Escitalopram is the (S)-enantiomer of the racemic selective serotonin reuptake inhibitor antidepressant citalopram. Clinical studies have shown that escitalopram is effective and well tolerated in the treatment of depression and anxiety disorders. Following oral administration, escitalopram is rapidly absorbed and reaches maximum plasma concentrations in approximately 3–4 hours after either single-or multiple-dose administration. The absorption of escitalopram is not affected by food. The elimination half-life of escitalopram is about 27–33 hours and is consistent with once-daily administration. Steady-state concentrations are achieved within 7–10 days of administration. Escitalopram has low protein binding (56%) and is not likely to cause interactions with highly protein-bound drugs. It is widely distributed throughout tissues, with an apparent volume of distribution during the terminal phase after oral administration (Vz/F) of about 1100L. Unmetabolised escitalopram is the major compound in plasma. S-demethylcitalopram (S-DCT), the principal metabolite, is present at approximately one-third the level of escitalopram; however, S-DCT is a weak inhibitor of serotonin reuptake and does not contribute appreciably to the therapeutic activity of escitalopram. The didemethyl metabolite of escitalopram (S-DDCT) is typically present at or below quantifiable concentrations. Escitalopram and S-DCT exhibit linear and dose-proportional pharmacokinetics following single or multiple doses in the 10–30 mg/day dose range. Adolescents, elderly individuals and patients with hepatic impairment do not have clinically relevant differences in pharmacokinetics compared with healthy young adults, implying that adjustment of the dosage is not necessary in these patient groups. Escitalopram is metabolised by the cytochrome P450 (CYP) isoenzymes CYP2C19, CYP2D6 and CYP3A4. However, ritonavir, a potent inhibitor of CYP3A4, does not affect the pharmacokinetics of escitalopram. Coadministration of escitalopram 20mg following steady-state administration of cimetidine or omeprazole led to a 72% and 51% increase, respectively, in escitalopram exposure compared with administration alone. These changes were not considered clinically relevant. In vitro studies have shown that escitalopram has negligible inhibitory effects on CYP isoenzymes and P-glycoprotein, suggesting that escitalopram is unlikely to cause clinically significant drug-drug interactions. The favourable pharmacokinetic profile of escitalopram suggests clinical utility in a broad range of patients.

The Clinical Pharmacokinetics of Escitalopram

The pharmacokinetics of escitalopram (S-citalopram) and its principal metabolite, S-demethylcitalopram (S-DCT), were investigated after intravenous and oral administration to healthy subjects. After intravenous infusion of escitalopram, the mean systemic clearance and volume of distribution were 31 L/h and 1,100 L, respectively. After oral administration of single or multiple doses, the absorption was relatively fast, with the maximum observed plasma or serum concentration (C(max)) attained after 3 to 4 hours. The mean half-lives were 27 and 33 hours, respectively; steady state was attained within 10 days. The area under the plasma or serum concentration time curve from time zero to 24 hours and C(max) was both linear and proportional to the dose. The apparent volume of distribution was around 20 L/kg. Comparison of the systemic and oral clearance implied a high absolute bioavailability. There was no evidence of interconversion from S-citalopram to R-citalopram either in plasma or in urine. Concurrent intake of food had no effect on the pharmacokinetics of escitalopram or its metabolite. All treatments were well tolerated.

The pharmacokinetics of escitalopram after oral and intravenous administration of single and multiple doses to healthy subjects.

SummaryBackground
The scale of depression in patients with chronic liver disease (CLD) and those who have received orthotopic liver transplantation (OLT) is poorly characterised Clinicians are uncertain of how best to manage depression within these patients

Aims
To review the literature evaluating both the prevalence and impact of depression in patients with CLD and post-OLT, and to assess the safety and efficacy of antidepressant use within this context

Methods
A PubMed search using the phrases ‘chronic liver disease’, ‘cirrhosis’, ‘liver transplantation’, ‘depression’, ‘antidepressant’ and the names of specific causes of liver disease and individual antidepressants

Results
Over 30% of cirrhotic patients have depressive features, and they experience worse clinical outcomes than nondepressed cirrhotic patients CLD patients with chronic hepatitis C are particularly prone to depression, partly related to the use of interferon therapy OLT patients with depression have higher mortality rates than nondepressed patients; appropriate antidepressant use reverses this effect Selective serotonin reuptake inhibitors (SSRIs) and selective noradrenaline reuptake inhibitors (SNRIs) are effective and generally safe in both CLD and OLT patients

Conclusions
Depression is much more prevalent in CLD or OLT patients than is generally recognised, and it adversely affects clinical outcomes The reasons for this relationship are complex and multifactorial Antidepressants are effective in both CLD and post-OLT, although lower doses or a reduced dosing frequency may be required to minimise side effects, eg exacerbation of hepatic encephalopathy Further research is needed to establish optimal management of depression in these patients, including the potential role of nonpharmacological treatments

https://onlinelibrary.wiley.com/doi/pdf/10.1111/apt.12925

Review article: depression and the use of antidepressants in patients with chronic liver disease or liver transplantation.

According to the World Health Organization, depression is one of the most debilitating disorders affecting humankind. The social and economic costs of chronic ill health resulting from untreated or inadequately treated depression are considerable and frequently underestimated.

The CINP established the Task Force on Antidepressant Medications in 2004 to examine all aspects of therapy with antidepressant drugs. This was considered necessary as, despite the availability of effective antidepressants for the past 50 years, a substantial minority of depressed patients either remains untreated or under treated. As the only international organization devoted to the promotion of research, education and the applications of neuropsychopharmacology to the clinic, the main task of the CINP is to extend the knowledge of the drugs that are available with the aim of improving the management of mental disorders. The purpose of this Task Force document was not to produce an academic monograph nor a set of guidelines, but to provide mental health and other professionals with comprehensive and objective information about the different aspects of the use of antidepressants important in clinical practice.

The Task Force consisted of 15 experts in psychiatry, psychopharmacology, public health, economics and family care. The majority of its members are senior members of the CINP. The Task Force was also advised to rely in the course of its work on advisors in different countries selected because of their outstanding expertise in the matters covered by the review. The report presented here was approved by the Executive Committee and the Council of the CINP at its meeting in Chicago in July 2006.

As a service to those engaged in mental health care and to ensure maximum impact, the Task Force review is being published as a supplement to the CINP's journal, the International Journal of Neuropsychopharmacology. In addition, the information will later …

Antidepressant medications and other treatments of depressive disorders: a CINP Task Force report based on a review of evidence

Citalopram is a selective serotonin re-uptake inhibitor that has demonstrated antidepressant efficacy in numerous controlled clinical trials. Additional studies have shown that the drug benefits patients with other illnesses that are related in some way to serotonergic dysfunction, including anxiety, panic disorder, obsessive-compulsive disorder, premenstrual dysphoria, alcohol dependence and the behavioural disturbances of dementia. This paper reviews the full spectrum of citalopram's clinical efficacy, as well as its safety and tolerability, in a range of patients.

Citalopram: a comprehensive review.

Objective: To compare the pharmacokinetics of the antidepressant citalopram and its metabolites demethylcitalopram and didemethylcitalopram in subjects with moderate renal insufficiency and subjects with hepatic cirrhosis with that in healthy subjects. Methods: Pharmacokinetic parameters from three individual, open-label, phase I trials were derived following single oral or intravenous citalopram dose (40 mg) to healthy subjects and a single oral dose (20 mg) to patients. Serum and urine concentrations of citalopram and metabolites were determined using a validated HPLC method. Results: The absolute bioavailability of citalopram tablets in healthy subjects was 80%. The renal clearance was a minor component (<20%) of the total elimination of citalopram. Serum Cmax and t

 max for citalopram were essentially unaffected by the occurrence of renal or hepatic disease. In comparison with healthy subjects, renal impairment was associated with a significant reduction in the renal elimination of citalopram and its two metabolites and a slight prolongation of serum citalopram t

 1/2 (49.5 h vs 36.8 h in healthy subjects).␣Cirrhosis resulted in significant decrease in citalopram CLoral␣(0.21 vs 0.33 l · h−1· kg−1 in healthy subjects) and increase in Vz· f −1, with an approximately twofold increase in t

 1/2 (83.4 h vs 36.8 h in healthy subjects). Indices of renal (creatinine or 51Cr-EDTA clearances) and hepatic (galactose elimination capacity or Child-Pugh score) function were poor predictors of the changes in the pharmacokinetics of citalopram and its metabolites in these populations. Conclusion: No reduction of citalopram dosage is warranted in patients with moderately impaired renal function. However, that may not apply for patients with severe renal failure. In patients with impaired hepatic function, prescription of a lower dosage of citalopram may be appropriate.

Single-dose pharmacokinetics of citalopram in patients with moderate renal insufficiency or hepatic cirrhosis compared with healthy subjects.

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Single-dose pharmacokinetics of citalopram in patients with moderate renal insufficiency or hepatic cirrhosis compared with healthy subjects.