Citalopram does not inhibit or induce CYP1A2, CYP3A4 and CYP2C9 in vivo. Risk for gastrointestinal adverse events in the form of nausea, diarrhoea, constipation and vomiting motivates vigilance against insufficient intake of food, especially of carbohydrate.

Citalopram is a selective serotonin (5-HT) reuptake inhibitor and is a racemic mixture. Citalopram is indicated for the treatment of depressive illness in the initial phase and as maintenance against potential relapse/recurrence, panic disorder with or without agoraphobia and obsessive compulsive disorder. Very common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are nausea, diarrhoea, vomiting and obstipation. Other common side effects are fatigue, reduced appetite, somnolence, insomnia, paraesthesia, myalgia, arthralgia and headache.

Citalopram is metabolised to the active demethylcitalopram by CYP2C19, CYP3A4 and CYP2D6. Citalopram and demethylcitalopram exhibits insignificant inhibition of CYP2C9, CYP2E1 and CYP3A4, and is a weak inhibitor of CYP1A2, CYP2C19 of CYP2D6 compared to other SSRI that are known to be significant inhibitors of these enzymes. Elimination half-life is about 1.5 days (SPC). When co-administrated, citalopram had no significantly effect on the pharmacokinetic characteristics of theophylline, a CYP1A2 substrate. This indicates that citalopram does not inhibit or induce CYP1A2 in vivo (Brøsen 2001 and Møller 2000). Citalopram did also not have any significant effect on the pharmacokinetics of carbamazepine, a CYP3A4 substrate (Brøsen 2001 and Møller 2001), or warfarin, a CYP2C9, CYP1A2 and CYP3A4 substrate (Brøsen 2001 and Priskorn 1997). This indicates that it does not inhibit or induce CYP2C9, CYP1A2 and CYP3A4 in vivo. A case study and a clinical study with co-administration of clozapine, a CYP1A2 substrate, and citalopram indicated conflicting results. The authors of the case study suggested that citalopram inhibited the metabolism of clozapine via CYP1A2 or CYP3A and therefore increased the serum concentrations of clozapine. The serum levels of clozapine without citalopram were however, not measured (Borba 2000 and Hilli 2009). The clinical study showed that there were no significant changes in plasma concentrations of clozapine when co-administrated with citalopram (Avenoso 1998 and Hilli 2009). This indicates that citalopram does not inhibit CYP1A2 in vivo.

Andersson; patient inquiry: used without ill effects (n=10); possible adverse reaction (n=1). Thunell: observation of possible biochemical activation (n=1).

Uneventful use reported in 11 patients with acute porphyria.