should be monitored for these symptoms when discontinuing treatment. A gradual reduction in the dose rather than abrupt cessation is recommended whenever possible. If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose may be considered. Subsequently, the physician may continue decreasing the dose but at a more gradual rate.

At least 14 days should elapse between discontinuation of an MAOI and initiation of LEXAPRO therapy. Similarly, at least 14 days should be allowed after stopping LEXAPRO before starting an MAOI (see CONTRAINDICATIONS and WARNINGS).

White to off-white, round, non-scored, film-coated. Imprint "FL" on one side of the tablet and "5" on the other side.

White to off-white, round, scored, film-coated. Imprint on scored side with "F" on the left side and "L" on the right side.

Pathologic changes (degeneration/atrophy) were observed in the retinas of albino rats in the 2-year carcinogenicity study with racemic citalopram. There was an increase in both incidence and severity of retinal pathology in both male and female rats receiving 80 mg/kg/day. Similar findings were not present in rats receiving 24 mg/kg/day of racemic citalopram for two years, in mice receiving up to 240 mg/kg/day of racemic citalopram for 18 months, or in dogs receiving up to 20 mg/kg/day of racemic citalopram for one year.

Additional studies to investigate the mechanism for this pathology have not been performed, and the potential significance of this effect in humans has not been established.

In a one-year toxicology study, 5 of 10 beagle dogs receiving oral racemic citalopram doses of 8 mg/kg/day died suddenly between weeks 17 and 31 following initiation of treatment. Sudden deaths were not observed in rats at doses of racemic citalopram up to 120 mg/kg/day, which produced plasma levels of citalopram and its metabolites demethylcitalopram and didemethylcitalopram (DDCT) similar to those observed in dogs at 8 mg/kg/day. A subsequent intravenous dosing study demonstrated that in beagle dogs, racemic DDCT caused QT prolongation, a known risk factor for the observed outcome in dogs.

Forest Pharmaceuticals, Inc.
Subsidiary of Forest Laboratories, Inc.
St. Louis, MO 63045 USA

PLEASE, DO NOT QUIT LEXAPRO COLD TURKEY. IT IS NOT SAFE TO SUDDENLY STOP TAKING THIS MEDICATION.

Lexapro has been approved by the FDA for treatment of major depression. We receive many reports each day of Lexapro being prescribed to treat headache, fingernail biting and a host of often minor ailments. Before you begin taking Lexapro review the side effects and weigh the reward and risk.

Common Lexapro Side Effects

Lexapro