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Citalopram

A Review of its Pharmacology, Clinical Efficacy and Tolerability in the Treatment of Depression

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Abstract

Synopsis

Citalopram is a selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitor (SSRI) which has been evaluated primarily in the treatment of major depression. In well controlled short term studies, Citalopram had efficacy similar to that of a number of but not all, tricyclic or tetracyclic antidepressants and was as effective as fluoxetine and fluvoxamine. There is some evidence of a faster onset of action for Citalopram compared with fluoxetine. Initial data suggest that Citalopram is effective in the prevention of depressive relapse and in the treatment of post-stroke depression.

The anticholinergic and cardiovascular adverse events often seen with tricyclic antidepressants generally occur less frequently or are infrequent with Citalopram, as with other SSRIs. Citalopram has been well tolerated in the elderly and in patients with existing cardiovascular disease. In vitro and in vivo pharmacodynamic studies suggest that Citalopram is a weak inhibitor of cytochrome P450 (CYP) 2D6, and data from several interaction studies in patients and healthy volunteers are consistent with this finding.

Thus, Citalopram is an effective and well tolerated SSRI which, like the other members of its class, represents a suitable first-line therapy for major depression. Additional efficacy data would be beneficial in clarifying the potential of Citalopram in the elderly and in patients with post-stroke depression or preexisting cardiovascular disorders, for whom anticholinergic or cardiovascular adverse events (caused by tricyclic antidepressants) are a serious concern. The main distinguishing feature of Citalopram within its class is its apparent low propensity to cause problematic drug interactions with CYP2D6 substrates; these include a number of commonly prescribed drug classes, such as antipsychotics, tricyclic antidepressants, antiarrhythmics and β-blockers. Thus, Citalopram may prove useful in the many patients with depression who require one or more such agents for treatment of additional psychiatric or general disorders.

Pharmacodynamic Properties

Citalopram is a potent in vitro inhibitor of serotonin (5-hydroxytryptamine; 5-HT) uptake. Its activity in this respect is more than 3000 times greater than that against noradrenaline (norepinephrine) uptake, making it the most serotonin-selective agent in its class. Citalopram has low affinity in vitro for adrenergic, muscarinic, dopaminergic and serotonergic receptors. Evidence from behavioural studies in animals supports a selective facilitatory effect of Citalopram on serotonergic neurotransmission.

Citalopram is a weaker in vitro and in vivo inhibitor of the hepatic cytochrome P450 (CYP) 2D6 isozyme than paroxetine and fluoxetine and therefore has a lower potential for pharmacokinetic interactions with cytochrome CYP2D6 substrates such as tricyclic antidepressants and antipsychotic agents.

Pharmacokinetic Properties

Peak plasma concentrations of Citalopram are observed 2 to 4 hours after single or multiple oral doses and steady-state plasma concentrations are reached after about 1 week of daily administration. The plasma concentration-dose relationship for Citalopram is linear for doses of 10 to 60mg.

Citalopram is converted by hepatic CYP isozymes to the metabolites demethyl- and didemethyl-citalopram which are less lipophilic than the parent molecule (and are weaker serotonin reuptake inhibitors).

Preliminary indications suggest that Citalopram may cause only moderate pharmacokinetic interactions or have no effect when coadministered with tricyclic antidepressants which are metabolised by CYP2D6, although formal studies of such interactions are limited. Available data suggest that coadministration of Citalopram and antipsychotic agents does not cause any significant pharmacokinetic interactions.

The elimination half-life of Citalopram following oral administration is about 30 hours, with an estimated clearance of 26 to 28 L/h. Approximately 12% of an oral dose of Citalopram is excreted unchanged into the urine.

Aging appears to be associated with increased plasma concentrations and decreased clearance of Citalopram. Similar effects are seen in patients with renal or hepatic dysfunction.

Clinical Efficacy

In well controlled clinical studies, score reductions for the Hamilton Depression Rating Scale (HDRS) or Montgomery-Åsberg Depression Rating Scale (MADRS) ranged from about 43 to 81% with Citalopram and from about 56 to 71 % with tricyclic or tetracyclic antidepressants. In the largest comparative study published to date, reductions in HDRS scores after 6 weeks were similar for Citalopram and imipramine in more than 400 patients from general practice. Furthermore, the proportions of patients whose HDRS score was reduced by ≥50% were similar for Citalopram and imipramine. In smaller studies, Citalopram had end-point efficacy similar to that of amitriptyline or maprotiline (2 studies each), although comparisons with mianserin have produced somewhat contradictory findings. Citalopram was less effective than clomipramine in a single study. Results from meta-analyses indicate that Citalopram is broadly similar to tricyclic agents (amitriptyline, clomipramine, nortriptyline and imipramine) in its antidepressant efficacy in clinical trials.

Citalopram had overall efficacy similar to that of fluoxetine in general practice patients and in psychiatrie inpatients and outpatients. However, analysis of 3 different clinical parameters after 2 weeks indicated that the effects of Citalopram were achieved significantly faster than those of fluoxetine in the general practice study; no significant difference between the two treatment groups was apparent at subsequent timepoints. A comparison of Citalopram with fluvoxamine in patients with major depression demonstrated equivalent efficacy for the 2 drugs.

Tolerability

Data from clinical trials and meta-analyses suggest that nausea and vomiting (20% incidence in a meta-analysis of 746 patients), increased sweating, dry mouth and headache were the most common adverse events experienced by Citalopram recipients. The anticholinergic and cardiovascular adverse events often seen with tricyclic antidepressants (dry mouth, constipation, tachycardia, orthostatic hypotension) appear to occur less frequently or to be infrequent with Citalopram in most large studies. Data from 2 comparative studies suggest that there are no major differences in tolerability between Citalopram and fluoxetine, although vomiting during the first week of treatment was significantly more common in Citalopram recipients (3.8%) than in fluoxetine recipients (0%) in one study (the Citalopram dosage in this trial was twice that recommended for initial treatment). Nausea and diarrhoea were significantly more common in patients receiving fluvoxamine 100 to 200 mg/day than in those receiving Citalopram 20 to 40 mg/day in a single study (the starting dosage of fluvoxamine was twice that normally recommended). This difference was apparent at all timepoints for nausea, but had disappeared by week 6 for diarrhoea.

Clinical and postmarketing experience with Citalopram suggests that it is not associated with serious cardiovascular toxicity, and is well tolerated in patients with existing cardiovascular conditions, in those who are receiving drugs that may cause ECG abnormalities and in the elderly. Like the other SSRIs, Citalopram appears to be less toxic than tricyclic antidepressants when taken in overdose during suicide attempts.

Dosage and Administration

The recommended oral treatment regimen for Citalopram in depressed patients is 20 to 60mg once daily, titrated to therapeutic effect, with a minimum treatment period of 6 months to prevent relapse. Citalopram 20 to 30mg once daily is currently recommended for elderly patients. Dosage adjustments are not necessary in patients with mild or moderate renal impairment; information on the use of Citalopram in patients with severe renal dysfunction is lacking. Citalopram 20 to 30mg is recommended as the maximum dose in patients with impaired hepatic function. Citalopram should not be given to patients who are taking monoamine oxidase inhibitors.

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References

  1. Wade AG, Lepola U, Koponen HJ, et al. The effect of Citalopram in panic disorder. Br J Psychiatry 1997 Jun; 170(6): 549–53

    PubMed  CAS  Google Scholar 

  2. Lepola U, Leinonen E, Turtonen J, et al. The effect of Citalopram in panic disorder and agoraphobia: a pilot study [abstract]. Psychopharmacology 1993 Apr; 111: B7

    Google Scholar 

  3. Humble M, Wistedt B. Serotonin, panic disorder and agoraphobia: short-term and long-term efficacy of Citalopram in panic disorders. Int Clin Psychopharmacol 1992 Jun; 6 Suppl. 5: 21–39

    PubMed  Google Scholar 

  4. Nyth AL, Gottfries CG. The clinical efficacy of Citalopram in treatment of emotional disturbances in dementia disorders: a Nordic multicentre study. Br J Psychiatry 1990 Dec; 157: 894–901

    PubMed  CAS  Google Scholar 

  5. Vartiainen H, Tiihonen J, Putkonen A, et al. Citalopram, a selective serotonin reuptake inhibitor, in the treatment of aggression in schizophrenia. Acta Psychiatr Scand 1995; 91: 348–51

    PubMed  CAS  Google Scholar 

  6. Andersen G, Vestergaard K, Rils JO. Citalopram for post-stroke pathological crying. Lancet 1993 Oct 2; 342: 837–9

    PubMed  CAS  Google Scholar 

  7. Hyttel J, Bogeso KP, Perregaard J, et al. The pharmacological effect of Citalopram resides in the (S)-(+)-enantiomer. J Neural Transm Gen Sect 1992; 88(2): 157–60

    PubMed  CAS  Google Scholar 

  8. Goodwin GM. How do antidepressants affect serotonin receptors? The role of serotonin receptors in the therapeutic and side effect profile of the SSRIs. J Clin Psychiatry 1996; 57 Suppl. 4: 9–13

    PubMed  CAS  Google Scholar 

  9. Moret C, Briley M. Effects of acute and repeated administration of Citalopram on extracellular levels of serotonin in rat brain. Eur J Pharmacol 1996; 295: 189–97

    PubMed  CAS  Google Scholar 

  10. Auerbach SB, Hjorth S. Effect of chronic administration of the selective serotonin (5-HT) uptake inhibitor Citalopram on extracellular 5-HT and apparent autoreceptor sensitivity in rat forebrain in vivo. Naunyn Schmiedebergs Arch Pharmacol 1995; 352: 597–606

    PubMed  CAS  Google Scholar 

  11. Arborelius L, Nomikos GG, Hertel P, et al. The 5-HT1A receptor antagonist (S)-UH-301 augments the increase in extracellular concentrations of 5-HT in the frontal cortex produced by both acute and chronic treatment with Citalopram. Naunyn Schmiedebergs Arch Pharmacol 1996; 353: 630–40

    PubMed  CAS  Google Scholar 

  12. Hjorth S, Auerbach SB. 5-HT1A autoreceptors and the mode of action of selective serotonin reuptake inhibitors (SSRI). Behav Brain Res 1996; 73: 281–3

    PubMed  CAS  Google Scholar 

  13. Arborelius L, Nomikos GG, Grillner P, et al. 5-HT1A receptor antagonists increase the activity of serotonergic cells in the dorsal raphe nucleus in rats treated acutely or chronically with Citalopram. Naunyn Schmiedebergs Arch Pharmacol 1995; 352: 157–65

    PubMed  CAS  Google Scholar 

  14. Milne RJ, Goa KL. Citalopram: a review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in depressive illness. Drugs 1991 Mar; 41: 450–77

    PubMed  CAS  Google Scholar 

  15. Hyttel J. Pharmacological characterization of selective serotonin reuptake inhibitors (SSRIs). Int Clin Psychopharmacol 1994 Mar; 9 Suppl. 1: 19–26

    PubMed  Google Scholar 

  16. Richelson E, Pfenning M. Blockade by antidepressants and related compounds of biogenic amine uptake into rat brain synaptosomes: most antidepressants selectively block norepinephrine uptake. Eur J Pharmacol 1984; 104: 277–86

    PubMed  CAS  Google Scholar 

  17. Hyttel J. Citalopram — pharmacological profile of a specific serotonin uptake inhibitor with antidepressant activity. Prog Neuropsychopharmacol Biol Psychiatry 1982; 6: 277–95

    PubMed  CAS  Google Scholar 

  18. Richelson M, Nelson A. Antagonism by antidepressants of neurotransmitter receptors of normal human brain in vitro. J Pharmacol Exp Ther 1984; 230(1): 94–102

    PubMed  CAS  Google Scholar 

  19. Hall H, Sallemark M, Wedel I. Acute effects of atypical antidepressants on various receptors in the rat brain. Acta Pharmacol Toxicol Copenh 1984 May; 54: 379–84

    PubMed  CAS  Google Scholar 

  20. Hyttel J, Arnt J, Sánchez C. The pharmacology of Citalopram. Rev Contemp Pharmacother 1995; 6(6): 271–85

    CAS  Google Scholar 

  21. Hyttel J, Overø KF, Arnt J. Biochemical effects and drug levels in rats after long-term treatment with the specific 5-HT-up-take inhibitor, Citalopram. Psychopharmacology (Berl) 1984; 83: 20–7

    CAS  Google Scholar 

  22. Garcha G, Smokcum RW, Stephenson JD, et al. Effects of some atypical antidepressants on β-adrenoceptor binding and adenylate cyclase activity in the rat forebrain. Eur J Pharmacol 1985 Jan 15; 108: 1–7

    PubMed  CAS  Google Scholar 

  23. Luo H, Richardson JS. A pharmacological comparison of Citalopram, a bicyclic serotonin selective uptake inhibitor, with traditional tricyclic antidepressants. Int Clin Psychopharmacol 1993; 8(1): 3–12

    PubMed  CAS  Google Scholar 

  24. Vetulani J, Antkiewicz-Michaluk L, Rokosz-Pelc A. Chronic administration of antidepressant drugs increases the density of cortical [3H]prazosin binding sites in the rat. Brain Res 1984 Sep 24; 310: 360–2

    PubMed  CAS  Google Scholar 

  25. Gobbi M, Crespi D, Foddi MC, et al. Effects of chronic treatment with fluoxetine and Citalopram on 5-HT uptake, 5-HT1B autoreceptors, 5-HT3 and 5-HT4 receptors in rats. Naunyn Schmiedebergs Arch Pharmacol 1997; 356: 22–8

    PubMed  CAS  Google Scholar 

  26. Tiihonen J, Kuoppamäki M, Någren K, et al. Serotonergic modulation of striatal D2 dopamine receptor binding in humans measured with positron emission tomography. Psychopharmacology 1996; 126: 277–80

    PubMed  CAS  Google Scholar 

  27. Christensen AV, Fjalland B, Pedersen V, et al. Pharmacology of a new phthalane (Lu 10-171), with specific 5-HT uptake inhibiting properties. Eur J Pharmacol 1977; 41: 153–62

    PubMed  CAS  Google Scholar 

  28. Fairweather DB, Dal Pozzo C, Kerr JS, et al. Citalopram compared to dothiepin and placebo: effects on cognitive function and psychomotor performance. Hum Psychopharmacol 1997; 12: 119–26

    CAS  Google Scholar 

  29. Sindrup SH, Brøsen K, Hansen MG, et al. Pharmacokinetics of Citalopram in relation to the sparteine and the mephenytoin oxidation polymorphisms. Ther Drug Monit 1993 Feb; 15: 11–7

    PubMed  CAS  Google Scholar 

  30. Crewe HK, Lennard MS, Tucker GT, et al. The effect of selective serotonin re-uptake inhibitors on cytochrome P4502D6 (CYP2D6) activity in human liver microsomes. Br J Clin Pharmacol 1992 Sep; 34: 262–5

    PubMed  CAS  Google Scholar 

  31. Skjelbo E, Brosen K. Inhibitors of imipramine metabolism by human liver microsomes. Br J Clin Pharmacol 1992 Sep; 34: 256–61

    PubMed  CAS  Google Scholar 

  32. Jeppesen U, Gram LF, Vistisen K, et al. Dose-dependent inhibition of CYP1A2, CYP2C19 and CYP2D6 by Citalopram, fluoxetine, fluvoxamine and paroxetine. Eur J Clin Pharmacol 1996; 51: 73–8

    PubMed  CAS  Google Scholar 

  33. Priskorn M, Larsen F, Segonzac A, et al. Pharmacokinetic interaction study of Citalopram and Cimetidine in healthy subjects. Eur J Clin Pharmacol 1997; 52: 241–2

    PubMed  CAS  Google Scholar 

  34. Kragh-Sørensen P, Overø KF, Petersen OL, et al. The kinetics of Citalopram: single and multiple dose studies in man. Acta Pharmacol Toxicol Copenh 1981 Jan; 48: 53–60

    PubMed  Google Scholar 

  35. Citalopram Product Monograph, H. Lundbeck A/S, 1994

  36. Overø KF. Preliminary studies of the kinetics of Citalopram in man. Eur J Clin Pharmacol 1978 Nov 9; 14: 69–73

    PubMed  Google Scholar 

  37. de Wilde J, Mertens C, Overø KF, et al. Citalopram versus mianserin: a controlled, double-blind trial in depressed patients. Acta Psychiatr Scand 1985 Jul; 72: 89–96

    PubMed  Google Scholar 

  38. Bouchard JM, Delaunay J, Delisle JP, et al. Citalopram versus maprotiline: a controlled, clinical multicentre trial in depressed patients. Acta Psychiatr Scand 1987 Nov; 76: 583–92

    PubMed  CAS  Google Scholar 

  39. Gravem A, Amthor KF, Astrup C, et al. A double-blind comparison of Citalopram (Lu 10-171) and amitriptyline in depressed patients. Acta Psychiatr Scand 1987 May; 75: 478–86

    PubMed  CAS  Google Scholar 

  40. Ahlfors UG, Elovaara S, Harma P, et al. Clinical multicentre study of Citalopram compared double-blindly with mianserin in depressed patients in Finland. Nord Psykiatr Tidsskr 1988; 42: 201–10

    Google Scholar 

  41. Overø KF. Kinetics of Citalopram in man; plasma levels in patients. Prog Neuropsychopharmacol Biol Psychiatry 1982; 6: 311–8

    Google Scholar 

  42. Bjerkenstedt L, Flyckt L, Overø KF, et al. Relationship between clinical effects, serum drug concentration and serotonin uptake inhibition in depressed patients treated with Citalopram: a double-blind comparison of three dose levels. Eur J Clin Pharmacol 1985; 28: 553–7

    PubMed  CAS  Google Scholar 

  43. Baumann P, Larsen F. The pharmacokinetics of Citalopram. Rev Contemp Pharmacother 1995; 6(6): 287–95

    CAS  Google Scholar 

  44. Leinonen E, Lepola U, Koponen H, et al. The effect of age and concomitant treatment with other psychoactive drugs on serum concentrations of Citalopram measured with a non-enantioselective method. Ther Drug Monit 1996; 18: 111–7

    PubMed  CAS  Google Scholar 

  45. Rochat B, Amey Y, Baumann P. Analysis of enantiomers of Citalopram and its demethylated metabolites in plasma of depressive patients using chiral reverse-phase liquid chromatography. Ther Drug Monit 1995; 17: 273–9

    PubMed  CAS  Google Scholar 

  46. Rochat B, Amey H, Van Gelderen H, et al. Determination of the enantiomers of Citalopram, its demethylated and propionic acid metabolites in human plasma by chiral HPLC. Chirality 1995; 7: 389–95

    PubMed  CAS  Google Scholar 

  47. Kobayashi K, Yamamoto T, Chiba K, et al. The effects of selective serotonin reuptake inhibitors and their metabolites on S-mephenytoin 4′-hydroxylase activity in human liver microsomes. Br J Clin Pharmacol 1995; 40: 481–5

    PubMed  CAS  Google Scholar 

  48. Kobayashi K, Chiba K, Yagi T, et al. Identification of cytochrome P450 isoforms involved in Citalopram N-demethylation by human liver microsomes. J Pharmacol Exp Ther 1997; 280(2): 927–33

    PubMed  CAS  Google Scholar 

  49. Rudorfer MV, Potter WZ. Pharmacokinetics of antidepressants. In: Meltzer HY, editor. Psychopharmacology: the third generation of progress. New York: Raven Press, 1987: 1353–63

    Google Scholar 

  50. Øyehaug E, Østensen ET, Salvesen B. High-performance liquid chromatographic determination of Citalopram and four of its metabolites in plasma and urine samples from psychiatric patients. J Chromatogr 1984 Jun 8; 308: 199–208

    PubMed  Google Scholar 

  51. Overø KF, Toft B, Christophersen L, et al. Kinetics of Citalopram in elderly patients. Psychopharmacology 1985; 86: 253–7

    Google Scholar 

  52. Foglia JP, Pollock BG, Kirshner MA, et al. Psychopharmacology in geriatric populations. Psychopharmacol Bull 1997; 33(1): 109–12

    PubMed  CAS  Google Scholar 

  53. Syvälahti EKG, Taiminen T, Saarijärvi S, et al. Citalopram causes no significnt alterations in plasma neuroleptic levels in schizophrenic patients. J Int Med Res 1997 Jan/Feb; 25(1): 24–32

    PubMed  Google Scholar 

  54. Baettig D, Bondolfi G, Montaldi S, et al. Tricyclic antidepressant plasma levels after augmentation with Citalopram: a case study. Eur J Clin Pharmacol 1993; 44(4): 403–5

    PubMed  CAS  Google Scholar 

  55. Gram LF, Hansen MGJ, Sindrup SH, et al. Citalopram: interaction studies with levomepromazine, imipramine, and lithium. Ther Drug Monit 1993 Feb; 15: 18–24

    PubMed  CAS  Google Scholar 

  56. Bondolfi G, Chautems C, Rochat B, et al. Non-response to Citalopram in depressive patients: pharmacokinetic and clinical consequences of a fluvoxamine augmentation. Psycho-pharmacology 1996; 128: 421–5

    CAS  Google Scholar 

  57. Priskhorn M, Sidhu JS, Larsen F, et al. Investigation of multiple dose Citalopram on the pharmacokinetics and pharmacodynamics of racemic warfarin. Br J Clin Pharmacol 1997; 44: 199–202

    Google Scholar 

  58. Hamilton M. Development of a rating scale for primary depressive illness. Br J Soc Clin Psychol 1967; 6: 278–96

    PubMed  CAS  Google Scholar 

  59. Montgomery SA, Åsberg M. A new depression scale designed to be sensitive to change. Br J Psychiatry 1979; 134: 382–9

    PubMed  CAS  Google Scholar 

  60. Guy W, editor. ECDEU assessment manual for psychopharmacology. Clinical Global Impressions (028-CGI). Washington, DC: USGPO, 1976

    Google Scholar 

  61. Feighner J, Overø K, Fieve R, et al. Fixed dose comparison of Citalopram versus placebo in the treatment of outpatients with moderate to severe depression [poster no. 419]. Presented at 150th Annual Meeting, American Psychiatric Association; 1997; San Diego

    Google Scholar 

  62. Mendels J, Overø K, Kiev A, et al. Citalopram versus placebo in the treatment of outpatients with moderate to severe depression [poster no. 465]. Presented at 150th Annual Meeting, American Psychiatric Association; 1997; San Diego

    Google Scholar 

  63. Andersen G, Vestergaard K, Lauritzen L. Effective treatment of poststroke depression with the selective serotonin reuptake inhibitor Citalopram. Stroke 1994 Jun; 25: 1099–104

    PubMed  CAS  Google Scholar 

  64. Montgomery SA, Rasmussen JGC, Lyby K. Dose response relationship of Citalopram 20mg, Citalopram 40mg and placebo in the treatment of moderate and severe depression. Int Clin Psychopharmacol 1992 Jun; 6 Suppl. 5: 65–70

    PubMed  Google Scholar 

  65. Nyth AL, Gottfries CG, Lyby K, et al. A controlled multicenter clinical study of Citalopram and placebo in elderly depressed patients with and without concomitant dementia. Acta Psychiatr Scand 1992 Aug; 86: 138–45

    PubMed  CAS  Google Scholar 

  66. Bech P, Cialdella P. Citalopram in depression — meta-analysis of intended and unintended effects. Int Clin Psychopharmacol 1992 Jun; 6 Suppl. 5: 45–54

    PubMed  Google Scholar 

  67. Montgomery SA, Pedersen V, Tanghøj P, et al. The optimal dosing regimen for Citalopram — a meta-analysis of nine placebo-controlled studies. Int Clin Psychopharmacol 1994 Mar; 9 Suppl. 1: 35–40

    PubMed  Google Scholar 

  68. Baumann P, Nil R, Souche A, et al. A double-blind, placebocontrolled study of Citalopram with and without lithium in the treatment of therapy-resistant depressive patients: a clinical, pharmacokinetic, and pharmacogenetic investigation. J Clin Psychopharmacol 1996; 16: 307–14

    PubMed  CAS  Google Scholar 

  69. Montgomery SA, Rasmussen JG, Tanghoj P. A 24-week study of 20mg Citalopram, 40mg Citalopram, and placebo in the prevention of relapse of major depression. Int Clin Psychopharmacol 1993 Fall; 8: 181–8

    PubMed  CAS  Google Scholar 

  70. Robert P, Montgomery SA. Citalopram in doses of 20-60mg is effective in depression relapse prevention: a placebo-controlled 6 month study. Int Clin Psychopharmacol 1995; 10 Suppl. 1: 29–35

    PubMed  Google Scholar 

  71. Shaw DM, Thomas DR, Briscoe MH, et al. A comparison of the antidepressant action of Citalopram and amitriptyline. Br J Psychiatry 1986 Oct; 149: 515–7

    PubMed  CAS  Google Scholar 

  72. Danish University Antidepressant Group. Citalopram: clinical effect profile in comparison with clomipramine: a controlled multicenter study. Psychopharmacology 1986; 90: 131–8

    Google Scholar 

  73. Rosenberg C, Damsbo N, Fuglum E, et al. Citalopram and imipramine in the treatment of depressive patients in general practice: a Nordic multicentre clinical study. Int Clin Psychopharmacol 1994 Mar; 9 Suppl. 1: 41–8

    PubMed  Google Scholar 

  74. Timmerman L, de Beurs P, Tan BK, et al. A double-blind comparative clinical trial of Citalopram vs maprotiline in hospitalized depressed patients. Int Clin Psychopharmacol 1987 Jul; 2: 239–53

    PubMed  CAS  Google Scholar 

  75. Anderson IM, Tomenson BM. The efficacy of selective serotonin re-uptake inhibitors in depression: a meta-analysis of studies against tricyclic antidepressants. J Psychopharmacol 1994; 8(4): 238–49

    PubMed  CAS  Google Scholar 

  76. Nuijten MJC, Hardens M, Souêtre E. A Markov process analysis comparing the cost effectiveness of maintenance therapy with Citalopram versus standard therapy in major depression. Pharmacoeconomics 1995; 8(2): 159–68

    PubMed  CAS  Google Scholar 

  77. Patris M, Bouchard J-M, Bougerol T, et al. Citalopram versus fluoxetine: a double-blind, controlled, multicentre, phase III trial in patients with unipolar depression treated in general practice. Int Clin Psychopharmacol 1996; 11: 129–36

    PubMed  CAS  Google Scholar 

  78. Bougerol T, Scotto J-C, Patris M, et al. Citalopram and fluoxetine in major depression: comparison of two clinical trials in a psychiatrist setting and in general practice. Clin Drug Invest. In press

  79. Haffmans PMJ, Timmerman L, Hoogduin CAL, et al. Efficacy and tolerability of Citalopram in comparison with fluvoxamine in depressed outpatients: a double-blind, multicentre study. Int Clin Psychopharmacol 1996; 11: 157–64

    PubMed  CAS  Google Scholar 

  80. Dencker SJ, Petersen HEH. Side-effect profile of Citalopram and reference antidepressants in depression. XXII Nordiske Psykiater-Kongres; 1988 Aug 10–13; Reykjavik, 31–42

    Google Scholar 

  81. Baldwin D, Johnson FN. Tolerability and safety of Citalopram. Rev Contemp Pharmacother 1995; 6(6): 315–25

    CAS  Google Scholar 

  82. Rudorfer MV, Manji HK, Potter WZ. Comparative tolerability profiles of the newer versus older antidepressants. Drug Saf 1994 Jan; 10: 18–46

    PubMed  CAS  Google Scholar 

  83. Lauerma H. Successful treatment of citalopram-induced anorgasmia by cyproheptadine. Acta Psychiatr Scand 1996; 93: 69–70

    PubMed  CAS  Google Scholar 

  84. Michael A, Herrod JJ. Citalopram-induced decreased libido [letter]. Br J Psychiatry 1997 Jul; 171: 90

    PubMed  CAS  Google Scholar 

  85. Berk M, Acton M. Citalopram-associated clitoral priapasm: a case series. Int Clin Psychopharmacol 1997; 12: 121–2

    PubMed  CAS  Google Scholar 

  86. Bouwer CD, Harvey BH. Phasic craving for carbohydrate observed with Citalopram. Int Clin Psychopharmacol 1996; 11: 273–8

    PubMed  CAS  Google Scholar 

  87. Risby E, Donnigan D, Nemeroff C. Pharmacotherapeutic considerations for psychiatric disorders: depression. Formulary 1997 Jan; 32: 46–59

    CAS  Google Scholar 

  88. Øström M, Erikkson A, Thorson J, et al. Fatal overdose with Citalopram [letter]. Lancet 1996 Aug 3; 348: 339–40

    PubMed  Google Scholar 

  89. Grundemar L, Wohlfart B, Lagerstedt C, et al. Symptoms and signs of severe Citalopram overdose. Lancet 1997 May 31; 349: 1602

    PubMed  CAS  Google Scholar 

  90. Personne M, Persson H, Sjöberg G. Citalopram toxicity [letter]. Lancet 1997 Aug 16; 350: 518–9

    PubMed  CAS  Google Scholar 

  91. Neuvonen PJ, Pohjola-Sintonen S, Tacke U, et al. Five fatal cases of serotonin syndrome after moclobemide-citalopram or moclobemide-clomipramine overdoses. Lancet 1993 Dec 4; 342: 1419

    PubMed  CAS  Google Scholar 

  92. Greenberg PE, Stiglin LE, Finkelstein SN, et al. The economic burden of depression in 1990. J Clin Psychiatry 1993 Nov; 54: 405–18

    PubMed  CAS  Google Scholar 

  93. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Arch Gen Psychiatry 1994 Jan; 51: 8–19

    PubMed  CAS  Google Scholar 

  94. Broadhead WE, Blazer DG, George LK, et al. Depression, disability days, and days lost from work in a prospective epidemiological survey. JAMA 1990 Nov 21; 264: 2524–8

    PubMed  CAS  Google Scholar 

  95. Kupfer DJ. Long-term treatment of depression. J Clin Psychiatry 1991 May; 52(5 Suppl.): 28–34

    PubMed  Google Scholar 

  96. Hirschfeld RMA. Long-term drug treatment of unipolar depression. Int Clin Psychopharmacol 1996; 11: 211–7

    PubMed  CAS  Google Scholar 

  97. Cohen LJ. Rational drug use in the treatment of depression. Pharmacotherapy 1997; 17(1): 45–61

    PubMed  CAS  Google Scholar 

  98. Sussman N, Stahl S. Update in the pharmacotherapy of depression. Am J Med 1996 Dec 30; 101 Suppl. 6A: 26S–36S

    PubMed  CAS  Google Scholar 

  99. de Jonghe F, Swinkels J. Selective serotonin reuptake inhibitors: relevance of differences in their pharmacological and clinical profiles. CNS Drugs 1997 Jun; 7(6): 452–67

    Google Scholar 

  100. van den Berg SJ. Comparing SSRIs: from chemistry to clinical choice. Hum Psychopharmacol 1995; 10: S199–209

    Google Scholar 

  101. van Harten J. Clinical pharmacokinetics of selective serotonin reuptake inhibitors. Clin Pharmacokinet 1993 Mar; 24: 203–20

    PubMed  Google Scholar 

  102. Baumann P, Rochat B. Comparative pharmacokinetics of selective serotonin reuptake inhibitors: a look behind the mirror. Int Clin Psychopharmacol 1995; 10 Suppl. 1: 15–21

    PubMed  Google Scholar 

  103. Brøsen K. The pharmacogenetics of the selective serotonin reuptake inhibitors. Clin Investig 1993 Dec; 71: 1002–9

    PubMed  Google Scholar 

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Correspondence to Stuart Noble.

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Various sections of the manuscript reviewed by: U.G. Ahlfors, Hesperia Hospital, Helsinki, Finland; G. Andersen, Department of Neurology, Aarhus Kommunehospital, Aarhus, Denmark; P. Baumann, Unité de Biochimie et Psychopharmacologie Clinique, Département Universitaire de Psychiatrie Adulte, Prilly-Lausanne, Switzerland; P. Bech, Department of Psychiatry, Frederiksborg General Hospital, Hillerød, Denmark; K. Brøsen, Department of Clinical Pharmacology, Odense University, Odense, Denmark; G.D. Burrows, Department of Psychiatry, University of Melbourne, Heidelberg, Victoria, Australia; F. de Jonghe, Psychiatrisch Ziekenhuis, Amsterdam, The Netherlands; R.R. Kydd, Department of Psychiatry and Behavioural Science, School of Medicine, University of Auckland, Auckland, New Zealand; S.A. Montgomery, Department of Psychiatry, St Mary’s Hospital Medical School, London, England; W.Z. Potter, Section on Clinical Pharmacology, National Institute of Mental Health, Bethesda, Maryland, USA; E. Richelson, Departments of Psychiatry and Pharmacology, Mayo Clinic and Foundation, Rochester, Minnesota, USA.

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Noble, S., Benfield, P. Citalopram. CNS Drugs 8, 410–431 (1997). https://doi.org/10.2165/00023210-199708050-00009

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