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Current Neuropharmacology 2024Antidepressants are a commonly used, easily accessible, and overall safe treatment option for post-traumatic stress disorder (PTSD). The present review aims to evaluate... (Review)
Review
Antidepressants are a commonly used, easily accessible, and overall safe treatment option for post-traumatic stress disorder (PTSD). The present review aims to evaluate the efficacy and safety of antidepressants in treating sleep disturbances in patients with PTSD. PubMed and the Cochrane Library were searched (July 2022) for systematic reviews and meta-analyses on the treatment of PTSD. Moreover, PubMed and ClinicalTrials.gov were searched for individual trials investigating the antidepressant treatment of PTSD (up to September 2022), and reference lists of all possibly relevant identified studies were screened. Sleep-related outcomes, i.e., total sleep time, sleep quality, dreams/ nightmares, insomnia, and somnolence, were extracted independently by at least two reviewers. Metaanalytic evaluations were performed wherever possible. 39 randomised controlled trials (RCTs) were identified; data from pooled analyses, reviews, and observational studies were used for antidepressants with a weak evidence base or when their findings were deemed important. Overall, scarce data exist on the effects of antidepressants on sleep outcomes among patients with PTSD. Some evidence may support the use of amitriptyline, nefazodone, paroxetine, and sertraline for improving sleep in patients with PTSD. Τhere was a meta-analytical trend indicating improvement of nightmares with fluoxetine, less insomnia with amitriptyline and more with brofaromine, as well as more somnolence with paroxetine vs. placebo, respectively. However, data from more than 1 RCT with a considerable number of patients were only available for paroxetine. Evidence is insufficient to draw safe conclusions. More and better-designed RCTs, with consistent reporting of sleep-related outcomes, are needed.
Topics: Humans; Stress Disorders, Post-Traumatic; Paroxetine; Amitriptyline; Sleep Initiation and Maintenance Disorders; Sleepiness; Systematic Reviews as Topic; Antidepressive Agents
PubMed: 37533247
DOI: 10.2174/1570159X21666230801144328 -
Journal of the American Association of... Jan 2015To systematically review the evidence related to the efficacy and tolerability of selective serotonin reuptake inhibitors (SSRIs) and serotonin/norepinephrine reuptake... (Review)
Review
PURPOSE
To systematically review the evidence related to the efficacy and tolerability of selective serotonin reuptake inhibitors (SSRIs) and serotonin/norepinephrine reuptake inhibitors (SNRIs) used for the treatment of vasomotor symptoms in perimenopausal and postmenopausal women.
DATA SOURCES
Medline, CINAHL, and the Cochrane Library databases were searched to identify randomized controlled trials (RCTs). Eighteen trials met the criteria for review.
CONCLUSIONS
Results from these trials indicate that paroxetine, citalopram, escitalopram, venlafaxine, and desvenlafaxine are effective in reducing the frequency and severity of hot flashes. Fluoxetine and sertraline appear to be less effective and should be considered second-line options for treatment.
IMPLICATIONS FOR PRACTICE
The SSRIs and SNRIs can reduce hot flashes by 65% and begin working within the first week. Patient response is variable and if one drug does not improve hot flashes, another can be tried after a 1- to 2-week drug trial. Paroxetine, citalopram, and escitalopram appear to have the fewest adverse effects. Considering cost, paroxetine and citalopram are the most cost-efficient.
Topics: Adult; Aged; Citalopram; Desvenlafaxine Succinate; Female; Fluoxetine; Hot Flashes; Humans; Menopause; Middle Aged; Paroxetine; Serotonin and Noradrenaline Reuptake Inhibitors; Sertraline; Vasomotor System; Venlafaxine Hydrochloride
PubMed: 24944075
DOI: 10.1002/2327-6924.12137 -
Future Microbiology May 2023To evaluate the antibacterial activity of paroxetine alone and associated with oxacillin against isolates of methicillin-sensitive and -resistant . The broth...
To evaluate the antibacterial activity of paroxetine alone and associated with oxacillin against isolates of methicillin-sensitive and -resistant . The broth microdilution and checkerboard techniques were used, with investigation of possible mechanisms of action through flow cytometry, fluorescence microscopy and molecular docking, in addition to scanning electron microscopy for morphological analysis. Paroxetine showed a MIC of 64 μg/ml and bactericidal activity, mostly additive interactions in combination with oxacillin, evidence of action on genetic material and membrane, morphological changes in microbial cells and influence on virulence factors. Paroxetine has antibacterial potential from the perspective of drug repositioning.
Topics: Humans; Staphylococcus aureus; Paroxetine; Methicillin-Resistant Staphylococcus aureus; Molecular Docking Simulation; Anti-Bacterial Agents; Oxacillin; Staphylococcal Infections; Microbial Sensitivity Tests
PubMed: 37213136
DOI: 10.2217/fmb-2022-0232 -
Journal of the American Board of Family... Jan 2024Existing guidelines for primary care clinicians (PCCs) on the detection and management of perinatal depression (PD) contain important gaps. This review aims to provide... (Review)
Review
INTRODUCTION
Existing guidelines for primary care clinicians (PCCs) on the detection and management of perinatal depression (PD) contain important gaps. This review aims to provide PCCs with a summary of clinically relevant evidence in the field.
METHODS
A narrative literature review was conducted by searching PubMed and PsycINFO for articles published between 2010 to 2023. Guidelines, systematic reviews, clinical trials, and/or observational studies were all examined.
RESULTS
Screening with the Edinburgh Postnatal Depression Scale or Patient Health Questionnaire-9 followed by a diagnostic evaluation for major depressive disorder in probable cases can enhance PD detection. At-risk individuals and mild to moderate PD should be referred for cognitive behavioral therapy or interpersonal psychotherapy when available. Selective serotonin reuptake inhibitors should be used for moderate to severe PD, with sertraline, escitalopram, or citalopram being preferred first. Using paroxetine or clomipramine in pregnancy, and fluoxetine or doxepin during lactation is generally not preferred. Gestational antidepressant use is associated with a small increase in risk of reduced gestational age at birth, low birth weight, and lower APGAR scores, though whether these links are causal is unclear. Sertraline and paroxetine have the lowest rate of adverse events during lactation. Consequences of untreated PD can include maternal and offspring mortality, perinatal complications, poor maternal-infant attachment, child morbidity and maltreatment, less breastfeeding, and offspring developmental problems.
CONCLUSIONS
These clinically relevant data can support the delivery of high-quality care by PCCs. Risks and benefits of PD treatments and the consequences of untreated PD should be discussed with patients to support informed decision making.
Topics: Pregnancy; Infant, Newborn; Female; Child; Humans; Paroxetine; Sertraline; Depression; Depressive Disorder, Major; Primary Health Care
PubMed: 37704392
DOI: 10.3122/jabfm.2023.230061R1 -
Asia-Pacific Psychiatry : Official... Dec 2014Previous studies have shown that varying acute-phase treatment periods of fluoxetine and paroxetine can result in varying antidepressive effects. We therefore did a... (Comparative Study)
Comparative Study Meta-Analysis Review
INTRODUCTION
Previous studies have shown that varying acute-phase treatment periods of fluoxetine and paroxetine can result in varying antidepressive effects. We therefore did a meta-analysis to ascertain the efficacy of fluoxetine versus paroxetine for depression by varying acute-phase treatment periods.
METHODS
PubMed, CCTR, Web of Science, Embase, CBM-disc, and CNKI were searched up to March 2013. The key search terms were "depression," "paroxetine," and "fluoxetine." No language restriction was imposed.
RESULTS
We included 17 studies with 3,110 patients. Three treatment period subgroups were created: 6, 8/10, and 12 weeks. In the 6-week subgroup, paroxetine was more efficacious than fluoxetine (odds ratio [OR]: 0.74; P < 0.05). In the 8/10-week subgroup, two drugs displayed comparative efficacy (OR, 0.85; P > 0.05). In the 12-week subgroup, fluoxetine was more efficacious than paroxetine (OR: 1.25; P < 0.05). There were no significant differences in acceptability. Significant heterogeneity and potential publication bias did not exist.
CONCLUSIONS
Patients' economic conditions, individual preference, and side effects of fluoxetine and paroxetine can be obstacles of successful treatment. Inappropriate acute-phase treatment, such as inadequate treatment periods, may result in pseudoresistance. Clinicians should take these information into consideration when prescribe fluoxetine or paroxetine for patients. Our results can aid clinicians in making an optimal treatment plan to increase odds of response.
Topics: Adult; Antidepressive Agents, Second-Generation; Depressive Disorder, Major; Fluoxetine; Humans; Paroxetine; Randomized Controlled Trials as Topic; Selective Serotonin Reuptake Inhibitors; Treatment Outcome
PubMed: 24150924
DOI: 10.1111/appy.12106 -
Journal of Psychopharmacology (Oxford,... Aug 2021Antidepressant drugs in adolescent depression are sometimes mired by efficacy issues and paradoxical effects. Transcranial direct current stimulation (tDCS) could...
BACKGROUND
Antidepressant drugs in adolescent depression are sometimes mired by efficacy issues and paradoxical effects. Transcranial direct current stimulation (tDCS) could represent an alternative.
AIMS/METHODS
We tested the antidepressant action of prefrontal tDCS and paroxetine (20 mg/kg, intraperitoneal) in olfactory bulbectomised (OBX) adolescent rats. Using enzyme-linked immunosorbent assays and in situ hybridisation, we examined treatment-induced changes in plasma brain-derived neurotrophic factor (BDNF) and brain serotonin transporter (SERT) and 5-HT-1A mRNA.
RESULTS
OBX-induced anhedonia-like reductions in sucrose preference (SP) correlated with open field (OF) hyperactivity. These were accompanied by decreased zif268 mRNA in the piriform/amygdalopiriform transition area, and increased zif268 mRNA in the hypothalamus. Acute paroxetine (2 days) led to a profound SP reduction, an effect blocked by combined tDCS-paroxetine administration. Chronic (14 days) tDCS attenuated hyperlocomotion and its combination with paroxetine blocked OBX-induced SP reduction. Correlations among BDNF, SP and hyperlocomotion scores were altered by OBX but were normalised by tDCS-paroxetine co-treatment. In the brain, paroxetine increased zif268 mRNA in the hippocampal CA1 subregion and decreased it in the claustrum. This effect was blocked by tDCS co-administration, which also increased zif268 in CA2. tDCS-paroxetine co-treatment had variable effects on 5-HT1A receptors and SERT mRNA. 5-HT1A receptor changes were found exclusively within depression-related parahippocampal/hippocampal subregions, and SERT changes within fear/defensive response-modulating brainstem circuits.
CONCLUSION
These findings point towards potential synergistic efficacies of tDCS and paroxetine in the OBX model of adolescent depression via mechanisms associated with altered expression of BDNF, 5-HT1A, SERT and zif268 in discrete corticolimbic areas.
Topics: Animals; Brain-Derived Neurotrophic Factor; Combined Modality Therapy; Depression; Disease Models, Animal; Male; Olfactory Bulb; Paroxetine; RNA, Messenger; Rats; Rats, Sprague-Dawley; Receptor, Serotonin, 5-HT1A; Serotonin Plasma Membrane Transport Proteins; Selective Serotonin Reuptake Inhibitors; Transcranial Direct Current Stimulation
PubMed: 33908307
DOI: 10.1177/02698811211000765 -
The Cochrane Database of Systematic... May 2017Approximately 20% of stroke patients experience clinically significant levels of anxiety at some point after stroke. Physicians can treat these patients with... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Approximately 20% of stroke patients experience clinically significant levels of anxiety at some point after stroke. Physicians can treat these patients with antidepressants or other anxiety-reducing drugs, or both, or they can provide psychological therapy. This review looks at available evidence for these interventions. This is an update of the review first published in October 2011.
OBJECTIVES
The primary objective was to assess the effectiveness of pharmaceutical, psychological, complementary, or alternative therapeutic interventions in treating stroke patients with anxiety disorders or symptoms. The secondary objective was to identify whether any of these interventions for anxiety had an effect on quality of life, disability, depression, social participation, caregiver burden, or risk of death.
SEARCH METHODS
We searched the trials register of the Cochrane Stroke Group (January 2017). We also searched the Cochrane Central Register of Controlled Trials (CENTRAL; the Cochrane Library; 2017, Issue 1: searched January 2017); MEDLINE (1966 to January 2017) in Ovid; Embase (1980 to January 2017) in Ovid; the Cumulative Index to Nursing and Allied Health Literature (CINAHL; 1937 to January 2017) in EBSCO; and PsycINFO (1800 to January 2017) in Ovid. We conducted backward citation searches of reviews identified through database searches and forward citation searches of included studies. We contacted researchers known to be involved in related trials, and we searched clinical trials registers for ongoing studies.
SELECTION CRITERIA
We included randomised trials including participants with a diagnosis of both stroke and anxiety for which treatment was intended to reduce anxiety. Two review authors independently screened and selected titles and abstracts for inclusion.
DATA COLLECTION AND ANALYSIS
Two review authors independently extracted data and assessed risk of bias. We performed a narrative review. We planned to do a meta-analysis but were unable to do so as included studies were not sufficiently comparable.
MAIN RESULTS
We included three trials (four interventions) involving 196 participants with stroke and co-morbid anxiety. One trial (described as a 'pilot study') randomised 21 community-dwelling stroke survivors to four-week use of a relaxation CD or to wait list control. This trial assessed anxiety using the Hospital Anxiety and Depression Scale and reported a reduction in anxiety at three months among participants who had used the relaxation CD (mean (standard deviation (SD) 6.9 (± 4.9) and 11.0 (± 3.9)), Cohen's d = 0.926, P value = 0.001; 19 participants analysed).The second trial randomised 81 participants with co-morbid anxiety and depression to paroxetine, paroxetine plus psychotherapy, or standard care. Mean levels of anxiety severity scores based on the Hamilton Anxiety Scale (HAM-A) at follow-up were 5.4 (SD ± 1.7), 3.8 (SD ± 1.8), and 12.8 (SD ± 1.9), respectively (P value < 0.01).The third trial randomised 94 stroke patients, also with co-morbid anxiety and depression, to receive buspirone hydrochloride or standard care. At follow-up, the mean levels of anxiety based on the HAM-A were 6.5 (SD ± 3.1) and 12.6 (SD ± 3.4) in the two groups, respectively, which represents a significant difference (P value < 0.01). Half of the participants receiving paroxetine experienced adverse events that included nausea, vomiting, or dizziness; however, only 14% of those receiving buspirone experienced nausea or palpitations. Trial authors provided no information about the duration of symptoms associated with adverse events. The trial of relaxation therapy reported no adverse events.The quality of the evidence was very low. Each study included a small number of participants, particularly the study of relaxation therapy. Studies of pharmacological agents presented details too limited to allow judgement of selection, performance, and detection bias and lack of placebo treatment in control groups. Although the study of relaxation therapy had allocated participants to treatment using an adequate method of randomisation, study recruitment methods might have introduced bias, and drop-outs in the intervention group may have influenced results.
AUTHORS' CONCLUSIONS
Evidence is insufficient to guide the treatment of anxiety after stroke. Further well-conducted randomised controlled trials (using placebo or attention controls) are required to assess pharmacological agents and psychological therapies.
Topics: Anti-Anxiety Agents; Antidepressive Agents; Anxiety; Buspirone; Depression; Humans; Middle Aged; Paroxetine; Pilot Projects; Psychotherapy; Randomized Controlled Trials as Topic; Relaxation Therapy; Stroke
PubMed: 28535332
DOI: 10.1002/14651858.CD008860.pub3 -
European Journal of Drug Metabolism and... Sep 2022Herein, hydroxylation activities at the 6β-position and 21-position of progesterone mediated by human cytochrome P450 (CYP) 2D6 and its variants and the effects of...
BACKGROUND AND OBJECTIVES
Herein, hydroxylation activities at the 6β-position and 21-position of progesterone mediated by human cytochrome P450 (CYP) 2D6 and its variants and the effects of psychotropic drugs on these hydroxylation activities were compared to clarify whether CYP2D6 polymorphisms and psychotropic drugs impact neurosteroid levels in the brain.
METHODS
Progesterone was incubated with CYP2D6.1, CYP2D6.2 (Arg296Cys, Ser486Thr), CYP2D6.10 (Pro34Ser, Ser486Thr), and CYP2D6.39 (Ser486Thr) in the absence or presence of typical psychotropic drugs (fluvoxamine, fluoxetine, paroxetine, fluphenazine, and milnacipran) and endogenous steroids (testosterone and cortisol). Then, 6β- and 21-hydroxyprogesterone levels were determined by high-performance liquid chromatography.
RESULTS
Although the Michaelis-Menten constants (K) for progesterone 6β- and 21-hydroxylation reactions mediated by the different CYP2D6 variants were similar, the maximal velocity (V) values of the reactions mediated by CYP2D6.1 and CYP2D6.2 were the highest, followed by those mediated by CYP2D6.39 and CYP2D6.10. Thus, the of progesterone 6β- and/or 21-hydroxylation reactions mediated by CYP2D6.1 and CYP2D6.2 showed the highest V/K values, followed by the reactions mediated by CYP2D6.39. All investigated compounds inhibited progesterone 21-hydroxylation mediated by CYP2D6 variants at high concentrations. Interestingly, at low concentrations, fluoxetine increased progesterone 21-hydroxylation mediated by CYP2D6.1, but not that mediated by CYP2D6.2 or CYP2D6.10. In addition, the K value for CYP2D6.2 was elevated in the presence of fluoxetine, whereas the value for CYP2D6.1 was unaltered; however, V values of both CYP2D6.1 and CYP2D6.2 were increased. Paroxetine competitively inhibited CYP2D6.1- and CYP2D6.2-mediated progesterone 21-hydroxylation.
CONCLUSIONS
These results suggest that CYP2D6 polymorphism can affect the stimulation/inhibition of progesterone 21-hydroxylation.
Topics: Humans; Cytochrome P-450 CYP2D6; Fluoxetine; Hydroxylation; Paroxetine; Progesterone; Psychotropic Drugs
PubMed: 35838883
DOI: 10.1007/s13318-022-00784-7 -
Journal of Clinical Sleep Medicine :... Jul 2020Sexsomnia is a parasomnia consisting of sexual behavior during non-rapid eye movement sleep. To date, there have been 116 clinical cases of sexsomnia reported and most...
Sexsomnia is a parasomnia consisting of sexual behavior during non-rapid eye movement sleep. To date, there have been 116 clinical cases of sexsomnia reported and most were treated with clonazepam. We present a case of an adult male with sexsomnia that started during his college days. He presented to us because of problems in his current marriage arising from sexual behavior during sleep. Polysomnography revealed no significant sleep-disordered breathing, electroencephalography abnormality, or abnormal movement during non-rapid eye movement and rapid eye movement (REM) sleep. Alcohol consumption was reported to worsen his sexsomnia. To avoid the neuro-depressant effects of benzodiazepines, paroxetine was administered and resulted in complete resolution of sexsomnia.
Topics: Adult; Humans; Male; Parasomnias; Paroxetine; Polysomnography; Sleep; Sleep Apnea Syndromes
PubMed: 32672534
DOI: 10.5664/jcsm.8478 -
Journal of Neurochemistry Sep 2022Selective serotonin reuptake inhibitor (SSRI) antidepressants are commonly prescribed treatments for depression, but their effects on serotonin reuptake and release are...
Selective serotonin reuptake inhibitor (SSRI) antidepressants are commonly prescribed treatments for depression, but their effects on serotonin reuptake and release are not well understood. Drosophila melanogaster, the fruit fly, expresses the serotonin transporter (dSERT), the major target of SSRIs, but real-time serotonin changes after SSRIs have not been characterized in this model. The goal of this study was to characterize effects of SSRIs on serotonin concentration and reuptake in Drosophila larvae. We applied various doses (0.1-100 μM) of fluoxetine (Prozac), escitalopram (Lexapro), citalopram (Celexa), and paroxetine (Paxil), to ventral nerve cord (VNC) tissue and measured optogenetically-stimulated serotonin release with fast-scan cyclic voltammetry (FSCV). Fluoxetine increased reuptake from 1 to 100 μM, but serotonin concentration only increased at 100 μM. Thus, fluoxetine occupies dSERT and slows clearance but does not affect concentration. Escitalopram and paroxetine increased serotonin concentrations at all doses, but escitalopram increased reuptake more. Citalopram showed lower concentration changes and faster reuptake profiles compared with escitalopram, so the racemic mixture of citalopram does not change reuptake as much as the S-isomer. Dose response curves were constructed to compare dSERT affinities and paroxetine showed the highest affinity and fluoxetine the lowest. These data demonstrate SSRI mechanisms are complex, with separate effects on reuptake or release. Furthermore, dynamic serotonin changes in Drosophila are similar to previous studies in mammals. This work establishes how antidepressants affect serotonin in real-time, which is useful for future studies that will investigate pharmacological effects of SSRIs with different genetic mutations in Drosophila.
Topics: Animals; Antidepressive Agents; Citalopram; Drosophila; Drosophila melanogaster; Fluoxetine; Mammals; Paroxetine; Serotonin; Selective Serotonin Reuptake Inhibitors
PubMed: 35736504
DOI: 10.1111/jnc.15658