Comparison of citalopram and other selective serotonin reuptake inhibitor ingestions in children

Abstract

Context. In adults, citalopram is more likely to cause seizures and ECG changes than other selective serotonin reuptake inhibitors (SSRIs). Data in children are lacking, yet the 2007 American Association of Poison Control Centers out-of-hospital citalopram consensus guideline mirrors the guideline for other SSRIs. Objective. To compare the clinical effects and hazard index of citalopram with other SSRIs in pediatric ingestions. Methods. An 11-year retrospective analysis of national poison center data was conducted. Acute, known-type SSRI ingestions in children younger than 6 years with known outcome were included. Clinical effects and hazard index (number of major or fatal outcomes/1000 SSRI ingestions) were compared. Citalopram dose-response was evaluated. Results. The 35 296 included cases by SSRI type were citalopram (3747), escitalopram (4815), fluoxetine (5946), fluvoxamine (273), paroxetine (7157), and sertraline (13 358). The overall hazard index was 0.340. The hazard index for citalopram (0.801) was 2.8-fold higher than for non-citalopram SSRIs (0.285). Comparing seizures (single or multiple discrete) and cardiac effects (conduction disturbances, other ECG changes or other dysrhythmia) of citalopram with the other SSRIs, pediatric citalopram ingestions were more likely to develop seizures (5 of 3747 [0.13%] vs. 10 of 31 549 [0.03%], OR = 4.2; 1.4–12.3) and cardiac toxicity (9 of 3747 [0.24%] vs. 25 of 31 549 [0.08%], OR = 3.0; 1.4–6.5). Clinical effects occurring more frequently with other SSRIs included tachycardia (p = 0.0236), oral irritation (p = 0.0412), vomiting (p = 0.0036), agitation/irritability (p = 0.0104), and hyperthermia (p = 0.0314). There was a dose response only for single or multiple discrete seizures, mydriasis and clinically significant responses (a predetermined subset of CNS and cardiopulmonary clinical effects). Meaningful triage thresholds for citalopram could not be determined due to the low frequency of significant clinical effects. Conclusion. Children develop minimal toxicity with SSRI ingestions. Seizures and ECG changes, while uncommon, occur more frequently with citalopram. Doses associated with significant outcomes suggest that the triage guideline for citalopram does not need to be modified.     

Use of selective serotonin-reuptake inhibitors in the treatment of depression in adults with HIV

OBJECTIVE: To review the safety and efficacy of selective serotonin-reuptake inhibitors (SSRIs) for the treatment of depression in adults with HIV. DATA SOURCES: We searched Pre-MEDLINE and MEDLINE (1966-May 2004) using terms including generic names of antidepressants and antiretrovirals, depression, HIV, and acquired immunodeficiency syndrome. All English-language articles were included in this review. DATA SYNTHESIS: SSRIs may be effective and better tolerated than tricyclic antidepressants in HIV-positive adults. SSRIs did not appear to affect CD4+ cell counts. CONCLUSIONS: Controlled trials comparing SSRIs are lacking; thus, it is difficult to determine whether one SSRI is more efficacious than another. It appears that most SSRIs may be used in HIV-positive adults. If drug-drug interactions are a concern, sertraline, citalopram, and possibly escitalopram may be considered.     

Anxiolytic-like effects of escitalopram, citalopram, and R-citalopram in maternally separated mouse pups

The S-enantiomer of citalopram, escitalopram, is a selective serotonin reuptake inhibitor (SSRI) that appears to be responsible for citalopram's antidepressant and anxiolytic effects. Clinically, escitalopram is reported to have fewer adverse side effects than do other SSRIs. This study compared escitalopram to other antidepressants in a preclinical procedure predicting anxiolytic-like effects of drugs. Carworth Farms Webster (CFW) mouse pups (7 days old) were separated from the dam and maintained at a temperature of 34 degrees C. Forty-five minutes after administering citalopram (0.56-10 mg/kg), escitalopram (0.0056-3 mg/kg), R-citalopram (1-10 mg/kg), paroxetine (0.3-3 mg/kg), fluoxetine (1-30 mg/kg), or venlafaxine (3-56 mg/kg) subcutaneously, the pups were placed individually on a 19.5 degrees C surface for 4 min. Ultrasonic vocalizations (USVs) (30-80 kHz), grid crossing, rolling (i.e., the pup turned on one side or its back), and colonic temperature were recorded. All the drugs reduced USV emission; escitalopram was the most potent (ED(50) 0.05 mg/kg), followed by paroxetine (0.17 mg/kg), citalopram (1.2 mg/kg), fluoxetine (4.3 mg/kg), R-citalopram (6 mg/kg), and venlafaxine (7 mg/kg). The doses that decreased USVs differed from those that increased motor activity. Increased grid crossing occurred after low doses of paroxetine (0.03 or 0.1 mg/kg) and fluoxetine (1 mg/kg), but only after the highest doses of the citalopram enantiomers and venlafaxine (0.3, 10, and 56 mg/kg, respectively). Except for escitalopram and venlafaxine, high doses of the treatments increased rolling. R-Citalopram caused a 10-fold rightward shift in escitalopram's dose-effect curve, suggesting that R-citalopram inhibits escitalopram's anxiolytic-like effects. These data support clinical findings that escitalopram is a potent, well tolerated SSRI with anxiolytic-like effects.     

Selective Serotonin Reuptake Inhibitor Use and Risk of Arrhythmia: A Nationwide,Population-Based Cohort Study

PurposeThis study compares the risks of arrhythmia among patients with depression receiving selective serotonin reuptake inhibitors (SSRIs) and those receiving other classes of antidepressants and among patients with depression receiving citalopram-escitalopram and those receiving other SSRIs.MethodsThis retrospective cohort study used data from the 2000–2011 National Health Insurance Research Database in Taiwan. Patients with depression who were new antidepressant users were included in the study sample. Propensity score matching was used to balance the covariates between the comparison groups. Crude incidence rates were generated by Poisson regressions, and Cox proportional hazards regression models were used to assess the rates of arrhythmia among SSRI users and nonusers of SSRI antidepressants as well as between citalopram-escitalopram users and users of other SSRIs.FindingsNeither SSRI (hazard ratio [HR] = 0.95; 95% CI, 0.83–1.08) nor citalopram-escitalopram (HR = 1.20; 95% CI, 0.95–1.51) exposure was associated with a risk of arrhythmia compared with other, newer non-SSRI antidepressants or noncitalopram SSRIs. An increase in mortality was, however, observed among citalopram-escitalopram users (HR = 1.21; 95% CI, 1.08–1.31).ImplicationsCitalopram, escitalopram, and other SSRIs were not associated with an elevated risk of arrhythmia compared with each other or with non-SSRI antidepressants. Nevertheless, citalopram and escitalopram were associated with an increase in mortality risk compared with other SSRIs and deserve further investigation.     

Glycine and a glycine dehydrogenase (GLDC) SNP as citalopram/escitalopram response biomarkers in depression: pharmacometabolomics-informed pharmacogenomics

Major depressive disorder (MDD) is a common psychiatric disease. Selective serotonin reuptake inhibitors (SSRIs) are an important class of drugs used in the treatment of MDD. However, many patients do not respond adequately to SSRI therapy. We used a pharmacometabolomics-informed pharmacogenomic research strategy to identify citalopram/escitalopram treatment outcome biomarkers. Metabolomic assay of plasma samples from 20 escitalopram remitters and 20 nonremitters showed that glycine was negatively associated with treatment outcome (P = 0.0054). This observation was pursued by genotyping tag single-nucleotide polymorphisms (SNPs) for genes encoding glycine synthesis and degradation enzymes, using 529 DNA samples from SSRI-treated MDD patients. The rs10975641 SNP in the glycine dehydrogenase (GLDC) gene was associated with treatment outcome phenotypes. Genotyping for rs10975641 was carried out in 1,245 MDD patients in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, and its presence was significant (P = 0.02) in DNA taken from these patients. These results highlight a possible role for glycine in SSRI response and illustrate the use of pharmacometabolomics to "inform" pharmacogenomics.     

Citalopram in the treatment of depression

OBJECTIVE: To review the efficacy and safety of citalopram in the treatment of depression. DATA SOURCES: MEDLINE search (1966-April 2000), Current Contents search, additional references listed in articles, and unpublished data obtained from the manufacturer were used to identify data from scientific literature. Studies evaluating citalopram (i.e., abstracts, clinical trials, data on file with the manufacturer) were considered for inclusion. STUDY SELECTION: English-language literature was reviewed to evaluate the pharmacology, pharmacokinetics, therapeutic use, and adverse effects of citalopram. DATA EXTRACTION: Controlled animal and human clinical studies published in the English-language literature were reviewed and evaluated. Clinical trials selected for inclusion were limited to those in human subjects and included data from animals if human data were not available. DATA SYNTHESIS: Citalopram is an antidepressant belonging to the class of selective serotonin-reuptake inhibitors (SSRIs) available for the treatment of depression. Citalopram offers therapeutic efficacy similar to that of the other SSRIs and a more favorable adverse effect profile than that of the tricyclic antidepressants (TCAs). Citalopram does not cause anticholinergic or cardiovascular adverse effects associated with the TCAs. Citalopram is the most selective SSRI and, unlike other SSRIs, seems to be relatively free of interaction mediated by the cytochrome P450 system. Citalopram is also the least expensive antidepressant available to date. This review of citalopram includes data from clinical trials comparing safety, tolerability, efficacy, and pharmacoeconomics with TCAs and SSRIs. CONCLUSIONS: Clinical trials demonstrate that citalopram's therapeutic efficacy is significantly greater than that of placebo and is comparable with that of other antidepressants. Citalopram has a favorable adverse effect profile, and thus may be useful in treating depressed patients who cannot tolerate anticholinergic or cardiovascular adverse effects associated with TCAs. It may also be useful in patients with comorbid illnesses requiring concomitant medicines.     

Patient compliance with SSRIs and gabapentin in painful diabetic neuropathy

BACKGROUND: Anticonvulsants are widely used for treatment of painful diabetic neuropathy. Selective serotonin reuptake inhibitors (SSRIs) are not first-line drugs but are commonly prescribed medicines for chronic pain. The majority of patients are hesitant to use these drug groups, thus their compliance remains an issue. OBJECTIVE: To compare patient compliance and the effectiveness of 2 SSRIs (paroxetine or citalopram) and 1 anticonvulsant (gabapentin) in patients with painful diabetic neuropathy. METHODS: This was a 6 months prospective trial in 101 patients with painful diabetic neuropathy and minimum score of 2 on a pain intensity scale ranging of 0 to 4. Compliance was assessed with patient interviews and pill counts. Adverse events, early discontinuation or satisfaction with treatment were also evaluated. RESULTS: Patients receiving SSRIs reported greater satisfaction and fewer concerns of the side-effects with their treatment (P<0.05) compared with the patients taking gabapentin. There was statistically significant better mood in the SSRI group (P<0.05). Overall, 43.5% of those taking SSRIs noticed no effect on the pain control, 50% felt better, and 6.5% felt worse. Among the patients taking gabapentin, 51% felt better, 40.5% noticed no effect, and 8.5% felt worse. Finally, on the pill count, more patients on SSRIs (93.5%) than on gabapentin (82.9%) were taking over the 75% of their medication (P<0.05). CONCLUSIONS: The lack of negative effects on quality of life, the better compliance, and the comparable efficiency of SSRIs suggest that these drugs may be considered as alternative to gabapentin in painful diabetic neuropathy.     

Relative Toxicity of Selective Serotonin Reuptake Inhibitors (SSRIs) in Overdose

Background: Selective serotonin reuptake inhibitors (SSRIs) have increasingly replaced tricyclic antidepressants (TCAs) in the treatment of depression. They appear to be safer in overdose, but there is little information on their spectrum of toxicity in overdose, or relative toxicity of each agent. Objective: To determine the effect of SSRIs in overdose, as a group, and the relative toxicity of five different SSRIs. Methods: A review of consecutive SSRI poisoning admissions to a single toxicology unit. Outcomes examined were length of stay [LOS], intensive care [ICU] admission rate, coma, seizures, electrocardiographic [ECG] abnormalities, and presence of serotonin syndrome [SS]. Logistic regression was used to model the outcome QTc > 440 msec. Results: There were 469 SSRI poisoning admissions analyzed after exclusions. The median LOS for all SSRI overdose admissions was 15.3 h (IQR: 10.5–21.3) and 30 of 469 (6.4%; 95% CI 4.3–9.0%) cases were admitted to ICU. The incidence of seizures was 1.9% and coma was 2.4%. Serotonin syndrome occurred in 14% of overdoses. Comparison of median QTc intervals of the five SSRIs was significantly different (p = 0.0002); citalopram (450 IQR: 436–484) was individually different to fluoxetine (p = 0.045), fluvoxamine (p = 0.022), paroxetine (p = 0.0002), and sertraline (p = 0.001). The proportion of citalopram overdoses with a QTc > 440 msec was 68%, differing significantly from sertraline (adjusted OR: 5.11 95% CI 2.32–11.27). Comparison of median QT intervals of the five SSRIs was statistically different (p = 0.026); citalopram (400 IQR: 380–440) was individually different from sertraline (p = 0.023). Conclusions: This study shows SSRIs are relatively safe in overdose despite serotonin syndrome being common. The exception was citalopram, which was significantly associated with QTc prolongation. We believe that cardiac monitoring should be considered in citalopram overdose, particularly with large ingestions and patients with associated cardiac disease.     

Differential effect of local infusion of serotonin reuptake inhibitors in the raphe versus forebrain and the role of depolarization-induced release in increased extracellular serotonin

Systemic administration of selective serotonin reuptake inhibitors (SSRIs) elicits larger increases in serotonin (5-HT) in raphe than in forebrain sites. Because serotonergic neuronal activity is suppressed, the mechanism underlying SSRI-induced increases in extracellular 5-HT is unclear. This study determined whether local infusion of SSRIs also elicited regionally selective increases in extracellular 5-HT, and whether changes depended on serotonergic neuronal depolarization. Conventional microdialysis methods were used to measure 5-HT in dorsal raphe (DRN), median raphe, nucleus accumbens (NAcc), and frontal cortex of unanesthetized rats. During infusion of SSRIs into each site, the maximum response was an approximately 6- to 7-fold increase in 5-HT in NAcc and frontal cortex, and an approximately 20-fold increase in DRN and median raphe. The larger increase in 5-HT in raphe was confirmed using zero-net-flux microdialysis. In NAcc, baseline 5-HT was 0.7 nM, and levels increased to a maximum of 3.1 nM during infusion of the SSRI citalopram. Baseline 5-HT in DRN was greater, 1.3 nM, and increased to 12.4 nM in response to citalopram. Consistent with evidence that autoreceptor activation inhibits serotonergic neuronal discharge, SSRI infusion into DRN produced a moderate decrease in 5-HT in NAcc. However, increases in 5-HT in DRN elicited by SSRI infusion were attenuated by 8-hydroxydipropylaminotetralin and tetrodotoxin. These data indicate that depolarization-dependent 5-HT release was not fully inhibited during SSRI infusion into DRN. In summary, SSRIs produce larger increases in extracellular 5-HT in raphe than in forebrain sites. Increases depend in part on depolarization-induced release, which may be greater in raphe than in forebrain.     

Serotonin syndrome caused by interaction between citalopram and fentanyl

OBJECTIVE: To report a case of serotonin syndrome associated with interaction between fentanyl and citalopram, as evidenced by medication history, clinical features and reversal following discontinuation of fentanyl. CASE SUMMARY: A 65-year-old patient chronically treated with the selective serotonin reuptake inhibitor (SSRI) citalopram developed confusion, agitation, tachycardia, tremors, myoclonic jerks and unsteady gait, consistent with serotonin syndrome, following initiation of fentanyl, and all symptoms and signs resolved following discontinuation of fentanyl. Based on the Naranjo probability scale, serotonin syndrome was a probable adverse reaction associated with co-administration of citalopram and fentanyl. DISCUSSION: Serotonin syndrome is a potentially lethal pharmacodynamic interaction between medications that increase serotonergic transmission at the synaptic junction. The development of new pharmacological agents with varied properties and actions has increased the risk of serotonin syndrome as a clinical diagnosis. SSRIs and fentanyl are commonly co-administered, especially in the setting of chronic or malignant pain, as underlying depression may contribute to the pathogenesis of pain. CONCLUSION: Healthcare professionals should be aware of the possible development of serotonin syndrome as a complication of initiation of fentanyl and other phenylpiperidine opioids in patients treated with SSRIs.     

Selective serotonin-reuptake inhibitors in the treatment of premature ejaculation

OBJECTIVE: To review the use of selective serotonin-reuptake inhibitors (SSRIs) in the treatment of premature ejaculation. DATA SOURCES: Articles were retrieved through a MEDLINE search (1966-January 2004). Search terms used to identify articles included serotonin uptake inhibitors, premature ejaculation, rapid ejaculation, and sexual behavior, as well as the generic names of currently available SSRIs: fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, and escitalopram. The literature search was limited to articles published in the English language containing human subjects. STUDY SELECTION AND DATA EXTRACTION: Articles obtained through the literature search were evaluated, and randomized controlled trials were included in this review. Information from noncontrolled trials or case reports was considered for inclusion if it contributed to the completeness of this review and if it was the highest level of evidence available. DATA SYNTHESIS: Premature ejaculation is a commonly reported sexual difficulty. Delayed ejaculation is a widely reported sexual adverse effect of SSRIs. In some men exhibiting premature ejaculation, the ability of the SSRIs to delay ejaculation has been therapeutic. Trials evaluating the ejaculation-delaying ability of SSRIs demonstrated that paroxetine, fluoxetine, sertraline, and citalopram produce a statistically significant increase in the ejaculation latency time compared with placebo. CONCLUSIONS: Taking advantage of the ejaculation-delaying effects of SSRIs increases the treatment options available to prescribers and patients. Convenience and minimal adverse effect profile make these agents an alternative to previously used behavior modalities and older pharmacologic agents. Although some questions still surround the details of their use, SSRIs have the potential to improve the quality of life for men with premature ejaculation and their partners.     

Premature ejaculation associated with citalopram withdrawal

OBJECTIVE: To report a case of premature ejaculation occurring subsequent to citalopram discontinuation.CASE SUMMARY: A 43-year-old white man being treated for depression with citalopram wished to discontinue treatment. Four or 5 days after stopping citalopram he reported that, during sexual intercourse, his genitals seemed to be extremely sensitive and orgasm was achieved within approximately 1 minute. These symptoms continued over the next 3-4 weeks and remitted after citalopram was restarted. Several subsequent attempts to discontinue citalopram resulted in a return of these symptoms despite using a slow tapering regimen. An objective causality assessment revealed a probable relationship between drug withdrawal and the observed symptoms.DISCUSSION: The ability of selective serotonin-reuptake inhibitors (SSRIs) to delay ejaculation has been well documented; however, discontinuation of these agents generally results in a return to baseline function. Although discontinuation of SSRI therapy has been associated with a number of withdrawal symptoms, this is the first report (MEDLINE, September 2003), to our knowledge, of the emergence of sexual adverse effects in someone with no previous history of these symptoms.CONCLUSIONS: Premature ejaculation is a possible withdrawal effect after SSRI discontinuation. Since patients are usually reluctant to spontaneously report sexual adverse effects, it is important to specifically inquire about them both when starting and stopping treatment with an SSRI.     

Treating functional impairment of autism with selective serotonin-reuptake inhibitors

OBJECTIVE: To review literature describing use of selective serotonin-reuptake inhibitors (SSRIs) in the management of functional impairments associated with autistic disorder. DATA SOURCES: EMBASE (1980-3rd quarter of 2003), International Pharmaceutical Abstracts (1970-August 2003), and MEDLINE (1966-August 2003) were searched. Search terms included autism, autistic disorder, citalopram, fluoxetine, fluvoxamine, paroxetine, selective serotonin-reuptake inhibitors, and sertraline. DATA SYNTHESIS: Studies and case reports evaluating treatment outcomes associated with the use of SSRIs in managing impairments of autism were reviewed. Multiple SSRI dosing ranges were evaluated in autistic patients of different ages with various functional impairments. No specific SSRI or dose range has been shown to improve a specific autistic symptom although some patients have demonstrated improvements. CONCLUSIONS: Benefits with SSRIs in treating functional impairments in autism have been observed. Response to therapy and adverse effects are individualized. Current evidence does not support selection of one SSRI over another for any impairment associated with autism.     

Pharmacokinetics of selective serotonin reuptake inhibitors

The five selective serotonin reuptake inhibitors (SSRIs), fluoxetine, fluvoxamine, paroxetine, sertraline, and citalopram, have similar antidepressant efficacy and a similar side effect profile. They differ, however, in their pharmacokinetic properties. Under steady-state concentrations, their half-lives range between 1 and 4 days for fluoxetine (7 and 15 days for norfluoxetine) and between 21 (paroxetine) and 36 (citalopram) hr for the other SSRIs. Sertraline and citalopram show linear and fluoxetine, fluvoxamine, and paroxetine nonlinear pharmacokinetics. SSRIs underlie an extensive metabolism with high interindividual variability, whereby cytochrome P450 (CYP) isoenzymes play a major role. Therefore, resulting blood concentrations are highly variable between individuals. Except for N-demethylated fluoxetine, metabolites of SSRIs do not contribute to clinical actions. Therapeutically effective blood concentrations are unclear so far, although there is evidence for minimal effective and upper-threshold concentrations that should not be exceeded. Paroxetine and, to a lesser degree, fluoxetine and norfluoxetine are potent inhibitors of CYP2D6 and fluvoxamine of CYP1A2 and CYP2C19. This can give rise to drug-drug interactions that may have no effect, lead to intoxication, or improve the therapeutic response. These different pharmacokinetic properties of the five SSRIs, especially their drug-drug interaction potential, should be considered when selecting a distinct SSRI for treatment of depression or other disorders with a suggested dysfunction of the serotonergic system in the brain.     

Comparison of Toxicity of Acute Overdoses with Citalopram and Escitalopram

Background: Seizures and QTc prolongation are associated with citalopram poisoning; however, overdose experience with escitalopram is more limited. Objectives: The goals of this study were to compare citalopram's vs. escitalopram's clinical effects in overdose, including the incidence of seizures. Methods: A retrospective review was conducted for single-substance acute overdoses with citalopram and escitalopram, managed in hospitals, that were reported to six U.S. poison centers from 2002–2005. Results: There were 374 citalopram and 421 escitalopram overdose cases. Gender and ages were similar between the two, with 68–70% females and a median age of 20 years for citalopram and 18 years for escitalopram. Median dose by history was 310 mg for citalopram and 130 mg for escitalopram. More serious outcomes were associated with citalopram overdoses (p < 0.001). Most frequently reported clinical effects with citalopram and escitalopram were tachycardia, drowsiness, hypertension, and vomiting. Seizures (30 vs. 1, respectively, p < 0.001) and tremor (32 vs. 13, respectively, p = 0.001) were more common with citalopram. QTc prolongation occurred in 14 citalopram cases and 7 escitalopram cases (p = 0.109). There was an association between increasing dose and severity of outcome for citalopram (p < 0.001) and escitalopram (p = 0.011). In children < 6 years old, 12 of 66 citalopram and 5 of 57 escitalopram cases experienced toxicity, such as drowsiness, nausea/vomiting, and tachycardia. There were no seizures in this age group. Conclusions: Escitalopram seems to be less toxic than citalopram after an acute overdose; seizures and tremors were more common with citalopram. Initial management of overdoses should include seizure precautions for citalopram and cardiac monitoring for both drugs.     

Irritable bowel syndrome in psychiatric perspectives: a comprehensive review

We comprehensively reviewed the irritable bowel syndrome (IBS) in terms of pathogenesis, psychiatric implications, general management and appropriate role of antidepressants, in particular selective serotonin uptake inhibitors (SSRIs) in the treatment of IBS. English language papers cited in MEDLINE and PychInfo from January 2000 to July 2006 were searched with a combination of the following key words: irritable bowel syndrome, 5-HT, pathogenesis, comorbid, psychiatry, treatment, psychotropic drugs, antidepressant, selective serotonin reuptake inhibitors (fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram and sertraline), tricyclic antidepressants, review, meta-analysis and placebo. The papers on IBS describing the clinical features, pathophysiology, evaluation, management, and clinical trials [randomised placebo-controlled trial (RCT), open-label study or case report] were selected for this review. Further literatures were also detected from references of the identified papers. The epidemiology, diagnostic criteria, pathophysiology, general management, bidirectional comorbidity, summary of currently available RCTs and open-label studies investigating antidepressant efficacy (focusing on SSRIs), and suggestions for SSRI use in IBS were relevantly synthesised based on through review of identified data. This article summarised an up-to-date clinical overview of IBS in psychiatric perspectives as well as to position a current role of SSRIs in the treatment of IBS. From this review, the routine use of SSRIs for IBS treatment cannot be conclusive due to a paucity of RCTs, although a handful of RCTs suggested a potentially beneficial effect of SSRIs over placebo.