Validation and clinical application of the Metacognitions Questionnaire in a sample of Brazilian generalized anxiety disorder patients: the effects of different treatment interventions

Abstract Introduction Metacognitive beliefs about worry may trigger anxiety. However, the effect of generalized anxiety disorder (GAD) treatment on metacognition has not yet been investigated. Objectives To validate the Metacognitions Questionnaire (MCQ-30) in a Brazilian GAD sample and verify whether different interventions reduce metacognitive beliefs. Method We recruited 180 GAD individuals and randomized them to Body in Mind Training (BMT), Fluoxetine (FLX), or an active control group (Quality of Life [QoL]) for 8 weeks. The MCQ-30 was assessed for internal consistency, was evaluated with confirmatory and exploratory factor analyses, and was tested for convergent validity with the Penn State Worry Questionnaire (PSWQ). Generalized estimating equations (GEE) were employed to analyze differences after the interventions. Results The MCQ-30 demonstrated good internal consistency and acceptability; the original five-factor model was supported. There was a positive moderate correlation between MCQ-30 scores and worry. GEE showed a significant group x time interaction (p < 0.001). Both BMT (mean difference [MD] = -6.04, standard error [SE] = -2.39, p = 0.034) and FLX (MD = -5.78, SE = 1.91, p = 0.007) reduced MCQ-30 scores. FLX was superior to QoL, but not BMT, at weeks 5 and 8. There were no differences between BMT and QoL. Conclusion The Brazilian-Portuguese version of MCQ-30 showed good psychometric properties. Furthermore, the positive effect of FLX and BMT on metacognition suggests it may represent a potential therapeutic target.

Cost variation analysis of various brands of selective serotonin reuptake inhibitors currently available in the Indian market: An observational study

Background: India being the world’s largest supplier of generic drugs provides 50% of the drugs globally. Selective Serotonin Reuptake Inhibitors (SSRI) (hereafter referred to as SSRI) is the most commonly prescribed drugs for depression (prevalence of 5.25%) and Anxiety (prevalence of 5.8%). The cost of these drugs influences the patient compliance with treatment and thereby the clinical outcome significantly. Aim and Objectives: The aim of the study was to analyze the cost-variation of SSRIs available in the Indian market. Materials and Methods: Maximum and minimum costs of various SSRIs used in the treatment of depression and anxiety were obtained from the monthly index of medical specialties (November 2020) online, Jan Aushadhi Sugam App (Generic drugs), and National Pharmaceutical Pricing Authority online. The cost of various SSRI being manufactured by different companies in the same strength and dosage form were compared. Cost ratio (Maximum cost/Minimum cost) and percentage cost variation ([{Max cost–Min cost}/Min cost] × 100) in INR (?) were calculated. Data were analyzed and represented using descriptive statistics. Results: Percentage cost variation was maximum with Fluoxetine 20 mg (3477.85%), followed by Sertraline 50 mg (1631.61%) and Escitalopram 10 mg (1288.89%). Percentage cost variation was minimum with Vilazodone 40 mg (16.31%). Conclusion: This study provides awareness about cost variation among different brands of SSRI used in the treatment of depression and anxiety. Wide variation can cause dissatisfaction, poor compliance, and economic burden among patients. It strengthens the usage of generic drugs among general population and healthcare providers.

Escitalopram-Induced Chronic Euvolemic Hyponatremia

Selective serotonin reuptake inhibitors (SSRIs), through the recent years have seen an increase in the number of prescriptions for a spectrum of mood disorders, especially in the geriatric population. Despite being a well-tolerated antidepressant, SSRIs have been associated with hyponatremia, a rare, but fatal adverse effect and the incidence ranges from 0.5%–32% in literature. Euvolemic hyponatremia is most commonly associated with syndrome of inappropriate secretion of antidiuretic hormone. An extensive review of literature was carried out, and we came across a total of 20 cases where escitalopram was reported as the causative agent of hyponatremia. We report a case of an 82-year-old female patient who had a history of acute onset, progressive memory impairment, and behavioral changes with depressive cognition precipitated by the death of her husband, for which she was treated with escitalopram 5 mg/day and clonazepam 0.5 mg/day. She was admitted to the hospital with presenting complaints of gait imbalance, tremors, irritability, confusion, decreased speech output and persecutory delusions. She was diagnosed with late-onset organic psychosis, precipitated and worsened by escitalopram-induced chronic uncontrolled euvolemic hyponatremia, with a sodium level of 115 mmol/L. On discontinuation of escitalopram, the patient’s serum sodium level improved gradually, and her consciousness became better. This is the second case with recurrent hyponatremia in the literature up to this date, with the other being reported by Tsai et al., in 2012. Furthermore, the dose of escitalopram was only 5 mg/day compared to other reported cases where the dose ranged between 10–20 mg/day.

Role of vitamin D supplementation as adjunctive therapy to escitalopram in patients of major depressive disorder: a 8 week prospective, randomized, interventional, clinical study

Background: Depression is a major public health problem and occurs in persons of all ages, and is associated with increased morbidity, soaring costs for treatment and reduced productivity and quality of life. Vitamin D is involved in numerous brain processes including neuroimmunomodulation, neuroprotection, neuroplasticity, regulation of neurotrophic factors, and making it biologically plausible to be associated with depression. Aim of the present study is to compare the therapeutic effects of vitamin D given along with escitalopram versus escitalopram given alone in patients with major depressive disorder. Methods: In this prospective, randomized, interventional clinical study, 60 patients with a diagnosis of major depressive disorder based on ICD-10 criteria were randomly assigned into two groups, one group received 60000IU vitamin D3 weekly plus 10 mg escitalopram OD daily while the other group received escitalopram10 mg OD daily alone for 8 weeks. Depression severity was assessed at 2-week intervals using the 24-item Hamilton Depression Rating Scale (HDRS). Serum 25(OH) vitamin D levels were measured in all the patients at baseline and after intervention.Result: Fifty nine patients completed the trial. Depression severity based on HDRS decreased significantly after intervention, with a significant difference between the two groups. The vitamin D3+escitalopram combination was significantly better than escitalopram alone from the fourth week of treatment. Conclusion: Role of vitamin D in mood disorder and its dietary supplementation is effective as an adjuvant treatment along with SSRIs in depressive disorders, especially in vitamin D deficient patients.

Research progress on the mechanism of 5-hydroxytryptamine in sepsis / 中华危重病急救医学

Sepsis has the characteristics of high morbidity and high mortality, which is the main cause of death in critically ill patients. Peripheral 5-hydroxytryptamine (5-HT) is mainly synthesized and secreted by enterochromaffin cells and plays a role in the development and progression of inflammation. This article focuses on 5-HT, 5-HT transporter (SERT) and selective serotonin reuptake inhibitors (SSRIs) in immune response, inflammatory factor release, oxidative stress, intestinal bacterial translocation and microcirculation of sepsis. The role of the review is to find new ideas for the clinical treatment of sepsis.

Progress in augmentation therapy mechanism of obsessive compulsive disorder / 上海交通大学学报（医学版）

Administration of selective serotonin reuptake inhibitors (SSRI) is a widely used pharmacotherapeutic approach for obsessive-compulsive disorder (OCD) today. However, nearly half of the OCD patients do not respond to SSRI. It has been shown that some antipsychotic drugs can augment the therapeutic effect of SSRI in the patients with OCD, but the augmentation’s effect is still ineffective for some patients. Therefore, it is of great significance to explore the augmentation’s mechanism for further improvement of the clinical treatment. This article reviews some common used augmentation for OCD and discusses the underlying mechanisms.

Selective serotonin reuptake inhibitor escitalopram inhibits 5-HT₃ receptor currents in NCB-20 cells

Escitalopram is one of selective serotonin reuptake inhibitor antidepressants. As an S-enantiomer of citalopram, it shows better therapeutic outcome in depression and anxiety disorder treatment because it has higher selectivity for serotonin reuptake transporter than citalopram. The objective of this study was to determine the direct inhibitory effect of escitalopram on 5-hydroxytryptamine type 3 (5-HT₃) receptor currents and study its blocking mechanism to explore additional pharmacological effects of escitalopram through 5-HT₃ receptors. Using a whole-cell voltage clamp method, we recorded currents of 5-HT₃ receptors when 5-HT was applied alone or co-applied with escitalopram in cultured NCB-20 neuroblastoma cells known to express 5-HT₃ receptors. 5-HT induced currents were inhibited by escitalopram in a concentration-dependent manner. EC50 of 5-HT on 5-HT₃ receptor currents was increased by escitalopram while the maximal peak amplitude was reduced by escitalopram. The inhibitory effect of escitalopram was voltage independent. Escitalopram worked more effectively when it was co-applied with 5-HT than pre-application of escitalopram. Moreover, escitalopram showed fast association and dissociation to the open state of 5-HT₃ receptor channel with accelerating receptor desensitization. Although escitalopram accelerated 5-HT₃ receptor desensitization, it did not change the time course of desensitization recovery. These results suggest that escitalopram can inhibit 5-HT₃ receptor currents in a non-competitive manner with the mechanism of open channel blocking.

Correlation of 5-hydroxytryptamine transporter gene-linked polymorphic region with lifelong premature ejaculation: Progress in studies / 中华男科学杂志

Premature ejaculation (PE), as one of the most common male sexual dysfunctions, has a serious negative impact on the sexual satisfaction of the patients and their sexual partners. Lifelong PE is a most common type and a current focus of research as well. The etiology and pathogenesis of this disease are not yet clear and genetic factors are considered to be closely related to lifelong PE. Studies show that the 5-hydroxytryptamine transporter (5-HTT) gene plays an important role in the development and progression of lifelong premature ejaculation and the 5-HTT-linked polymorphic region (5-HTTLPR) has attracted much attention in recent years. This article presents an overview on the correlation between 5-HTTLPR and lifelong PE.

Antidepressant drug paroxetine blocks the open pore of Kv3.1 potassium channel

In patients with epilepsy, depression is a common comorbidity but difficult to be treated because many antidepressants cause pro-convulsive effects. Thus, it is important to identify the risk of seizures associated with antidepressants. To determine whether paroxetine, a very potent selective serotonin reuptake inhibitor (SSRI), interacts with ion channels that modulate neuronal excitability, we examined the effects of paroxetine on Kv3.1 potassium channels, which contribute to highfrequency firing of interneurons, using the whole-cell patch-clamp technique. Kv3.1 channels were cloned from rat neurons and expressed in Chinese hamster ovary cells. Paroxetine reversibly reduced the amplitude of Kv3.1 current, with an IC₅₀ value of 9.43 µM and a Hill coefficient of 1.43, and also accelerated the decay of Kv3.1 current. The paroxetine-induced inhibition of Kv3.1 channels was voltage-dependent even when the channels were fully open. The binding (k₊₁) and unbinding (k₋₁) rate constants for the paroxetine effect were 4.5 µM⁻¹s⁻¹ and 35.8 s⁻¹, respectively, yielding a calculated K(D) value of 7.9 µM. The analyses of Kv3.1 tail current indicated that paroxetine did not affect ion selectivity and slowed its deactivation time course, resulting in a tail crossover phenomenon. Paroxetine inhibited Kv3.1 channels in a usedependent manner. Taken together, these results suggest that paroxetine blocks the open state of Kv3.1 channels. Given the role of Kv3.1 in fast spiking of interneurons, our data imply that the blockade of Kv3.1 by paroxetine might elevate epileptic activity of neural networks by interfering with repetitive firing of inhibitory neurons.

Study on the effect of SSRI and SNRI combined with psychological intervention on the executive function in patients with depression untreated / 中国生化药物杂志

Objective To observe the effect of SSRI and SNRI drugs combined with clinical nursing path of untreated depression in patients with executive function. Methods From October 2014 to April 2016, the third people's Hospital of Yuyao was admitted to the 4 people's Hospital, who met the criteria of diagnosis and inclusion criteria. 80 cases of untreated depressive patients were randomly divided into two groups, according to clinical medication and nursing methods were defined as SSRI group, SSRI group and SNRI group, SNRI group, SSRI group were treated with 8 cycles of Pa Rossi Dean oral treatment, during the treatment group were given routine clinical care, SNRI group were given venlafaxine 8 During the period of oral treatment, treatment group Ⅱ were given clinical nursing path on the basis of conventional nursing, treatment and nursing care of patients before and after the change of executive function evaluation. Results SSRI Ⅱ, SNRI Ⅱ group WCST scores were better than SSRI Ⅰ, SNRI Ⅰ group; SNRI group Ⅱ WCST scores were better than SSRI group; SSRI group, SNRI group Ⅱ TMT evaluation results is better than that of SSRI group, SNRI group; SNRI group Ⅱ TMT evaluation results is better than that of SSRI group; the SSRI Ⅱ SNRI Ⅱ group the experimental results of TOL is better than that of SSRI group, SNRI group; SNRI group Ⅱ TOL experimental results better than SSRI Ⅱ group. Conclusion SSRI and SNRI drug treatment untreated depression patients exactly, combined with clinical nursing path can effectively improve the patients with degree of functional recovery, is worthy of clinical application.

Blockade of Kv1.5 by paroxetine, an antidepressant drug

Paroxetine, a selective serotonin reuptake inhibitor (SSRI), has been reported to have an effect on several ion channels including human ether-a-go-go-related gene in a SSRI-independent manner. These results suggest that paroxetine may cause side effects on cardiac system. In this study, we investigated the effect of paroxetine on Kv1.5, which is one of cardiac ion channels. The action of paroxetine on the cloned neuronal rat Kv1.5 channels stably expressed in Chinese hamster ovary cells was investigated using the whole-cell patch-clamp technique. Paroxetine reduced Kv1.5 whole-cell currents in a reversible concentration-dependent manner, with an IC50 value and a Hill coefficient of 4.11 microM and 0.98, respectively. Paroxetine accelerated the decay rate of inactivation of Kv1.5 currents without modifying the kinetics of current activation. The inhibition increased steeply between -30 and 0 mV, which corresponded with the voltage range for channel opening. In the voltage range positive to 0 mV, inhibition displayed a weak voltage dependence, consistent with an electrical distance delta of 0.32. The binding (k(+1)) and unbinding (k(-1)) rate constants for paroxetine-induced block of Kv1.5 were 4.9 microM(-1)s(-1) and 16.1 s-1, respectively. The theoretical K(D) value derived by k(-1)/k(+1) yielded 3.3 microM. Paroxetine slowed the deactivation time course, resulting in a tail crossover phenomenon when the tail currents, recorded in the presence and absence of paroxetine, were superimposed. Inhibition of Kv1.5 by paroxetine was use-dependent. The present results suggest that paroxetine acts on Kv1.5 currents as an open-channel blocker.

Blockade of Kv1.5 channels by the antidepressant drug sertraline

Sertraline, a selective serotonin reuptake inhibitor (SSRI), has been reported to lead to cardiac toxicity even at therapeutic doses including sudden cardiac death and ventricular arrhythmia. And in a SSRI-independent manner, sertraline has been known to inhibit various voltage-dependent channels, which play an important role in regulation of cardiovascular system. In the present study, we investigated the action of sertraline on Kv1.5, which is one of cardiac ion channels. The eff ect of sertraline on the cloned neuronal rat Kv1.5 channels stably expressed in Chinese hamster ovary cells was investigated using the whole-cell patch-clamp technique. Sertraline reduced Kv1.5 whole-cell currents in a reversible concentration-dependent manner, with an IC50 value and a Hill coefficient of 0.71 microM and 1.29, respectively. Sertraline accelerated the decay rate of inactivation of Kv1.5 currents without modifying the kinetics of current activation. The inhibition increased steeply between -20 and 0 mV, which corresponded with the voltage range for channel opening. In the voltage range positive to +10 mV, inhibition displayed a weak voltage dependence, consistent with an electrical distance delta of 0.16. Sertraline slowed the deactivation time course, resulting in a tail crossover phenomenon when the tail currents, recorded in the presence and absence of sertraline, were superimposed. Inhibition of Kv1.5 by sertraline was use-dependent. The present results suggest that sertraline acts on Kv1.5 currents as an open-channel blocker.

Serum Levels of Brain-Derived Neurotrophic Factor at 4 Weeks and Response to Treatment with SSRIs

OBJECTIVE: It is important to predict a response to an antidepressant in early time after starting the antidepressant. We previously reported that serum brain-derived neurotrophic factor (BDNF) levels in responders to treatment with antidepressants were increased, whereas, those in nonresponders were not. Therefore, we hypothesized that the changes in serum levels of BDNF from baseline (T0) to 4 weeks (T4) after treatment with selective serotonin reuptake inhibitors (SSRIs) predict the response to the treatment at 8 weeks (T8) in depressed patients. To confirm the hypothesis, we measured serum BDNF at T0, T4, and T8 during the treatment with SSRIs (paroxetine, sertraline, and fluvoxamine). METHODS: One hundred fifty patients (M/F; 51/99, age; 50.4+/-15.1 years) met major depressive disorder (MDD) using by DSM-IV-TR enrolled in the present study. We measured serum BDNF concentrations at T0, T4, and T8 in patients with MDD treated with SSRIs. RESULTS: The changes in serum BDNF, age, sex, dose of SSRIs, and HAMD-17 score did not predict the response to SSRIs at T8. CONCLUSION: These results suggest that the changes in serum BDNF levels from T0 to T4 could not predict the subsequent responses to SSRIs at T8.

No Association between the Response to the Addition of an Atypical Antipsychotic Drug to an Selective Serotonin Reuptake Inhibitor or Serotonin Norepinephrine Reuptake Inhibitor and the Brain-Derived Neurotrophic Factor (Val66Met) Polymorphism in Refracto

OBJECTIVE: This study examined the association between the brain-derived neurotrophic factor (BDNF) (Val66Met) polymorphism and the response to the addition of an atypical antipsychotic drug to a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) in treatment-refractory depression. METHODS: The study enrolled 64 patients meeting the Diagnostic and Statistical Manual of Mental Disorders-IV criteria for major depressive disorder who were treated with at least two courses of a single antidepressant, but who had Hamilton Depression Rating Scale (HAMD-17) scores > or =15 points that were reduced less than 50% over at least a 4-week treatment period. There were 24 males and 40 females (age range 27-68 years; mean+/-SD, 48+/-13 years). The patients' clinical improvement was evaluated using the HAMD-17. Patients with at least a 50% decrease in the HAMD-17 score were defined as responders. Serum BDNF levels were assayed using enzyme-linked immunosorbent assays and the presence of the BDNF (Val66Met) polymorphism was determined using the TaqMan genotyping assay. RESULTS: No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug. No differences were observed in the changes in the serum BDNF levels and HAMD-17 scores between Val66Val and Met-carriers. In addition, in patients who experienced remission, the atypical antipsychotic drug was discontinued after at least 3 months of treatment and the patients were then followed for 1 year; 14 of 27 patients (52%) relapsed within 1 year. CONCLUSION: These results suggest that the BDNF (Val66Met) polymorphism is not associated with the response to the augmentation of a SSRI or SNRI with an atypical antipsychotic drug, and that the combination of an atypical antipsychotic drug and a SSRI or SNRI should be continued for 3 months or more in refractory depressed patients in the Japanese population.

Influence of buspirone on sexual function and plasma prolactin in rehabilitative female major depressive patients / 中华行为医学与脑科学杂志

ObjectiveTo determine the influence of buspirone on sexual function and plasma prolactin in rehabilitative female major depressive patients.MethodsThe female major depressive patients,who had a total HAMD-17 less than 7,were living with a sexual partner and receiving SSRI antidepressant monotherapy for at least six months were recruited.Sexual dysfunction (SD) was assessed using the Arizona Sexual Experience Scale (ASEX).The patients with SD were treated with buspirone 15 ～ 30 mg by 4 weeks.Sexua function and blood samples were compared among the control,non-SD patients,and the SD patients before or after treating with buspirone.The clinical risk factor of SD was also investigated with correlation analysis.ResultsThe general incidence of SD in rehabilitative female major depressive patients was 33.3％.The improvement rate of SD was 60％ after the treatment of buspirone.The ASEX score and it 5 items were significantly decreased in the depressive patients after the treatment of buspirone (P ＜ 0.01 ).Prolactin in subjects treated with buspirone ( ( 20.38 ± 11.91 )ng/ml) was significantly higher than control ( ( 14.2 ± 12.15 ) ng/ml),but not higher than the period prior to treatment with buspirone ( ( 18.15 ±9.84) ng/ml).The ASEX score was significantly correlated the dose of fluoxetine( r=0.504,P=0.002) and paroxetine ( r=0.377,P=0.013).There was no significantly correlation between ASEX score and prolactin in the control,non-SD patients,and the patients before or after treating with buspirone.ConclusionBuspirone can release sexual dysfunction induced by SSRI antideptressant in the depressive patients.

Retrospective Analyses of Long-Term Use of SSRI in Children and Adolescents with Autism Spectrum Disorder

OBJECTIVES: The purpose of this study was to investigate clinical profile, efficacy, and safety of long-term treatment with selective serotonin reuptake inhibitors (SSRIs) in Korean autism spectrum disorders (ASDs) patients. METHODS: Effectiveness was assessed through a retrospective review of self-reported target symptom improvement at the last follow-up visit. Changes in illness severity and improvement were measured using the Clinical Global Impression-Severity (CGI-S) of illness and Clinical Global Impression-Improvement (CGI-I) Scales. Tolerability was assessed through a review of the reason for discontinuation of SSRI and documented adverse events. RESULTS: A total of 21 ASDs patients (aged 9 to 19 years) treated with SSRI during July 2010 to July 2011 in department of child and adolescent psychiatry of Seoul National Hospital were identified. The mean duration of SSRI treatment was 47.9 (standard deviation = 36.9) months (range 0.7-114.5), and the mean fluoxetine equivalent dosage of SSRIs was 27.1 +/- 10.8 mg. Nineteen (90.5%) patients were using concomitant medication. We found that SSRIs were prescribed for symptoms of agitation, stereotyped behavior, aggression, depression, impulsivity and self-injury in ASDs. Ten patients (47.6%) reported improvement in their target symptom after SSRI treatment based on CGI-I scores (CGI-I < or = 2). The side effects were reported in 5 patients (23.8%) ; vomiting (n = 2, 9.5%), excessive mood elevation (n = 1, 4.8%), insomnia (n = 1, 4.8%), somnolence (n = 1, 4.8%) and decreased appetite (n = 1, 4.8%). Self-injurious behavior was reported in one patient (4.8%). CONCLUSIONS: The results of this study suggest that SSRIs may be used effectively in children and adolescents diagnosed with ASDs. However, safety issues need to be considered carefully when choosing SSRIs for treatment. Future controlled trials are needed to confirm these findings.

Wide Spectrum of Inhibitory Effects of Sertraline on Cardiac Ion Channels

Sertraline is a commonly used antidepressant of the selective serotonin reuptake inhibitors (SSRIs) class. In these experiments, we have used the whole cell patch clamp technique to examine the effects of sertraline on the major cardiac ion channels expressed in HEK293 cells and the native voltage-gated Ca2+ channels in rat ventricular myocytes. According to the results, sertraline is a potent blocker of cardiac K+ channels, such as hERG, IKs and IK1. The rank order of inhibitory potency was hERG >IK1> IKs with IC50 values of 0.7, 10.5, and 15.2 microM, respectively. In addition to K+ channels, sertraline also inhibited INa and ICa, and the IC50 values are 6.1 and 2.6 microM, respectively. Modification of these ion channels by sertraline could induce changes of the cardiac action potential duration and QT interval, and might result in cardiac arrhythmia.

SSRIs and SNRIs for Management of Hot Flushing / 대한폐경학회지

For postmenopausal women who fear hormone therapy, women 60 years of age with continuous, severe hot flushing or women with a history of breast cancer, we should consider selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs) as therapeutic agents. Base on the results from a meta-analysis and clinical trials regarding hot flushing, paroxetine and the conetrolled-release formultation of paroxetine have been shown to effectively reduce hot flushing by 30~40% and 60~70%, respectively, and 13~41% more reductions as compared to placebo. Venlafaxine reduced hot flushes by 30~60% (133% reductions compared to placebo), and desvenlafaxine reduced hot flushes by 30~70%. Fluoxetine and citalopram were shown to be less effective than paroxetine and venlafaxine, by 20% (113% reductions compared to placebo) and 40~50%, respectively. Sertraline reduced hot flushes 3~18% compared to the placebo group, but was considered ineffective. Citalopram (20 mg), paroxetine (10 mg), venlafaxine (37.5~150 mg), and desvenlafaxine (100~200 mg) not only reduced vasomotor symptoms, but demonstrated additional beneficial outcomes with respect to sleep disturbances, mood, the vigor index, and improved quality of life. Citalopram (20 mg), fluoxetine (20 mg), paroxetine (10 mg), venlafaxine (75~150 mg), and desvenlafaxine (150 mg) are recommended at the corresponding doses after weighing the risks and benefits of these medications. SSRIs and SNRIs were shown to interrupt the conversion of tamoxifen into the active metabolite, endoxifen, and thus SSRIs and SNRIs must not be used in breast cancer patients who are taking tamoxifen. Paroxetine suppressed vasomotor symptoms most potently, followed by fluoxetine, sertraline, citalopram, and venlafaxine.

A Case of Paroxetine-Related Hyperprolactinemia / 대한정신약물학회지

Although selective serotonin reuptake inhibitors (SSRIs) have been widely used in both psychiatry and other medicine, few cases have been reported SSRI-related hyperprolactinemia and/or galactorrhea. We experienced one case which showed both galactorrhea and hyperprolactinemia following treatment with paroxetine. In the case, a 37-year-old multiparous woman reported galactorrhea after 8-weeks paroxetine treatment for her depression. After 1 month prescription of bromocriptine, dopamine agonist, as well as switching medication from paroxetine to venlafaxine, serotonin-norepinephrine reuptake inhibitor, both galactorrhea and hyperprolactinemia were disappeared. Both hyperprolactinemia and galactorrhea have not been observed even after the cessation of bromocriptine prescription.

Selective Serotonin Reuptake Inhibitors for the Treatment of Premature Ejaculation / 대한남성과학회지

Premature ejaculation (PE) affects the 20~30% men among general population regardless of their age. PE may be classified as lifelong (primary) or acquired (secondary) type. Diagnosis of PE is mainly based on subjective complaints of sexual symptoms. Recently proposed diagnostic system of PE is based on many aspects; intravaginal ejaculatory latency time (IELT), control over ejaculation, stress and interpersonal difficulty according to the PE problem. Standard treatment of lifelong PE is mainly pharmacotherapy. Among many treatment options, selective serotonin reuptake inhibitors (SSRIs) are recommended for off-label use by American Urologic Association and International Consultation on Sexual Medicine. SSRIs were reported to improve the PE symptom by lengthening IELT. However, daily intake of SSRIs often increases the possibility of adverse effects, such as nausea, diarrhea, loss of libido, and even erectile dysfunction. Recently, dapoxetine hydrochloride, newer SSRI with short half life, was tailored to target the PE. Dapoxetine was proved its efficacy on PE over placebo. Clinicians should keep in mind that the sexual dysfunction can be the primary complaints or the results of the intake of antidepressants at the same time.