Doses above 40 mg/day are not recommended because of the risk for QT prolongation.
Initial, 20 mg/day orally as a single dose in the morning or evening;
Dose increases should usually occur in increments of 20 mg at intervals of no less than one week; max., 40 mg/day
A test of the GRIK4 gene can be made in order to know if a depressed patient will respond to the citalopram.
Initially 10 mg for a week, then 20 mg. Sometimes it is necessary to increase the dose to maximum 40 mg
There is controversy over selective publishing of SSRI clinical trials by pharmaceutical companies. A meta-analysis analyzing published as well as unpublished trials found the benefits of SSRIs over placebos to be insignificant in all but the severe cases of depression (benefits over placebo were substantial in severe cases).
According to other authors citalopram is an established first-line antidepressant, of comparable efficacy to other antidepressants. In NICE (National Institute for Health and Clinical Excellence) ranking of the 10 antidepressants for efficacy and cost-effectiveness  citalopram is fifth in effectiveness (after mirtazapine, escitalopram, venlafaxine and sertraline) and fourth in cost effectiveness. The ranking results were based on the metaanalysis by Andrea Cipriani In another analysis by Cipriani citalopram turned out to be more efficacious than paroxetine and reboxetine and more acceptable than tricyclics, reboxetine and venlafaxine, however it seemed to be less efficacious than escitalopram.
Citalopram is licensed in the UK and other European countries  for panic disorder, with or without agoraphobia. The dose is 10 mg/d for a week, increasing to 20–30 mg/d, with a maximum of 60 mg/d. It appears equally effective as escitalopram.
SSRI’s develop their action over 2 weeks, but most studies were not powered to detect earlier onset. Some authors suggest that onset of action may be quicker than 2 weeks, although there are contrary opinions.
It has been shown to be effective in 85% patients with GAD (Generalized Anxiety Disorder), including some who had failed with other SSRIs It also appears to be as effective as fluvoxamine and paroxetine in obsessive-compulsive disorder. Some data suggests the effectiveness of intravenous infusion of citalopram in resistant OCD. Citalopram 40 mg/d is well tolerated and as effective as moclobemide in social anxiety disorder (SAD). There are studies suggesting that citalopram can be useful in reducing aggressive and impulsive behavior. It appears to be superior to placebo for behavioural disturbances associated with dementia. It has also been used successfully for hypersexuality in early Alzheimer’s disease.
A metaanalisys including studies with fluoxetine, paroxetine, sertraline, escitalopram and citalopram versus placebo showed that SSRI’s are effective in reducing symptoms of premenstrual syndrome (PMS), whether taken continuously or just in the luteal phase. Citalopram has produced a modest, reduction in alcoholic drink intake and increase in drink-free days in studies of alcoholics, possibly by decreasing desire or reducing the reward 
A 2009 multisite randomized controlled study found no benefit and some adverse effects in autistic children from citalopram, raising doubts whether SSRIs are effective for treating repetitive behavior in children with autism.
Some research suggests that citalopram interacts with cannabinoid protein-couplings in the rat brain, and this is put forward as a potential cause of some of the drug's antidepressant effect.
Citalopram is typically taken in one dose, either in the morning or evening. Citalopram can be taken with or without food. The absorption of citalopram does not increase when taken with food, but doing so can help prevent nausea. Nausea is often caused when the 5HT3 receptors actively absorbs free serotonin, as this receptor is present within the digestive tract. The 5HT3 receptors stimulate vomiting. This side effect, if present, should subside as the body adjusts to the medication.
Sexual dysfunction is often a side effect with SSRIs. Specifically, common side effects include difficulty becoming aroused, lack of interest in sex, and anorgasmia (trouble achieving orgasm). Genital anesthesia, loss of or decreased response to sexual stimuli, and ejaculatory anhedonia are also possible. Although usually reversible, in some people these sexual side effects become permanent after the drug has been completely withdrawn. This is known as post-SSRI sexual dysfunction. One study showed however that when remission of major depressive disorder is achieved, quality of life is reported to be higher in spite of sexual side effects.
Citalopram theoretically causes side effects by increasing the concentration of serotonin in other parts of the body (e.g., the intestines). Other side effects, such as increased apathy and emotional flattening, may be caused by the decrease in dopamine release that is associated with increased serotonin. Citalopram is also a mild antihistamine, which may be responsible for some of its sedating properties.:104
In August 2011, the US Food and Drug Administration (FDA) announced that “Citalopram causes dose-dependent QT interval prolongation. Citalopram should no longer be prescribed at doses greater than 40 mg per day”. Further clarification issued in March 2012  restricted the maximum dose to 20 mg for subgroups of patients, including those older than 60 years and those taking an inhibitor of cytochrome P450 2 C19.7 This change, affecting the most widely prescribed antidepressant in the US, left clinicians unclear about appropriate next-step strategies because of the lack of data comparing citalopram with other antidepressants. In a cross-sectional study using electronic health records with almost 40 000 participants modest dose dependent QTc prolongation was confirmed . It was also true for escitalopram and amitriptyline  although the effect sizes were small and there is no epidemiological evidence for higher risk of cardiac arythmia. It is clear that randomised investigation is still required in this field. Another large study found no elevated risks of ventricular arrhythmia or all-cause, cardiac, or noncardiac mortality associated with citalopram dosages >40 mg/day. Higher dosages were associated with fewer adverse outcomes, and similar findings were observed for a comparison medication, sertraline, not subject to the FDA warning. Based on these results the authors suggest that continued merit of the FDA warning should be considered.
Citalopram appears safe after the MI (myocardial infarction) and response to citalopram and mirtazapine may improve mortality after the MI  Although QTc prolongation warning must be taken into account especially in case of acute myocardial infarction, heart failure decompensation, in patients with bradycardia, low potassium and magnesium levels and in case of dose higher than 40 mg 
Bone cell function
Some data suggests that SSRIs increase bone fragility and fracture risk through inhibition of bone cell function via apoptosis. Citalopram seems to have the weakest effect of the SSRIs tested, as order of potency is: sertraline>fluoxetine>paroxetine>fluvoxamine>citalopram
As other SSRI’s citalopram can cause increase in serum prolactine level. Citalopram has no significant effect on insulin sensitivity in women of reproductive age  no changes in glycaemic control were seen in another trial 
Exposure in pregnancy
Antidepressant exposure (including citalopram) during pregnancy is associated with shorter duration of gestation (by 3 days), increased risk of preterm delivery (by 55%), lower birth weight (by 75 g), and lower Apgar scores (by <0.4 points). Antidepressant exposure is not associated with an increased risk of spontaneous abortion.
Citalopram should not be taken with St John's wort, tryptophan or 5-HTP as the resulting drug interaction could lead to serotonin syndrome. With St John's wort, this may be caused by compounds in the plant extract reducing the efficacy of the hepaticcytochrome P450 enzymes that process citalopram. It has also been suggested that such compounds, including hypericin, hyperforin and flavonoids, could have SSRI-mimetic effects on the nervous system, although this is still subject to debate. One study found that Hypericum extracts had similar effects in treating moderate depression as citalopram, with fewer side effects. Tryptophan and 5-HTP are precursors to serotonin and can cause a rise in serotonin. When taken with an SSRI, such as citalopram, this can lead to levels of serotonin that can be lethal. This may also be the case when SSRI's are taken with SRA's (Sertonin Releasing Agents) such as in the case of MDMA. It's possible that SSRI's could reduce the effects associated due an SRA, due to the fact that SSRI's stop the reuptake of Serotonin by blocking SERT. This would allow less Serotonin in and out of the transporters, thus decreasing the likelihood of neurotoxic effects. However, these concerns are still disputed as the exact pharmacodynamic effects of Citalopram and MDMA have yet to be fully identified.
When taken with Omeprazole, the clearance of citalopram may be reduced, leading to higher blood levels of citalopram. Prilosec inhibits the CYP450 2C19 enzyme, one of the two primary enzymes responsible for the metabolism of citalopram. Dosage adjustments may be needed to counter this effect.
SSRI discontinuation syndrome has been reported when treatment is stopped. It includes sensory, gastrointestinal symptoms, dizziness, lethargy, and sleep disturbances, as well as psychological symptoms such as anxiety/agitation, irritability, and poor concentration. Electric shock-like sensations are typical for SSRI discontinuation. Tapering off citalopram therapy, as opposed to abrupt discontinuation, is recommended in order to diminish the occurrence and severity of discontinuation symptoms. Some doctors may choose to switch a patient to Prozac (Fluoxetine) when discontinuing Citalopram as Fluoxetine has a much longer half-life (i.e. stays in the body longer compared to Citalopram). This may avoid many of the severe withdrawal symptoms associated with Citalopram discontinuation. This can be done either by administering a single 20 mg dose of Fluoxetine or by beginning on a low dosage of Fluoxetine and slowly tapering down. Either of these prescriptions may be written in liquid form to allow a very slow and gradual tapering down in dosage. Alternatively, a patient wishing to stop taking Citalopram may visit a compounding pharmacy where his or her prescription may be re-arranged into progressively smaller dosages.
Overdosage may result in vomiting, sedation, disturbances in heart rhythm, dizziness, sweating, nausea, tremor, and rarely amnesia, confusion, coma, or convulsions.:105 Overdose deaths have occurred, sometimes involving other drugs but also with citalopram as the sole agent. Citalopram and N-desmethylcitalopram may be quantized in blood or plasma to confirm a diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Blood or plasma citalopram concentrations are usually in a range of 50-400 μg/L in persons receiving the drug therapeutically, 1000-3000 μg/L in patients who survive acute overdosage and 3–30 mg/L in those who do not survive. It is the most dangerous of SSRIs in overdose.
In the United States, citalopram, like other antidepressants, carries a black box warning stating that it may increase suicidal thinking and behavior in those under age 24.
Citalopram is sold as a racemic mixture, consisting of 50% (R)-(−)-citalopram and 50% (S)-(+)-citalopram. Only the (S)-(+) enantiomer has the desired antidepressant effect.Lundbeck now markets the (S)-(+) enantiomer, the generic name of which is escitalopram. Whereas citalopram is supplied as the hydrobromide, escitalopram is sold as the oxalate salt (hydrooxalate). In both cases, the salt forms of the amine make these otherwise lipophilic compounds water-soluble.
Citalopram is metabolized in the liver mostly by CYP 2 C19, but also by CYP 3A4 and CYP 2D6. Metabolites desmethylcitalopram and didesmethylcitalopram are significantly less energetic and their contribution to the overall action of citalopram is negligible. The half-life of citalopram is about 35 hours. In 85% it is eliminated by the liver and in 25% by kidneys. The elimination process is slower in the elderly and in patients with hepatic or renal failure. With once daily dosing steady plasma concentrations are achieved in about a week. Potent inhibitors of CYP2C19 and 3A4 might decrease citalopram clearance. It was found that tobacco smoke exposure inhibits the biotransformation of citalopram in animals. The half-life of the racemic mixture of citalopram after intragastric administration was increased by about 287%.
Citalopram was originally created in 1989 by the pharmaceutical company Lundbeck. The patent expired in 2003, allowing other companies to legally produce generic versions. Lundbeck has recently released an updated formulation called escitalopram, which is the S-enantiomer of the racemic citalopram (see b), and acquired a new patent for it. In the United States, Forest Labs manufactures and markets the drug.
Citalopram is sold under the brand-names Celexa (U.S. and Canada, Forest Laboratories, Inc.), Citalopram (USA, United Kingdom, Denmark, Spain, Switzerland), Citta, Denyl (Brazil), Cipramil (Australia, Brazil, Belgium, Finland, Germany, Netherlands, Ireland, Israel, Norway, Sweden, United Kingdom, New Zealand, South Africa, Russia), Elopram (Italy), Clitoram (United Kingdom), Citol (Russia), Vodelax (Turkey), Citrol, Seropram, Talam (Europe and Australia), Citabax, Citaxin (Poland), Citalec (Slovakia, Czech Republic), Recital (Israel, Thrima Inc. for Unipharm Ltd.), Zetalo (India), Celapram, Ciazil (Australia, New Zealand), Zentius, Cimal (South America, by Roemmers and Recalcine), Ciprapine (Ireland), Cilift, Cilate (South Africa), Citox (Mexico), Temperax (Chile, Peru, Argentina), Talohexal (Australia), Citopam (Australia), Akarin (Denmark, Nycomed), Cipram (Turkey, Denmark, H. Lundbeck A/S), Dalsan (Eastern Europe), Pram (Russia), Pramcit (Pakistan), Cipraned (Greece), Humorup (Argentina), Humorap (Peru), Humorap (Bolivia), Oropram (Iceland, Actavis), Opra (Russia), and Zylotex (Portugal),Citalo (Egypt), Citalex (Iran), Sepram (Finland).
European Commission fine
On 19 June 2013, the European Commission imposed a fine of €93.8 million on the Danish pharmaceutical company Lundbeck, plus a total of €52.2 million on several generic pharmaceutical producing companies. This was in response to Lundbeck entering an agreement with the companies to delay their sales of generic citalopram after Lundbeck's patent on the drug had expired, thus reducing competition in breach of European antitrust law.
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