Poor clinical outcomes among pneumonia patients with depressive disorder.
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ABSTRACT:
SUBMITTER: Kao LT
PROVIDER: S-EPMC4281227 | biostudies-other | 2014
REPOSITORIES: biostudies-other
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Project description:Background: The difficulty in timely evaluating patient response to antidepressants has brought great challenge to the treatment of major depressive disorder (MDD). Some studies found that the electroencephalogram (EEG) microstates might be a reliable marker to evaluate patient response to treatment. The present study aims to evaluate the relationship between EEG microstate parameters and MDD symptoms before and after treatment to identify predictive biological markers for patient response. Methods: Thirty drug-naïve MDD patients (20 females and 10 males) were enrolled in this study. All the patients received effective dosages of selective serotonin reuptake inhibitors, and EEG recordings were collected at baseline and 2 weeks of treatment. Brain activities during the eyes-closed state were recorded using 64-channel electroencephalography, and the patients' microstates were clustered into four maps according to their topography (labeled A, B, C, and D). The differences of EEG microstates before and after treatment were compared using paired t-test. Spearman correlation coefficients were calculated to identify the relationships between the improvement of depression and anxiety symptoms and microstate parameters. Results: The mean duration (69.67 ± 10.33 vs. 64.00 ± 7.70, p < 0.001) and occurrence (4.06 ± 0.69, vs. 3.69 ± 0.70, p = 0.002) of microstate B decreased significantly after treatment. The proportion of microstate B also decreased (27.53 ± 5.81, vs. 23.23 ± 4.61, p < 0.001), while the occurrence of microstate A increased after treatment. A significant negative correlation was found between the change of score of Hamilton Rating Scale for Anxiety and the increase of the occurrence of microstate A (r = -0.431, p < 0.05) after 2 weeks of treatment. The reduction of the duration of microstate B was found to be predictive of patient response to antidepressants after 3 months. Conclusion: This study explored the relationship between changes of EEG microstates and patient response to antidepressants. Depression symptoms might be associated with the duration of microstate B and anxiety symptoms related to the occurrence of microstate A. Therefore, the duration of microstate B and the occurrence of microstate A are potential biological markers for MDD patients' early response and further clinical outcomes.
| S-EPMC8415359 | biostudies-literature
Project description:PurposeTo compare treatment outcomes in patients with major depressive disorder treated with duloxetine, escitalopram, fluoxetine, paroxetine, or sertraline for up to 6 months.Patients and methodsData were taken from a 6-month prospective, observational study that included 1,549 major depressive disorder patients without sexual dysfunction in 12 countries. We report the overall results and those from Asian countries. Depression severity was measured using the Clinical Global Impression and the 16-item Quick Inventory of Depressive Symptomatology Self-Report (QIDS-SR16). Clinical and functional remissions were defined as having a QIDS-SR16 <6, and as having a rating of <3 on all three Sheehan Disability Scale items and no reduced productivity, respectively. Mixed effects modeling with repeated measures analysis and generalized estimating equation models were used. Propensity scores were included in the models.ResultsThe mixed effects modeling with repeated measures regression models showed that the Clinical Global Impression rating during follow-up was significantly lower in those patients treated with duloxetine compared with escitalopram (0.40, 95% CI 0.25 to 0.56); fluoxetine (0.22, 95% CI 0.05 to 0.38); paroxetine (0.38, 95% CI 0.23 to 0.54); and sertraline (0.32, 95% CI 0.16 to 0.49). The QIDS-SR16 of duloxetine-treated patients was significantly lower than those treated with escitalopram (1.58, 95% CI 1.03 to 2.12); fluoxetine (1.48, 95% CI 0.90 to 2.06); paroxetine (1.53, 95% CI 1.00 to 2.07); and sertraline (1.19, 95% CI 0.61 to 1.78). The probability of clinical remission of the patients treated with escitalopram, fluoxetine, paroxetine, and sertraline was lower than those treated with duloxetine (OR 0.46, 95% CI 0.33 to 0.64; OR 0.42, 95% CI 0.29 to 0.61; OR 0.40, 95% CI 0.29 to 0.56; OR 0.50, 95% CI 0.35 to 0.71; respectively). The regression analysis of functional remission also showed more favorable results for duloxetine, with OR ranging from 0.43, 95% CI 0.31 to 0.60 for paroxetine to 0.49, 95% CI 0.35 to 0.70 for sertraline. The results for the Asian countries were generally consistent.ConclusionDuloxetine-treated patients had better 6-month outcomes in terms of depression severity and clinical and functional remission, compared with selective serotonin reuptake inhibitor-treated patients.
| S-EPMC6165742 | biostudies-literature
Project description:Uncertainties exist about the rates, predictors, and outcomes of major depressive disorder (MDD) among individuals with traumatic brain injury (TBI).To describe MDD-related rates, predictors, outcomes, and treatment during the first year after TBI.Cohort from June 2001 through March 2005 followed up by structured telephone interviews at months 1 through 6, 8, 10, and 12 (data collection ending February 2006).Harborview Medical Center, a level I trauma center in Seattle, Washington.Five hundred fifty-nine consecutively hospitalized adults with complicated mild to severe TBI.The Patient Health Questionnaire (PHQ) depression and anxiety modules were administered at each assessment and the European Quality of Life measure was given at 12 months.Two hundred ninety-seven of 559 patients (53.1%) met criteria for MDD at least once in the follow-up period. Point prevalences ranged between 31% at 1 month and 21% at 6 months. In a multivariate model, risk of MDD after TBI was associated with MDD at the time of injury (risk ratio [RR], 1.62; 95% confidence interval [CI], 1.37-1.91), history of MDD prior to injury (but not at the time of injury) (RR, 1.54; 95% CI, 1.31-1.82), age (RR, 0.61; 95% CI, 0.44-0.83 for > or = 60 years vs 18-29 years), and lifetime alcohol dependence (RR, 1.34; 95% CI, 1.14-1.57). Those with MDD were more likely to report comorbid anxiety disorders after TBI than those without MDD (60% vs 7%; RR, 8.77; 95% CI, 5.56-13.83). Only 44% of those with MDD received antidepressants or counseling. After adjusting for predictors of MDD, persons with MDD reported lower quality of life at 1 year compared with the nondepressed group.Among a cohort of patients hospitalized for TBI, 53.1% met criteria for MDD during the first year after TBI. Major depressive disorder was associated with history of MDD and was an independent predictor of poorer health-related quality of life.
| S-EPMC3090293 | biostudies-literature
Project description:Search for the biomarkers of major depressive disorder (MDD) has facilitated from the genes expressed in the patientâs blood cells. Because the severity of depressive symptoms and characteristics in patients with MDD are differed by the age at onset of first depressive episode, the potential transcriptomic markers in blood cells may also be different by the age at onset of MDD. In this study, we searched the transcriptomic markers of late-onset (onset ages ⥠50 years) MDD (LOD) from the expressed genes in blood cells, and identified state-dependent biomarkers in the patients. We assessed the expressed genes in blood cells by the microarray and found that the expression levels of 3,066 probes were state-dependently changed in the blood cells of patients with LOD. Elderly (age â¥50 years) outpatients and inpatients with MDD corresponding to a DSM-IV diagnosis of the melancholy type of MDD episodes were studied. The depressive state was measured using the Structured Interview Guide for the Hamilton Depression (SIGH-D) rating scale. Syndromal remission was defined as a stage in which a participant did not meet the diagnosis of a MINI major depressive episode for a period of 2 consecutive months and had a SIGH-D score of less than 8. Twelve healthy individuals were also recruited. Blood was obtained from the participants and analyzed using an Agilent SurePrint G3 Human GE 8Ã60K v2 Microarray (Design ID: 039494).
2016-01-14 | E-GEOD-76826 | biostudies-arrayexpress
Project description:Depression frequently co-occurs with paediatric obsessive-compulsive disorder (OCD), yet the clinical correlates and impact of depression on CBT outcomes remain unclear. The prevalence and clinical correlates of depression were examined in a paediatric specialist OCD-clinic sample (N = 295; Mean = 15 [7 - 18] years, 42 % female), using both dimensional (Beck Depression Inventory-youth; n = 261) and diagnostic (Development and Wellbeing Assessment; n = 127) measures of depression. The impact of depressive symptoms and suspected disorders on post-treatment OCD severity was examined in a sub-sample who received CBT, with or without SSRI medication (N = 100). Fifty-one per-cent of patients reported moderately or extremely elevated depressive symptoms and 26 % (95 % CI: 18 - 34) met criteria for a suspected depressive disorder. Depressive symptoms and depressive disorders were associated with worse OCD symptom severity and global functioning prior to CBT. Individuals with depression were more likely to be female, have had a psychiatric inpatient admission and less likely to be attending school (ps < 0.01). OCD and depressive symptom severity significantly decreased after CBT. Depressive symptoms and depressive disorders predicted worse post-treatment OCD severity (βs = 0.19 and 0.26, ps < 0.05) but became non-significant when controlling for pre-treatment OCD severity (βs = 0.05 and 0.13, ns). Depression is common in paediatric OCD and is associated with more severe OCD and poorer functioning. However, depression severity decreases over the course of CBT for OCD and is not independently associated with worse outcomes, supporting the recommendation for treatment as usual in the presence of depressive symptoms.
| S-EPMC4465665 | biostudies-literature
Project description:Background: Major Depressive Disorder (MDD) is a moderately heritable disorder with a high lifetime prevalence. At present, laboratory blood tests to support MDD diagnosis are not available. Methods: We used a classifier approach on blood gene expression profiles of a unique set of non-medicated subjects (MDD patients and controls) to select genes of which expression is predictive for disease status. To reveal blood gene expression changes related to MDD disease, we applied a powerful ex vivo stimulus to the blood, i.e. incubation with lipopolysaccharide (LPS; 10 ng/ml blood). Results: Based on LPS-stimulated blood gene expression using whole-genome microarrays in 42 subjects (primary cohort; 21 MDD patients (mean age 42.3 years), 21 healthy controls (mean age 41.9 years)), we identified a set of genes (CAPRIN1, CLEC4A, KRT23, MLC1, PLSCR1, PROK2, ZBTB16) that serves as a molecular signature of MDD. These findings were validated for the primary cohort using an independent quantitative PCR method (P = 0.007). The difference between depressive patients and controls was confirmed (P = 0.019) in a replication cohort of 13 patients with MDD (mean age 42.8 years) and 14 controls (mean age 45.6 years). The MDD-signature score comprised of expression levels of 7 genes could discriminate depressive patients from controls with sensitivity of 76.9% and specificity of 71.8%. Conclusions: We show for the first time that molecular analysis of stimulated blood cells can be used as an endophenotype for MDD diagnosis, which is a milestone in establishing biomarkers for neuropsychiatric disorders with moderate heritability in general. Our results may provide a new entry point for following and predicting treatment outcome, as well as prediction of severity and recurrence of MDD. In total, 33 MDD patients and 34 healthy controls were analyzed using basal gene expression in whole blood, and gene expression from whole blood that was stimulated with LPS for 5-6 h, using microarrays. Patients were arbitrarily selected from all patients to serve as primary cohort (nMDD = 21 (MDD01-MDD21); nControls = 21 (Con01-Con21)), or replication cohort (nMDD = 12 (MDD22-MDD35); nControls = 13 (Con22-Con37)) using microarrays. This submission does not include Samples CON21_LPS or CON30_LPS.
2011-10-04 | E-GEOD-19738 | biostudies-arrayexpress
Project description:BackgroundLymphopenia is a marker of poor prognosis in patients with community-acquired pneumonia (CAP), yet its impact on outcomes in patients with CAP and sepsis remains unknown. We aim to investigate the impact of lymphopenia on outcomes, risk of intensive care unit (ICU) admission, and mortality in CAP patients with sepsis.MethodsThis was a retrospective, observational study of prospectively collected data from an 800-bed tertiary teaching hospital (2005-2019).ResultsOf the 2203 patients with CAP and sepsis, 1347 (61%) did not have lymphopenia, while 856 (39%) did. When compared with the nonlymphopenic group, patients with sepsis and lymphopenia more frequently required ICU admission (P = .001), had a longer hospital length of stay (P ˂ .001), and presented with a higher rate of in-hospital (P ˂ .001) and 30-day mortality (P = .001). Multivariable analysis showed that C-reactive protein ≥15 mg/dL, lymphopenia, pleural effusion, and acute respiratory distress syndrome within 24 hours of admission were risk factors for ICU admission; age ≥80 years was independently associated with decreased ICU admission. In addition, age ≥80 years, chronic renal disease, chronic neurologic disease, being a nursing home resident, lymphopenia, and pleural effusion were independently associated with increased 30-day mortality, whereas pneumococcal vaccination, diabetes mellitus, and fever were independently associated with reduced 30-day mortality.ConclusionsLymphopenia was independently associated with risk of ICU admission and higher in-hospital and 30-day mortality in patients with CAP and sepsis. Early identification of lymphopenia could help identify septic patients with CAP who require or will shortly require critical care.
| S-EPMC8231373 | biostudies-literature
Project description:ImportanceMajor depressive disorder (MDD) is an important risk factor of suicidal behavior, but the added burden of suicidal behavior and MDD on the patient and societal level, including all-cause mortality, is not well studied. Also, the contribution of various prognostic factors for suicidal behavior has not been quantified in larger samples.ObjectiveTo describe the clinical and societal outcomes, including all-cause mortality, of suicidal behavior in patients with MDD and to explore associated risk factors and clinical management to inform future research and guidelines.Design, setting, and participantsThis population-based cohort study used health care data from the Stockholm MDD Cohort. Patients aged 18 years or older with episodes of MDD diagnosed between January 1, 2012, and December 31, 2017, in any health care setting were included. The dates of the data analysis were February 1 to November 1, 2022.ExposuresPatients with MDD with and without records of suicidal behavior.Main outcomes and measuresThe main outcome was all-cause mortality. Secondary outcomes were comorbid conditions, medications, health care resource utilization (HCRU), and work loss. Using Region Stockholm registry variables, a risk score for factors associated with suicidal behavior within 1 year after the start of an MDD episode was calculated.ResultsA total of 158 169 unipolar MDD episodes were identified in 145 577 patients; 2240 (1.4%) of these episodes, in 2219 patients, included records of suicidal behavior (mean [SD] patient age, 40.9 [18.6] years; 1415 episodes [63.2%] in women and 825 [36.8%] in men). A total of 11 109 MDD episodes in 9574 matched patients with MDD without records of suicidal behavior were included as controls (mean [SD] patient age, 40.8 [18.5] years; 7046 episodes [63.4%] in women and 4063 [36.6%] in men). The all-cause mortality rate was 2.5 per 100 person-years at risk for the MDD-SB group and 1.0 per 100 person-years at risk for the MDD-non-SB group, based on 466 deaths. Suicidal behavior was associated with higher all-cause mortality (hazard ratio, 2.62 [95% CI, 2.15-3.20]), as well as with HCRU and work loss, compared with the matched controls. Patients with MDD and suicidal behavior were younger and more prone to have psychiatric comorbid conditions, such as personality disorders, substance use, and anxiety, at the start of their episode. The most important factors associated with suicidal behavior within 1 year after the start of an MDD episode were history of suicidal behavior and age, history of substance use and sleep disorders, and care setting in which MDD was diagnosed.Conclusions and relevanceThis cohort study's findings suggest that high mortality, morbidity, HCRU, and work loss associated with MDD may be substantially accentuated in patients with MDD and suicidal behavior. Use of medication aimed at decreasing the risk of all-cause mortality during MDD episodes should be systematically evaluated to improve long-term outcomes.
| S-EPMC10433143 | biostudies-literature
Project description:Search for the biomarkers of major depressive disorder (MDD) has facilitated from the genes expressed in the patient’s blood cells. Because the severity of depressive symptoms and characteristics in patients with MDD are differed by the age at onset of first depressive episode, the potential transcriptomic markers in blood cells may also be different by the age at onset of MDD. In this study, we searched the transcriptomic markers of late-onset (onset ages ≥ 50 years) MDD (LOD) from the expressed genes in blood cells, and identified state-dependent biomarkers in the patients. We assessed the expressed genes in blood cells by the microarray and found that the expression levels of 3,066 probes were state-dependently changed in the blood cells of patients with LOD.
2016-01-14 | GSE76826 | GEO
Project description:Major depressive disorder (MDD) exhibits numerous clinical, epidemiological, and molecular features that are consistent with partially inherited and partially acquired epigenetic misregulation. We performed microarray based DNA modification study of MDD, utilizing affected and unaffected samples from white blood cells from monozygotic twins discordant for MDD, post-mortem prefrontal cortex tissues, and sperm samples. We performed DNA methylome analysis on white blood cells from monozygotic twins discordant for depression (n=200), pre-frontal cortex (n=71), and germline samples (n=33) from affected individuals and controls (total n=304). DNA samples were enriched for unmodified fraction of the genome using DNA-modification sensitive restriction enzyme digestion followed by adaptor-mediated PCR. The enriched fractions were labelled with a fluorescent dye (Cy5) and hybridized onto the array with a common reference pool (Cy3) generated from individuals unrelated to this study.
2012-04-27 | E-GEOD-37579 | biostudies-arrayexpress