ORIGINAL ARTICLE

Escitalopram Treatment of Depression in Human

Immunodeficiency Virus/Acquired Immunodeficiency Syndrome
A Randomized, Double-Blind, Placebo-Controlled Study
Jacqueline Hoare, MD, FCPsych, Mphil,* Paul Carey, PhD, John A. Joska, MMed, FCPsych,*
Henri Carrara, MPH, Katherine Sorsdahl, PhD,* and Dan J. Stein, FCPsych, PhD*

Abstract: Depression can be a chronic and impairing illness in people with

human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome. Large randomized studies of newer selective serotonin reuptake inhibitors such as escitalopram in the treatment of depression in HIV, examining
comparative treatment efficacy and safety, have yet to be done in HIV-positive
patients. This was a fixed-dose, placebo-controlled, randomized, double-blind
study to investigate the efficacy of escitalopram in HIV-seropositive subjects
with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,
major depressive disorder. One hundred two participants were randomly
assigned to either 10 mg of escitalopram or placebo for 6 weeks. An analysis
of covariance of the completers found that there was no advantage for
escitalopram over placebo on the Montgomery-Asberg Depression Rating
Scale ( p = 0.93). Sixty-two percent responded to escitalopram and 59%
responded to placebo on the Clinical Global Impression Scale. Given the
relatively high placebo response, future trials in this area need to be selective
in participant recruitment and to be adequately powered.
Key Words: Randomized controlled study, depression, HIV
(J Nerv Ment Dis 2014;202: 133Y137)

epression can be a chronic and impairing illness in people living

with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS). Depression occurs in almost twice as
many people with HIV when compared with the general population
in the developed world (Ciesla and Roberts, 2001). In lower- and
middle-income countries, indications are that depression affects upward of 30% of HIV clinic attendees (Olley et al., 2004).
In a South African primary care context, identification of depression was generally poor (Carey et al., 2003) and perhaps even
worse in clinics focused on chronic medical illnesses including HIV
(Evans et al., 1996). Later in the illness, overlap with HIV symptoms
(Jacobsberg and Perry, 1992) and side effects from antiretroviral
treatment in more advanced disease may serve to complicate diagnosis (Kalichman et al., 2000). There is little doubt that a significant
proportion of patients with comorbid depression and HIV go
unrecognized and untreated.
Depression in HIV is associated with greater delays initiating
antiretroviral treatment (Fairfield et al., 1999) and poorer adherence

*Department of Psychiatry and Mental Health, University of Cape Town, Cape

Town, South Africa; Department of Psychiatry, Faculty of Health Sciences,
Stellenbosch University, Tygerberg Hospital, Cape Town, South Africa; and
School of Public Health and Family Medicine, University of Cape Town,
Cape Town, South Africa.
Send reprint requests to Jacqueline Hoare, MD, FCPsych, Mphil, Department of
Psychiatry and Mental Health, University of Cape Town, Anzio Road Observatory, 7925, Cape Town, South Africa. E-mail: hoare.jax@googlemail.com.
Copyright * 2014 by Lippincott Williams & Wilkins
ISSN: 0022-3018/14/20202Y0133
DOI: 10.1097/NMD.0000000000000082

The Journal of Nervous and Mental Disease

to antiretroviral medication (Gordillo et al., 1999). Depression is

important not only because of its psychological impact but also because of its impact on the course of HIV. Evidence suggests that
depression accelerates HIV disease progression (Leserman et al.,
1999) and is independently associated with increased HIV mortality
and a more rapid decline in CD4+ lymphocyte counts (Ickovics et al.,
2001). Compliant selective serotonin reuptake inhibitor (SSRI) use
has been associated with improved antiretroviral adherence and laboratory parameters (Horberg et al., 2008). It is possible that early and
effective treatment of depression in HIV may significantly improve
quality of life and that longer-term use may have an influence on HIV
disease progression and associated morbidity.
Expert consensus suggests that selective SSRIs are first-line
treatments of depression in HIV (Caballero and Nahata, 2004).
SSRIs may be as effective as and better tolerated than tricyclic antidepressants (TCAs) in HIV-positive adults (Caballero and Nahata,
2004). However, published controlled studies in this area are limited
to trials with fluoxetine versus placebo (Rabkin et al., 1999) and
paroxetine versus imipramine (Elliott et al., 1998), with comparable
response rates as in depressed cohorts without HIV. A recent metaanalysis of the use of SSRIs for depression in HIV argued that the
lack of data prevented conclusions being drawn on the most useful
SSRIs in this context (Ferrando and Freyberg, 2008). Because of
fluoxetines properties as an inhibitor of cytochrome P450 isoforms
2D6 and 3A4 and its long half-life, interactions with antiretrovirals
may occur. Newer SSRIs such as citalopram and escitalopram offer a
theoretically lower potential for drug-drug interactions, but large randomized studies examining comparative treatment efficacy and safety
have yet to be done in HIV-positive patients. A recent meta-analysis of
12 new-generation antidepressant drugs in non-HIV cohorts in the
treatment of depression found, for both efficacy and acceptability, in
favor of escitalopram and sertraline (Cipriani et al., 2009).
Escitalopram, the most selective SSRI available (Owens et al.,
2001), may offer a particular advantage for treating depression in
HIV. Aside from the established efficacy of escitalopram in non-HIV
depression (Burke et al., 2002; Lepola et al., 2003; Wade et al.,
2002), escitalopram mediates a more rapid and robust treatment response than its predecessor citalopram (Gorman et al., 2002) and
has only weak or negligible effects on hepatic enzymes crucial to the
metabolism of most medicines including those frequently used in
highly active antiretroviral therapy (Brosen and Naranjo, 2001;
Gutierrez et al., 2003; von Moltke et al., 2001). This drug-drug interaction remains relevant in South Africa because patients are still prescribed protease inhibitors (PIs). The South African antiretroviral
roll out programme consists of a nonnucleoside reverse transcriptase
inhibitor (NNRTI) based first-line regimen and a ritonavir-boosted
protease inhibitor (PI) containing second-line regimen. Ten milligrams of escitalopram per day is effective and well tolerated in the
treatment of depression in primary care (Burke et al., 2002).
Therefore, the present study aimed to investigate the efficacy
and tolerability of escitalopram for the treatment of Diagnostic and

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Hoare et al.

Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV ),

major depressive disorder (MDD) in people with stage III HIV
infection.

METHODS
This study was a fixed-dose, placebo-controlled, randomized,
double-blind study to investigate the efficacy of escitalopram in HIVseropositive subjects with DSM-IV MDD. Patients meeting inclusion
and exclusion criteria were recruited from primary and secondary
level clinics and then referred to Tygerberg Hospital, University of
Stellenbosch South Africa, to participate in this study. Participant
selection was a semirandom, convenience sample of consecutively
screened patients attending primary care antiretroviral therapy clinics
in Tygerberg Hospital and in the community clinics. Protocol was
approved by the ethics committee of the University of Stellenbosch,
and the patients signed informed written consent.

Participants
Eligible participants were HIV seropositive (World Health
Organization stage III); ranged in age from 18 to 60 years; and met
criteria for a DSM-IV diagnosis of a current major depressive episode
without psychosis, according to the Mini-international neuropsychiatric interview-plus neuropsychiatric interview. Exclusion criteria
included patients who currently or in the last 6 months have fulfilled
criteria for DSM-IV alcohol or substance abuse/dependence, lifetime
history of bipolar disorder, history of schizophrenia, or other psychotic disorders or dementia; patients presenting at screening with evidence of mild cognitive impairment and who were unable to score 10
or higher on the HIV Dementia Scale and 23 or higher on the MiniMental State Examination (MMSE); and patients with a positive
urine screen for any prohibited substance (including amphetamines,
barbiturates, cocaine, marijuana, methadone, opiates, phencyclidine, or
propoxyphene) or medication (benzodiazepines) at the screening visit.

Procedure
The participants received an initial screening and evaluation,
including a review of medical and psychiatric history. This first visit
was followed by 7 days (T3) of single-blind placebo to exclude early
placebo responders and to monitor compliance. Thereafter, the subjects were randomized to treatment of 10 mg per day of either
escitalopram or matching placebo for the full 6 weeks of the study.
Clinical examination (including full systemic examination,
weight, blood pressure, pulse, and electrocardiogram) and laboratory
tests (full blood count, electrolytes, renal function, liver function,
thyroid function tests, pregnancy screen, and urine drug screen) were
conducted at screening. HIV disease stage (CD4, CD8) was done at
baseline and at successful completion of the study as a final assessment, whereas efficacy measures were collected every week. Safety
and tolerability measures were done at weeks 1, 2, 4, and 6 by the
study nurse. Adherence was monitored in dispensing packs weekly
and with patient report.

Measures
Primary Outcome Measure
Montgomery-Asberg depression rating scale
The 10-item MADRS (Montgomery and Asberg, 1979) is
widely used and validated for assessing symptom severity in depression. It has been shown to be a reliable measure to detect depression in
HIV-positive subjects (Cockram et al., 1999) and has been found to
respond robustly to effective pharmacotherapy in a number of conditions with neurovegetative symptoms, including Parkinsons disease
(with a preponderance of subcortical cognitive decline; Leentjens et al.,
2003, 2000), headache (Walker et al., 1998), and cognitive impairment
(Gabryelewicz et al., 2004).
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Secondary Outcome Measures

Hospital anxiety and depression scale
The Hospital Anxiety and Depression Scale (Zigmond and
Snaith, 1983) is a reliable and well-validated self-report measure of
depressive and anxiety symptom severity in medically ill populations
including HIV (Savard et al., 1998).
Hamilton depression rating scale
The Hamilton Depression Rating Scale (Hamilton, 1960) is an
observer-rated 17-item measure of depression severity that reliably
differentiates depressed from nondepressed subjects in HIV disease
(Cockram et al., 1999) and other medical illnesses (Leentjens et al.,
2000) and has been widely used in treatment studies of depression in
HIV (Elliott et al., 1998; Rabkin et al., 1999; Zisook et al., 1998).
Clinical global impression scale of severity and improvement
The Clinical Global Impression Scale of Severity (CGI-S) and
Improvement (CGI-I; Guy, 1976) is a well-validated, clinician-rated
global assessment of disease severity (CGI-S) and improvement.
CGI responder status is defined as a week 6 score of 2 (much improved) or 1 (very much improved) in the global assessment of improvement (CGI-I) from baseline.
Sheehan disability scale
The Sheehan Disability Scale (SDS; Sheehan, 1983) is a
patient-rated three-item visual analog scale for assessing impairment
in the domains of work, family, and social life.
HIV dementia scale
The HIV Dementia Scale (HDS; Berghuis et al., 1999; Power
et al., 1995) is a brief and reliable measure of global cognitive
function that is reliably able to identify early cognitive decline of a
subcortical pattern.
Mini-Mental State Examination
The MMSE (Folstein et al., 1975) is a widely used and validated screening tool for cognitive impairment that was used in addition to the HDS. The MMSE is a reliable brief screening tool used
to identify cognitive decline of a cortical pattern. The pattern of HIVassociated brain loss may be changing from a subcortical to a cortical
disease among HIV-positive patients (Cohen et al., 2010). Assessment of cognitive functioning on all subjects at screening was designed
to exclude significant cognitive impairment that may negatively influence the ability to comply with the study protocol.
Blood was taken to measure CD4 and CD8 counts.

Analysis
All analyses were conducted using the Statistical Package for
the Social Sciences and Stata version 11.1 (StataCorp LP, 4905
Lakeway Dr, College Station, TX 77845). A sample size of 56 patients per treatment group was required to detect a 3-point difference
on MADRS scores at week 6 between the treatment and placebo
groups, with significance at 5% level, assuming a 20% dropout rate.
An intention-to-treat analysis was not conducted because of the very
low dropout rate. The efficacy of escitalopram over placebo was tested
using an analysis of covariance (ANCOVA) model including the
baseline score as a covariate. CD4 counts were square root transformed
to achieve a normal distribution, and all other outcome measures were
assessed to be normally distributed using the Shapiro-Wilks test. The
Friedmans test was conducted on the MMSE and the international HIV
dementia scale (IHDS) because the data were not normally distributed and could not be transformed to achieve a normal distribution.
Treatment-emergent adverse events (hereafter referred to as adverse
events) were analyzed. The chi-square test was performed for the incidence of adverse events in the escitalopram group versus that in the
placebo group.
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RESULTS
A total of 105 participants, predominantly women (86%),
participated in the study and were randomly assigned to either the
treatment or control groups. With three participants lost to follow-up
in the first 2 weeks (in the treatment group), a total of 102 patients
completed baseline and all weekly assessments (51 in the treatment
group and 51 in the control group). All participants included in the
study were 100% adherent to treatment. The dropout rate was 2.9%.
Reasons for loss to follow-up were unrelated to side effects, and all
three participants withdrew within the first 2 weeks of the first study
visit. Both groups were well matched regarding the baseline demographic characteristics and the mean group scores on the outcome
measures used in the study, with the exception of the CGI severity
measure, in which the mean for the treatment group (5.09) was significantly higher than that for the control group (4.74; Table 1).
The results of the ANCOVA models are presented in Table 2.
The primary efficacy analysis showed an adjusted mean change in
MADRS total score from baseline to week 6 of j14 points in the
escitalopram group and j13 points in the placebo group. The treatment
difference was not statistically significant ( p = 0.93). Given that the
MADRS was the primary outcome of interest, we further explored
this variable using cross-sectional time series regression analysis to
account for changes during the six visits. The results of this analysis did
not alter the conclusion that there was no statistically significant difference according to treatment group ( p = 0.2). The MADRS improved
over time in both the placebo and escitalopram groups, p G 0.001
(see Fig. 1). Similar findings were also reported for changes in SDS
( p 9 0.001) and HDS ( p 9 0.001) scores in both groups.
In addition, after controlling for baseline scores, there was no
significant effect of escitalopram on the remaining secondary outcome measures. Overall, 62% responded to escitalopram and 59%
responded to placebo on the CGI. Furthermore, the proportion of the
escitalopram-treated patients in complete remission (28%) was not
statistically significantly higher than that of the placebo-treated patients at week 6 (35%; p = 0.47).
Treatment-emergent side effects were relatively uncommon, and
the only one that differed between the treatment groups was nausea and

Escitalopram in HIV Depression

vomiting. Nausea and vomiting was more frequently reported in those

in taking escitalopram than the placebo group ( p = 0.012).

DISCUSSION
This study found no statistically significant advantage for
escitalopram over placebo in the treatment of depression in HIV. A
high placebo response (59%) was evident. There was also no significant effect of escitalopram on the remaining secondary outcome
measures. Treatment-emergent side effects were relatively uncommon, with nausea and vomiting more frequently reported in those
taking escitalopram than the placebo group. In terms of safety, the
study did not find a negative effect of escitalopram on CD4 cell
counts. However CD4 cell counts did not decline significantly over
time, and no positive effects on CD4 cell count were observed.
High placebo response rates have been reported in a number
of SSRI double-blind randomized controlled trials in HIV. In a previous randomized, double-blind, placebo-controlled prospective trial
examining the efficacy of fluoxetine in treating depression in HIVpositive subjects, Rabkin et al. (1999), in an intent-to-treat analysis,
found the difference between the fluoxetine and placebo groups in
improving depression to be nonsignificant. The failure of these differences to be ultimately significant was attributed to an unusually
high placebo response. Elliott et al. (1998), in a randomized, blinded,
placebo-controlled prospective trial comparing the efficacy of an
SSRI, paroxetine, versus a TCA, imipramine, showed that although
both paroxetine and imipramine were effective through week 8 of the
study, paroxetine was not superior to placebo at week 12; this finding
may be explained by an unusually high placebo response at week 12.
A range of factors may be contributing to the placebo response, including sex, empathy and compassion of the clinical staff, setting of the
trial, frequency of the visits, and severity of symptoms (Stein et al.,
2006). Of note is that the study participants in this trial were receiving
care that was significantly better than treatment as usual. Inadequate
services exist for the diagnosis, treatment, and management of mental
health problems in many clinics specializing in treatment of people
living with HIV. It is also notable that attrition of 2.9% was lower than
that reported in other studies of HIV-positive patients. It is our clinical

TABLE 1. Group Characteristics at Baseline

Escitalopram
n

Variable

Sex
Male
Female
Age, median (range)
Race
Black
White
Colored
Indian
MADRS, mean (SD)
HAM-D, mean (SD)
MMSE, median (range)
IHDS, median (range)
SDS total, mean (SD)
CD4 count, median (range)
CD8 count, mean (SD)
CGI severity, mean (SD)

n (%)

Control
n

n (%)

0.22
51
51
51
51

51
51
51
51
50
48
47
51

4 (7.8)
47 (92.2)
34 (23Y56)
35 (68.6)
1 (1.96)
12 (23.53)
1 (1.96)
31.73 (4.74)
21.33 (5.20)
29 (23Y30)
11 (10Y12)
20.80 (6.27)
425.5 (144Y1072)
1278.64 (535.86)
4.80 (0.80)

51
51
51
51

51
51
50
51
51
48
47
51

8 (15.7)
43 (84.3)
34 (24Y54)
28 (54.9)
0 (0)
21 (41.2)
0 (0)
30.11 (5.58)
19.64 (5.51)
29 (23Y30)
11.5 (10Y12)
18.76 (6.86)
350.5 (3Y1144)
1135.94 (526.69)
5.16 (0.73)

0.82
0.26

0.12
0.11
0.37
0.55
0.12
0.37
0.2
0.02*

*Significant difference at baseline.

HAM-D indicates 17-item Hamilton Depression Rating Scale.

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Hoare et al.

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TABLE 2. ANCOVA of Follow-up Scores as a Function of Treatment Baseline Scores as Covariate

Placebo
Baseline,
Mean (SD)

Outcome

MADRS
HAM-D
MMSEa
IHDSa
SDS total
CD4 count
CD8 count

51
30.1 (5.6)
51
19.6 (5.5)
50
29 (23Y30)
51
11.5 (10Y12)
51
18.8 (6.9)
48 404.1 (218.5)
47 1135.9 (526.7)

Follow-up,
Mean (SD)

50
17.0 (10.5)
50
11.8 (8.4)
43
29 (23Y30)
45
12 (9Y12)
49
13.9 (8.1)
41 436.8 (210.6)
41 1159.8 (486.1)

Escitalopram
Change From
Baseline

j13.2
j8
0
0.5
j4.6
43.3b
j13c

Baseline,
Mean (SD)

51
31.7 (4.7)
51
21.3 (5.2)
51
29 (23Y30)
51
11 (10Y12)
50
20.8 (6.3)
48 454.3 (29.5)
47 1278.6 (535.9)

Follow-up,
Mean (SD)

50
17.8
48
12.3
44
29
45
12
51 12.84
37 433.6
37 1205.8

(9.5)
(1.0)
(26Y30)
(10Y12)
(7.23)
(214.9)
(448.05)

Change From
Baseline

Treatment
Diff (SE)

j14
j9
0
1
j8.1
j10.7
j54.6

0.9 (2.0)
1.1 (1.7)
0.0
0.5
3.5 (1.8)
54.0 (35.6)
41.5 (90.4)

0.93
0.98
0.7
0.86
0.3
0.2
0.96

Not normally distributed; therefore, median and range were reported.

Complete data on 39 patients.
Complete data on 38 patients.
diff indicates difference.

b
c

impression that the excellent supportive care given by the study nurse to
the participants was crucial in retaining participants in the study;
however, possibly, it also responsible for the high placebo response rate.
If placebo responses in clinical trials are due to frequent patient evaluation and increased attention, then high placebo response rates underscore the power of the expectancy effect created by the relationship
with the trial team and the therapeutic context (Stein et al., 2006). A
review of the placebo response in escitalopram placebo-controlled trials
found that a higher placebo response rate was predicted by decreased
baseline disorder severity (Stein et al., 2006).
Our study is noteworthy in so far as it is one of the first
conducted in a lower- and middle-income country that comprises
predominantly African women. The participants were recruited from
primary and secondary level clinics specializing in treatment of
people living with HIV and were invited if they had a diagnosis of
depression. Recent studies showed that HIV-positive women may be
more likely to be on antiretroviral therapy (antiretroviral therapy;
Nattrass, 2006). For example, in South Africa, men who present for
antiretroviral therapy are sicker on average than women, suggesting
delays by men in getting tested or care seeking once tested (Bekker
et al., 2006). A study of HIV-positive men in the Cape Town area found
that additional barriers included the notion that clinics are places for
women and HIV/AIDS is a womens issue (Kagee et al., 2011). In a
cross-sectional study examining the correlates of depression in a public
sector antiretroviral program, most of the study participants were female (75.7%; Pappin et al., 2012). Previous studies on depression in
HIV have overrepresented gay/bisexual male participants and underrepresented female and African HIV-positive participants, possibly because of the fact that most studies have been conducted in
higher-income countries. Factors that may contribute to depression

FIGURE 1. MADRS improvement over time in both placebo

and treatment group.
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in this HIV-infected population include stigmatization, lack of social

support, and the death of a loved one from HIV/AIDS. Individuals
may therefore respond well to a supportive intervention of the kind
provided by a clinical research trial.

CONCLUSIONS
Future studies could focus on a longer treatment duration with
escitalopram or be more selective in participant recruitment. In this
case, a more selective approach would be to include only severe/
persistent MDD.
DISCLOSURES
This study was funded by Lundbeck. Lundbeck South Africa
(SA) is a subsidiary of H. Lundbeck A/S, an international, Danish,
research-based pharmaceutical company focusing on the central
nervous system. Jacqueline Hoare is funded by the Discovery Foundation. Dan J. Stein is funded by the Medical Research Council of
South Africa (MRC). John A. Joska is funded by the National Research Foundation of South Africa.
The authors declare no conflict of interest.
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