Effect of sertraline in the treatment and prevention of poststroke depression: A meta-analysis.
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ABSTRACT: Background
Morbidity of poststroke depression (PSD) remains high worldwide. Additionally, PSD causes multiple sequelae. Although sertraline has been reported to be effective in treating PSD, many studies remain inconsistent.Methods
PubMed, Embase, Scopus, Cochrane Central Register of Controlled Trials, Clinical trials. gov, Wan fang Data (Chinese), VIP (Chinese), and CNKI (Chinese) were retrieved from inception to April 2017. Randomized controlled trials (RCTs) and self-controlled trials (SCTs) were recruited, which met the inclusion criteria in our study. The depression rating scores, the incidence of PSD, activities of daily living (ADL), neurological impairment scores, and adverse effects were assessed.Results
Around 11 studies were recruited in our work, including 1258 participants. For trials enrolled, the results were depicted: the reduction of depression rating scores was significant in sertraline groups (WMD -6.38; 95% CI -8.63 to -4.14; P?0.05). However, in sensitivity analyses, the conclusions of the reduction of depression rating scores and the improvement of ADL were altered.Conclusions
The study suggests that sertraline has a potentially protective role compared with control groups and demonstrates sertraline is safe. However, the reduction of depression rating scores and the improvement of ADL should be considered carefully.
SUBMITTER: Feng R
PROVIDER: S-EPMC6310584 | biostudies-literature | 2018 Dec
REPOSITORIES: biostudies-literature
Publications
Effect of sertraline in the treatment and prevention of poststroke depression: A meta-analysis.
Feng Rongfang R Wang Peng P Gao Chenhao C Yang Jianbo J Chen Zixiao Z Yang Yaoyao Y Jiao Jiawei J Li Mengmeng M Fu Bo B Li Ling L Zhang Zhenxiang Z Wang Shiguang S
Medicine 20181201 49
<h4>Background</h4>Morbidity of poststroke depression (PSD) remains high worldwide. Additionally, PSD causes multiple sequelae. Although sertraline has been reported to be effective in treating PSD, many studies remain inconsistent.<h4>Methods</h4>PubMed, Embase, Scopus, Cochrane Central Register of Controlled Trials, Clinical trials. gov, Wan fang Data (Chinese), VIP (Chinese), and CNKI (Chinese) were retrieved from inception to April 2017. Randomized controlled trials (RCTs) and self-controlle ...[more]
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Project description:ObjectiveThe aim of this study is to create a rank order of the comparative efficacy and acceptability (risk of all-cause discontinuation) of antidepressant treatment in poststroke depression (PSD) by integrating direct and indirect evidence.DesignMultiple-treatments meta-analysis of randomised controlled trials.ParticipantsPatients with depression following stroke.Interventions10 antidepressants and placebo in the acute treatment of PSD.Outcome measuresThe primary outcomes were the overall efficacy, defined as the mean change of the total depression score. The secondary outcome was the acceptability, defined as risk of all-cause discontinuation. These estimates as standardised mean differences or ORs with 95% CIs.ResultsWe identified 12 suitable trials, with data from 707 participants. All drugs were significantly more effective than placebo apart from sertraline, nefiracetam and fluoxetine. Most of the comparisons for acceptability revealed no significant differences except that paroxetine had significantly lower all-cause discontinuation than doxepin, citalopram and fluoxetine. Standardised mean differences compared with placebo for efficacy varied from -6.54 for the best drug (reboxetine) to 0.51 for the worst drug (nefiracetam). ORs compared with placebo for acceptability ranged from 0.09 for the best drug (paroxetine) to 3.42 for the worst drug (citalopram). For the efficacy rank, reboxetine, paroxetine, doxepin and duloxetine were among the most efficacious treatments, the cumulative probabilities of which were 100%, 85.7%, 83.2%, 62.4%, respectively. With respect to the acceptability rank, paroxetine, placebo, sertraline and nortriptyline were among the most acceptable treatments, the cumulative probabilities of which were 92.4%, 63.5%, 57.3%, 56.3%.ConclusionAfter weighing the efficacy and acceptability, we conclude that paroxetine might be the best choice when starting acute treatment for PSD, and fluoxetine might be the worst choice.Trial registration numberThis systematic review has been registered in the Prospective Register of Systematic Review Protocols (PROSPERO) public database (CRD42017054741; http://www.crd.york.ac.uk/PROSPERO).
| S-EPMC5629745 | biostudies-literature
Project description:Depression is a proposed risk factor for heart failure based largely on epidemiological data; few experimental data addressing this hypothesis are available.Depression was evaluated in relation to cardiac structural and functional phenotypes assessed by transthoracic echocardiography in 42 adult female cynomolgus monkeys that consumed a Western-like diet for 3 years. Half of the monkeys were treated with sertraline HCl for 18 months, and depressive behavior was assessed for 12 months before echocardiography.Depressed monkeys (the 19/42 with depressive behavior rates above the mean rate) had higher heart rates (HRs; 171 [4.1[ versus 152 [6.1]) and smaller body surface area (0.13 [0.003] versus 0.15 [0.004]), left ventricular (LV) end-systolic dimension (0.75 [0.05] versus 0.89 [0.04]), LV systolic (0.76 [0.08] versus 1.2 [0.11]) and diastolic (2.4 [0.23] versus 3.4 [0.26]) volumes, and left atrial volumes (1.15 [0.14] versus 1.75 [0.12]; p values < .05). Doppler profiles of depressed monkeys indicated greater myocardial relaxation (higher e' and higher e'/a' ratio) and lower filling pressures (lower E/e') compared to nondepressed monkeys (p values < .05). Although sertraline treatment reduced HR (150 [5.8] versus 171 [4.8]) and modestly increased chamber dimensions (LV end-systolic dimension: 0.91 [0.05] versus 0.74 [0.03]; LV end-diastolic dimension, body surface area adjusted 1.69 [0.05] versus 1.47 [0.06]; p values < .05), it did not overtly affect systolic or diastolic function (p values > .10).These data suggest that behavioral depression in female primates is accompanied by differences in cardiac function, although not in ways classically associated with subclinical heart failure. Selective serotonin reuptakes show promise in supporting heart function by reducing HR and perhaps improving LV filling; however, further investigation is needed.
| S-EPMC3971435 | biostudies-literature
Project description:BackgroundPoststroke depression (PSD) is a common form of stroke patients. Whether the risk of PSD is influenced by the stroke lesion location and sex remains a matter of debate. The objective of this study was to examine the association between the risk of PSD and the stroke lesion location and sex by performing a systematic meta-analysis.MethodsSubgroup analyses were performed according to the time interval after stroke onset to assessment for PSD. A total of 31 reports involving 5,309 subjects (for lesion location analysis) and 5,489 subjects (for sex analysis) suffering from stroke were included in this meta-analysis.ResultsThe pooled odds ratio (OR) of PSD after a left-hemisphere stroke, compared with a right-hemisphere stroke was 1.11 (95% confidence interval [CI] 0.82-1.49) and OR of PSD after a male stroke, compared with a female stroke was 0.68 (95% CI 0.58-0.81). Subacute poststroke subgroup (1-6 months) significantly favored PSD occurring after a left hemisphere stroke (OR = 1.50, 95% CI 1.21-1.87). Furthermore, there was a statistically significant association between PSD and female stroke for studies with acute poststroke group (OR = 0.73, 95% CI 0.62-0.86) and subacute poststroke stroke phase (OR = 0.69, 95% CI 0.56-0.86).ConclusionsThis systematic review suggests that patients with left hemisphere stroke may be more susceptible to PSD during subacute phase of stroke and female stroke may be more susceptible to PSD during acute and subacute phase of stroke.
| S-EPMC5651383 | biostudies-literature
Project description:Depression is common in Alzheimer disease (AD), and antidepressants are commonly used for its treatment, however, evidence for antidepressant efficacy in this population is lacking. The authors conducted a multicenter, randomized, placebo-controlled trial titled "Depression in Alzheimer's Disease-2" to assess the efficacy and tolerability of sertraline for depression in AD.One hundred thirty-one participants from five U.S. medical centers with mild-to-moderate AD (Mini-Mental State Examination scores 10-26) and depression of AD were randomized to double-blinded treatment with sertraline (N = 67) or placebo (N = 64), with a target dosage of 100 mg daily. Efficacy was assessed using logistic regressions and mixed effects models in an intention-to-treat analysis with imputation of missing data. Principal outcome measures were modified Alzheimer's Disease Cooperative Study-Clinical Global Impression of Change (mADCS-CGIC), change in Cornell Scale for Depression in Dementia (CSDD) scores, and remission defined by both mADCS-CGIC score <or=2 and CSDD score <or=6.mADCS-CGIC ratings (odd ratio [OR = 1.01], 95% confidence interval [CI]: 0.52-1.97, p = 0.98), CSDD scores (median difference at 12 weeks 1.2, 95% CI: 1.65-4.05, p = 0.41), and remission at 12 weeks of follow-up (OR = 2.06, 95% CI: 0.84-5.04, p = 0.11) did not differ between sertraline (N = 67) and placebo (N = 64). Sertraline-treated patients experienced more adverse events, most notably gastrointestinal and respiratory, than placebo-treated patients.Sertraline did not demonstrate efficacy for the treatment depression symptoms in patients with AD. In addition, its use was associated with an increased incidence of adverse events. Thus, selective serotonin reuptake inhibitors may be of limited value for treating depression in patients with AD.
| S-EPMC2842121 | biostudies-literature
Project description:ObjectiveChaihu Jia Longgu Muli decoction (CLMD) is widely used in the treatment of poststroke depression (PSD) in China. Some evidences show that it has advantages, but there lacks reliable evidence. This study aims to systematically evaluate the efficacy and safety of CLMD in the treatment of PSD.MethodsAll randomized controlled trials (RCTs) of CLMD in the treatment of PSD were searched from the following databases: PubMed, Cochrane Library, Embase, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang Database, VIP Database, and Chinese Biomedical Literature Service System (CBM), from their inception to May 2021. Two researchers independently screened the literature, extracted the data, and evaluated the risk of bias in the included studies. Meta-analysis was performed using RevMan5.3 software.ResultsA total of 13 RCTs involving 1665 patients were finally included in this study, among which 5 RCTs were oral CLMD alone versus antidepressants, and 8 RCTs were oral CLMD with antidepressants versus antidepressants. Meta-analysis results showed that oral administration of CLMD could improve Hamilton's Depression Scale (HAMD) and the Modified Edinburgh-Scandinavian Stroke Scale (MESSS) scores, improve the Barthel index, and have a low rate of adverse reactions, but there was no significant difference in the total effective rate (p=0.21 > 0.05) and the National Institute of Health Stroke Scale (NIHSS) score (p=0.47 > 0.05) between the antidepressants group and the oral administration of the CLMD group. Oral CLMD combined with antidepressants could improve the total effective rate, HAMD, and MESSS score, but there was no significant difference in Barthel index (p=0.06 > 0.05) and the adverse reaction rate (p=0.14 > 0.05) between the two groups.ConclusionCurrent evidence suggests that oral CLMD alone or with antidepressants is more effective and safer in the treatment of PSD than oral antidepressants. Due to the limitation of the quality and quantity of the included studies, more high-quality studies are needed to confirm the above conclusion.
| S-EPMC8397549 | biostudies-literature
Project description:Poststroke depression (PSD) constitutes an important complication of stroke, leading to great disability as well as increased mortality. Since which treatment for PSD should be preferred are still matters of controversy, we are aiming to compare and rank these pharmacological and nonpharmacological interventions.We will employ a network meta-analysis to incorporate both direct and indirect evidence from relevant trials. We will search PubMed, the Cochrane Library Central Register of Controlled Trials, Embase, and the reference lists of relevant articles for randomized controlled trials (RCT) of different PSD treatment strategies. The characteristics of each RCT will be summarized, including the study characteristics, the participant characteristics, the outcome measurements, and adverse events. The risk of bias will be assessed by means of the Cochrane Collaboration's risk of bias tool. The primary outcome was change in Hamilton Depression Scale (HAMD) score. Secondary outcomes involve patient response rate (defined as at least a 50% score reduction on HAMD), and remission rate (defined as no longer meeting baseline criteria for depression). Moreover, we will assess the acceptability of treatments according to treatment discontinuation. We will perform pairwise meta-analyses by random effects model and network meta-analysis by Bayesian random effects model.Formal ethical approval is not required as primary data will not be collected. Our results will help to reduce the uncertainty about the effectiveness and safety of PSD management, which will encourage further research for other therapeutic options. The review will be disseminated in peer-reviewed publications and conference presentations.CRD42016049049.
| S-EPMC5319512 | biostudies-other
Project description:Depression and antidepressant use are common in Alzheimer disease (AD), but the effect of antidepressant treatment for depression on longer term outcomes is unknown. The authors report the Week-24 outcomes of patients who participated in a 12-week efficacy study of sertraline for depression of AD.One hundred thirty-one participants (sertraline = 67, placebo = 64) with mild-moderate AD and depression participated in the study. Patients who showed improvement on the modified Alzheimer's Disease Cooperative Study Clinical Global Impression-Change (mADCS-CGIC) after 12 weeks of randomized treatment with sertraline or placebo continued double-blinded treatment for an additional 12 weeks. Depression response and remission at 24 weeks were based on mADCS-CGIC score and change in Cornell Scale for Depression in Dementia (CSDD) score. Secondary outcome measures included time to remission, nonmood neuropsychiatric symptoms, global cognition, function, and quality of life.One hundred seventeen (89.3%) participants completed all study assessments and 74 (56.5%; sertraline = 38, placebo = 36) completed all 24 weeks on randomized treatment. By 24 weeks, there were no between-group differences in depression response (sertraline = 44.8%, placebo = 35.9%; odds ratio [95% CI] = 1.23 [0.64-2.35]), change in CSDD score (median difference = 0.6 [95% CI: -2.26 to 3.46], chi2 [df = 2] = 1.03), remission rates (sertraline = 32.8%, placebo = 21.8%; odds ratio [95% CI] = 1.61 [0.70-3.68]), or secondary outcomes. Common selective serotonin reuptake inhibitor-associated adverse events, specifically diarrhea, dizziness, and dry mouth, and pulmonary serious adverse events were more frequent in sertraline-randomized patients than in placebo subjects.Sertraline treatment is not associated with delayed improvement between 12 and 24 weeks of treatment and may not be indicated for the treatment of depression of AD.
| S-EPMC2849739 | biostudies-literature
Project description:ContextDepression occurs in more than half of patients who have experienced a stroke. Poststroke depression has been shown in numerous studies to be associated with both impaired recovery in activities of daily living and increased mortality. Prevention of depression thus represents a potentially important goal.ObjectiveTo determine whether treatment with escitalopram or problem-solving therapy over the first year following acute stroke will decrease the number of depression cases that develop compared with placebo medication.Design, setting, and participantsA multisite randomized controlled trial for prevention of depression among 176 nondepressed patients was conducted within 3 months following acute stroke from July 9, 2003, to October 1, 2007. The 12-month trial included 3 groups: a double-blind placebo-controlled comparison of escitalopram (n = 59) with placebo (n = 58), and a nonblinded problem-solving therapy group (n = 59).Main outcome measuresThe main outcome measure was the development of major or minor poststroke depression based on symptoms elicited by the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) (DSM-IV) and the diagnostic criteria from DSM-IV for depression due to stroke with major depressive-like episode or minor depression (ie, research criteria).ResultsPatients who received placebo were significantly more likely to develop depression than individuals who received escitalopram (11 major and 2 minor cases of depression [22.4%] vs 3 major and 2 minor cases of depression [8.5%], adjusted hazard ratio [HR], 4.5; 95% confidence interval [CI], 2.4-8.2; P < .001) and also more likely than individuals who received problem-solving therapy (5 major and 2 minor cases of depression [11.9%], adjusted HR, 2.2; 95% CI, 1.4-3.5; P < .001). These results were adjusted for history of mood disorders and remained significant after considering possible confounders such as age, sex, treatment site, and severity of impairment in the model. Using an intention-to-treat conservative method of analyzing the data, which assumed that all 27 patients who did not start randomized treatment would have developed depression, and controlling for prior history of mood disorders, escitalopram was superior to placebo (23.1% vs 34.5%; adjusted HR, 2.2; 95% CI, 1.2-3.9; P = .007), while problem-solving therapy was not significantly better than placebo (30.5% vs 34.5%; adjusted HR, 1.1; 95% CI, 0.8-1.5; P = .51). Adverse events, including all-cause hospitalizations, nausea, and adverse effects associated with escitalopram were not significantly different between the 3 groups.ConclusionsIn this study of nondepressed patients with recent stroke, the use of escitalopram or problem-solving therapy resulted in a significantly lower incidence of depression over 12 months of treatment compared with placebo, but problem-solving therapy did not achieve significant results over placebo using the intention-to-treat conservative method of analysis.Trial registrationclinicaltrials.gov Identifier: NCT00071643.
| S-EPMC2743160 | biostudies-literature
Project description:INTRODUCTION:A number of observational studies have indicated that poststroke depression could increase the risk of stroke outcomes. There is a meta-analysis indicating that poststroke depression is a risk factor of all-cause mortality. This paper reports the protocol for a systematic review and meta-analysis to clarify the associations of poststroke depression with stroke recurrence and mortality in order to determine whether poststroke depression is a predictor of stroke outcomes according to data extracted from relevant observational studies. METHODS AND ANALYSIS:MEDLINE, Web of Science databases, EMBASE, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews will be used to conduct the search. Published studies written in English will be included. The risk of bias for the studies included in the systematic review or meta-analysis will be assessed by the Newcastle-Ottawa Quality Assessment Scale. HRs for stroke recurrence and mortality with 95% CIs will be included as primary outcomes. Subgroup analyses and meta-regression will be performed. ETHICS AND DISSEMINATION:Ethics approval will not be needed because the data used in this systematic review will be extracted from published studies. The results of the systematic review focusing on whether depression after stroke is a predictor for stroke recurrence and mortality will be disseminated by publication in a peer-reviewed journal. PROSPERO REGISTRATION NUMBER:CRD42018107944.
| S-EPMC6303620 | biostudies-literature
Project description:The purpose of this study was to explore the relationship between lesion location and poststroke depression using statistical parametric mapping.First episode patients with stroke were assessed within 12?days and at 1-month poststroke. Patients with an a priori defined cut-off score of 11 on the Hospital Anxiety and Depression Scale (HADS) at follow-up were further assessed using the Mini-International Neuropsychiatric Interview (MINI) to confirm a clinical diagnosis of major or minor depression in accordance with Diagnostic and Statistical Manual-IV (DSM-IV) inclusion criteria. Participants were included if they were aged 18-85?years, proficient in English and eligible for MRI. Patients were excluded if they had a confounding diagnosis such as major depressive disorder at the time of admission, a neurodegenerative disease, epilepsy or an imminently life-threatening comorbid illness, subarachnoid or subdural stroke, a second episode of stroke before follow-up and/or a serious impairment of consciousness or language. Infarcts observed on MRI scans were manually segmented into binary images, linearly registered into a common stereotaxic coordinate space. Using statistical parametric mapping, we compared infarct patterns in patients with stroke with and without depression.27% (15/55 patients) met criteria for depression at follow-up. Mean infarct volume was 19±53?mL and National Institute of Health Stroke Scale (NIHSS) at Time 1 (within 12?days of stroke) was 4±4, indicating a sample of mild strokes. No voxels or clusters were significant after a multiple comparison correction was applied (p>0.05). Examination of infarct maps showed that there was minimal overlap of infarct location between patients, thus invalidating the voxel comparison analysis.This study provided inconclusive evidence for the association between infarcts in a specific region and poststroke depression.
| S-EPMC4091263 | biostudies-other