Journal of Sex & Marital Therapy, 31:257–262, 2005Copyright 2005 Brunner-RoutledgeISSN: 0092-623X printDOI: 10.1080/00926230590513474
Improvements in SSRI/SNRI-Induced Sexual Dysfunction by Switching to Escitalopram School of Medicine, State University of New York at Buffalo, Buffalo, New York, USAAntidepressants, especially serotonin reuptake inhibiting agents,are associated with sexual dysfunction. The newest drug of thisclass, escitalopram, claims greater tolerability than older alterna-tives. This study evaluated patient experiences with switching fromone serotonin enhancing antidepressant to escitalopram in indi-viduals who already were complaining of antidepressant-inducedsexual dysfunction. We found that 68.1% of patients experiencedimprovement with their sexual function. The ability to obtain a sat-isfactory clinical response at relatively low doses may explain thisfinding. We performed gender, phase of sexual response, and doseanalyses. This article discusses results and significance.
Sexual dysfunction is a common side effect of selective serotonin reuptakeinhibiting/serotonin norepinephrine reuptake inhibiting antidepressants(SSRI/SNRI; Clayton et al., 2002). Unfortunately, this side effect tends notto wear off. The largest published study to date revealed that only 9.8% ofpatients taking SSRI/SNRIs had this side effect dissipate, even when thesepatients were followed up for up to 38 months (Ashton & Rosen, 1998). Sexual dysfunction is among the top three side effects that patients withdepression wish to avoid when taking antidepressants (Jamerson et al.,2001). Given patients’ desire to avoid or manage this chronic, difficult-to-live-with side effect, a number of strategies have been developed (Ashton,Young, & LoPiccolo, 2001; Balon, 1995). One strategy commonly employedis selecting an antidepressant less likely to cause sexual dysfunction (Balon,1995). Unfortunately, if a patient requires a serotonin agent, it is not clear
Address correspondence to Adam Keller Ashton, Clinical Professor of Psychiatry, State Uni-
versity of New York at Buffalo, School of Medicine, 6245 Sheridan Dr., Suite 316, Williamsville,NY, 14221.
that substituting any particular alternative SSRI/SNRI is helpful. Althoughindividual patients may lose this side effect, these antidepressants as a classcommonly cause the same sexual problems. One recently published reportdescribed a single case of reversal of fluoxetine-induced sexual dysfunctionby switching to the newest SSRI, escitalopram (Ashton, 2004). We reporthere an expansion of this analysis to 47 consecutively treated psychiatricpatients. To evaluate likelihood of reversal of SSRI/SNRI-induced sexualdysfunction, we switched them to a dose of escitalopram required to treattheir primary psychiatric diagnosis.
We systematically evaluated over 1,000 medical charts of an outpatient psy-chiatric private practice for reports of sexual dysfunction. Charts were re-viewed for diagnoses, type, and dose of SSRI/ SNRI and adjunctive medi-cations. Demographic data, including marital status, age, and gender wereobtained at baseline. SSRI/SNRI-induced sexual dysfunction was defined asa new impairment in libido, arousal, or orgasm appearing within 4 weeksof beginning treatment with an SSRI or SNRI. Ratings of improvement werebased on clinical interviews by each patient’s treating psychiatrist.
We found 47 charts in which patients were switched to escitalopram
because of SSRI/SNRI-induced sexual dysfunction, with and without con-comitant lack of efficacy in managing symptoms of the primary psychiatricdisorder. All were included in data analysis. Diagnoses included, in de-creasing order of occurrence (n), major depressive disorder (15), obsessive-compulsive disorder (15), dysthymia (14), panic disorder (9), generalizedanxiety disorder (8), social anxiety disorder (2), posttraumatic stress disor-der (1), and undifferentiated somatoform disorder (1). In addition, somepatients had more than one diagnosis. Using a visual analog scale, we di-vided patients into categories of worsening, no improvement, mild improve-ment, or much improvement in sexual dysfunction symptoms of impairedlibido, arousal, and orgasm after switch to escitalopram. Ratings of improve-ments were based on clinical interviews by the patient’s treating psychiatrist. These patients were followed for at least 2–3 months after switch to escitalo-pram for reports on sexual dysfunction symptoms. Dose of escitalopram wasstarted at 10 mg q.d. and adjusted based on clinical response. The data of pa-tients enrolled with SSRI/SNRI-induced sexual dysfunction are summarizedin Figure 1.
Our study revealed that 32 of 47 (68.1%) patients showed mild or markedimprovement in SSRI/SNRI-induced sexual dysfunction by switching their
Improvements in SSRI/SNRI-Induced Sexual DysfunctionSEXUAL DYSFUNCTION: SSRI/SNRI USED SSRI/SNRI USED SSRI/SNRI USED SEXUAL DYSFUNCTION SEXUAL DYSFUNCTION FIGURE 1. Sexual dysfunction and SSRI/SNRI use in 47 patients
original serotonin agent to escitalopram. In contrast, 15 of 47 (31.9%) patientsdid not find this improved their sexual functioning. Subanalysis revealed avariety of interesting data. Dose required to treat the primary psychiatricdisorder appeared to play a role in whether patients showed improvementin sexual dysfunction. As seen in Table 1, 19 of 26 (73.1%) patients on 10 mgshowed mild or marked improvement in sexual functioning versus 12 of 19(63.2%) patients on 20 mg and 1 of 2 (50%) patients on 30 mg of escitalopram. When one looks at degree of response according to patient self-report, 15of 26 (57.7%) patients at the 10 mg dose described “much improvement.”At 20 mg, 10 of 19 (52.6%) patients described this degree of response. At30 mg, 0 of 2 (0%) patients reported much improvement, again suggestingthat a lower dose may result in a greater degree of success in reversingSSRI/SNRI-induced sexual dysfunction.
Gender analysis also appeared to show a trend toward male response
over female response, although the study was not designed or powered toshow statistical differences. Table 2 reveals that 20 of 26 men (76.9%), com-pared with 12 of 21 women (57.1%), showed mild or much improvementin SSRI/SNRI-induced sexual dysfunction in switching to escitalopram. Four-teen of 15 men (93.3%) on 10 mg of escitalopram showed mild or muchimprovement versus 6 of 12 women (50%). At 20 mg, 6 of 11 men (54.5%)
TABLE 1. Comparison of Dose of Escitalopram and Change in Sexual Dysfunction TABLE 2. Comparison of Improvement in Sexual Dysfunction Based on Dose and Gender after Switch to Escitalopram
showed mild or much improvement in SSRI/SNRI-induced sexual dysfunc-tion, compared with 5 of 7 women (71.4%). No men were taking 30 mg ofescitalopram, however, 1 of 2 women (50%) showed improvement at thisdose.
The final analysis examined improvement in SSRI/SNRI-induced sexual
dysfunction depending on phase of sexual response impaired. We reportedcomparable results regardless of which phase was impacted. Among thosewhose desire was impaired, 13 of 24 patients (54.2%) described mild ormuch improvement by switching to escitalopram. For those with arousaldysfunction, 8 of 11 patients (72.7%) reported this response. For those withorgasm dysfunction, described as delayed or absent orgasm, 26 of 37 patients(70.3%) described improvement. The total number of sexual complaints ex-ceeded the number of patients enrolled because many patients describedmore than one SSRI/SNRI-induced sexual dysfunction. In all, there were 72sexual complaints (1.53 per patient) prior to initiation of escitalopram and 25complaints (0.53 per patient) after switch to escitalopram, a 65.3% reduction,comparable to the 68.1% improvement in percentage of patients who expe-rienced improvement in sexual dysfunction after switching to escitalopram. This data is shown in Table 3.
This study described extent of changes, if any, in sexual dysfunction inpatients exhibiting a vulnerability to SSRI/SNRI-induced sexual dysfunction
TABLE 3. Change in Type of Sexual Com- plaint before and after Switch to Escitalopram Improvements in SSRI/SNRI-Induced Sexual Dysfunction
by switching from their original agent to escitalopram in clinically effec-tive dosages. The majority of patients in this trial exhibited mild or markedimprovement in sexual dysfunction by discontinuing their SSRI/SNRI andcommencing on a trial of escitalopram. It is notable that no one described aworsening of sexual dysfunction after switch to escitalopram.
The likely explanation for the degree of improvement in sexual dysfunc-
tion on escitalopram is the fact that most patients (27/47, 57.4%) could bemaintained on a 10 mg dose. Because sexual dysfunction is thought to be adose-related side effect, a lower dose is less likely to cause problems than ahigher dose. Certainly, there may be other mechanisms that are responsiblefor the lower likelihood of sexual dysfunction caused by escitalopram, butthese have yet to be identified.
There are obvious limitations to this study. Lack of a placebo-control
restricts a clearer interpretation of this data. Certainly, many of these patientscould have displayed a placebo response, although their historic impair-ment would suggest, if anything, a higher risk of SSRI/SNRI-induced sexualdysfunction then in a na¨ıve population; if so, this low rate of escitalopram-induced sexual dysfunction betters the incidence seen in other large-scalestudies (Clayton et al., 2002; Montejo-Gonzalez et al., 1997).
These patients may not yet have developed an escitalopram-induced
sexual dysfunction, although this side effect usually, begins within the firstmonth of initiating treatment with an offending agent (Coleman et al., 1999;Croft et al., 1999), and this study followed patients for at least 2 to 3 months inall cases and followed many patients for over 12 months. Also, because all ofthese patients entered the study already suffering from a medication-inducedsexual dysfunction, one could speculate that this is a population that wouldbe more likely to continue to experience sexual dysfunction when placedon a medication with a mechanism of action similar to the original offendingagent.
Perhaps this was not a representative clinical population; thus, the results
may not be applicable to a wider population. However, the fact that over halfof the patients had more than one Axis I diagnosis and most were middleaged population would more likely make it difficult to achieve improvementin sexual dysfunction. A psychiatrically sicker and older group, in fact, shouldincrease failure rate simply by raising the likelihood of a negative samplingbias caused by co-prescribing of other agents and age effect. The greaterpercentage of males enrolled in this study potentially affects our ability toextrapolate this data to the usual psychiatric patient demographic that wouldnormally reflect a higher percentage of female patients. Nevertheless, thefemale response, although not as robust, mimicked that seen in males.
Future studies, preferably large scale and with a placebo control, would
be helpful in further identifying the extent of improvement that patients couldexpect by following the protocol described in this article. Use of a validatedtool to assess sexual functioning prior to and following a switch may also
clarify these issues and would be more useful in additional, active comparatortrials. Our study revealed that patients who experience SSRI/SNRI-inducedsexual dysfunction are no worse and are frequently less impaired by switch-ing to escitalopram. This is especially true if the dose does not need to bemaximized.
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