Escitalopram is an inhibitor of CYP1A2 in vivo, but is not listed as a mechanism-based inhibitor of CYP1A2 or any other major CYP enzymes. Risk for gastrointestinal adverse events in the form of nausea, diarrhoea, constipation and vomiting motivates vigilance against insufficient intake of food, especially of carbohydrate.

Escitalopram is the S-enantiomer of citalopram and a selective serotonin (5-HT) reuptake inhibitor.

Escitalopram is indicated for the treatment of major depressive episodes, panic disorder, social anxiety disorder, generalised anxiety disorder and obsessive-compulsive disorder. 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, constipation and vomiting. Other common side effects are reduced or increased appetite, insomnia, somnolence, dizziness, paraesthesia, tremor, arthralgia, myalgia, fatigue and pyrexia.

Escitalopram is mainly metabolised by CYP2C19 with minor contribution by CYP3A4 and CYP2D6 (SPC). It is metabolised to S-demethylcitalopram and S-didemthylcitalopram which has no pharmacological activity in vivo (Pastoor 2014). Half-life elimination is approximately 30 hours. In vitro studies have shown that escitalopram and its metabolites are negligible inhibitors of CYP2C19 (SPC), CYP1A2, CYP2C9, and CYP3A4 (Spina 2012). Others have shown that escitalopram does not inhibit CYP3A4, CYP1A2, CYP2C19 and CYP2E1 in vitro (Pastoor 2014). Escitalopram did not significantly affect the pharmacokinetics of ritonavir, a CYP3A4 substrate, when co-administrated (Gutierrez 2003 and Rao 2007). This indicates that escitalopram is not an inhibitor or inducer of CYP3A4 in vivo. Escitalopram increased the AUC of rasagiline (CYP1A2 substrate) by 42% when co-administrated (Hilli 2009 and Spina 2012). This indicates that escitalopram is an inhibitor of CYP1A2 in vivo. It is however, not listed as a mechanism-based inhibitor of CYP1A2, or inhibitor or inducer of any other major CYP enzymes (FDA, Hisaka 2010, Isoherranen 2009 and Pelkonen 2008). Another in vivo study showed that escitalopram increased the serum concentration of apiprazole (CYP3A4 and CYP2D6 substrate) by 20% when co-administrated (Spina 2012). Escitalopram is listed as a weak inhibitor of CYP2D6 in vivo (FDA, Isoherranen 2009 and SPC).

Uneventful use reported in 7 patients with acute porphyria.