Navegando por Palavras-chave "Major depressive disorder"

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    Antidepressant combination for major depression in incomplete responders-a systematic review
    (Elsevier B.V., 2013-01-10) Rocha, Fabio Lopes; Fuzikawa, Cintia; Riera, Rachel [UNIFESP]; Ramos, Melissa Guarieiro; Hara, Claudia; Universidade Federal de Minas Gerais (UFMG); Universidade Federal de São Paulo (UNIFESP); Fac Ciencias Med Minas Gerais
    Background: Antidepressant combination has been suggested as a strategy to increase treatment efficacy. the objective of this study was to perform a systematic review and meta-analysis of studies that assessed the effect of antidepressant combination for major depression in patients with incomplete response to an initial antidepressant.Methods: Studies were retrieved from PubMed (1966-February, 2012), Cochrane Library (-February, 2012), Embase (1980-February, 2012), PsycINFO (1980-February, 2012), Lilacs (1982-February, 2012), clinical trials registry, thesis database (www.capes.gov.br), and secondary references. Included studies had an open label phase in which an initial antidepressant was used for the treatment of major depression and a double blind phase for the incomplete responders that compared monotherapy with the first antidepressant versus the association of a second antidepressant to the first one.Results: Out of the 4,884 studies retrieved, only five satisfied the inclusion criteria. the total number of patients included was 483. Only two small trials reported benefits of adding a second antidepressant to the initial antidepressant. Dropouts due to side effects were not reported in three studies. Meta-analysis was not performed due to the small number of studies, the inconsistency in the direction of effect and the possible instability of effect size. Only limited kinds of combination, involving mianserin, mirtazapine and desipramine were studied. Some properties of the first two drugs such as the anxiolytic, sedative, and orexigenic effects, can mimic depression improvement.Limitations: Publication bias cannot be ruled out. Only one study included a monotherapy arm with the antidepressant used for augmentation of the first antidepressant.Conclusions: the practice of using a combination of antidepressants for major depression in incomplete responders is not warranted by the literature. (C) 2012 Elsevier B.V. All rights reserved.
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    Avaliação da efetividade da escetamina subcutânea para o tratamento da anedonia em pacientes com episódio depressivo resistente ao tratamento
    (Universidade Federal de São Paulo (UNIFESP), 2021) Delfino, Rodrigo Simonini [UNIFESP]; Lacerda, Acioly Luiz Tavares de [UNIFESP]; http://lattes.cnpq.br/9732472446053745; http://lattes.cnpq.br/7143698895016669; Universidade Federal de São Paulo
    A anedonia é um sintoma associado a piores desfechos no tratamento da depressão, incluindo maior resistência ao tratamento, maior impacto funcional e taxas maiores de suicidalidade. Poucas intervenções se têm mostrado eficazes para o tratamento da anedonia, tanto na depressão unipolar quanto na depressão bipolar. A cetamina, um antagonista NMDA, teve sua eficácia demonstrada na melhora rápida da anedonia em episódios depressivos agudos. O principal objetivo do presente estudo é avaliar o efeito antianedônico da escetamina, o enantiômero S da cetamina – recentemente aprovada para depressão resistente ao tratamento – em episódios depressivos agudos em indivíduos com depressão maior ou depressão bipolar resistentes ao tratamento. Métodos: Em um estudo de mundo real, aberto 70 pacientes com episódio depressivo agudo (unipolar ou bipolar) foram tratados com 6 infusões semanais de escetamina subcutânea (0,5-1mg/kg). A anedonia foi medida por meio do item 8 da escala MADRS antes e 24h após cada infusão. Resultados: Foi observada redução significativa da gravidade da anedonia (p <0,0001) após 6 infusões de escetamina. O efeito já se mostrou estatisticamente significativo 24h após a primeira infusão (p <0,001) em ambos os grupos unipolar e bipolar e se manteve clinicamente e estatisticamente significativo ao longo de toda a série de infusões subcutâneas. O efeito antianedônico da escetamina não diferiu entre os grupos. A escetamina apresentou um bom perfil de tolerabilidade e segurança, com efeitos adversos transitórios de intensidade baixa a moderada. Não foi registrado evento adverso sério durante o estudo. Limitações: Este é um estudo aberto, de mundo real. A falta de cegamento e de grupo controle limita a interpretação e generalização dos resultados. Conclusão: Embora preliminares, os presentes achados sugerem que infusões repetidas de escetamina subcutânea são efetivas para o tratamento da anedonia em pacientes com depressão unipolar e bipolar. Esses resultados precisam ser confirmados por meio de replicação em ensaios clínicos duplocegos, randomizados e controlados.
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    Depressão e hipotireoidismo: uma revisão sistemática
    (Universidade Federal de São Paulo, 2023-01-16) Souza, Eduarda Silva [UNIFESP]; Chriguer, Rosangela Soares [UNIFESP]; Mazzaia, Maria Cristina [UNIFESP]; http://lattes.cnpq.br/6423662828098950; http://lattes.cnpq.br/7277226334658321; http://lattes.cnpq.br/5553635228903547; Universidade Federal de São Paulo (UNIFESP)
    A presença de sintomas depressivos em pacientes com hipotireoidismo e a influência da glândula tireoide no humor e nas cognições é bem reconhecida no meio científico e na prática clínica. Nesse contexto, esta revisão sistemática sem metanálise, teve como objetivo analisar as produções científicas dos últimos cinco anos nas bases de dados PubMed, Embase e CAPES utilizando o método PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) sobre a relação entre hipotireoidismo e sintomas depressivos, além de investigar a influência da desregulação hormonal tireoidiana em pacientes diagnosticados com depressão. Foram incluídos 14 artigos (n= 430.692) com tamanho amostral variando de 88 até 220.545 participantes os resultados indicam que há uma forte associação entre hipotireoidismo e depressão, com a prevalência sendo maior em mulheres e a relação podendo influenciar na gravidade dos sintomas depressivos. Essa relação se mantém mesmo em pacientes que já fazem terapia de reposição hormonal. No entanto, a associação entre hipotireoidismo subclínico e depressão foi menos expressiva. Estes resultados sugerem a importância da avaliação da função tireoidiana em pacientes com sintomas depressivos, especialmente em mulheres.
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    Evaluation of periodontitis in hospital outpatients with major depressive disorder. A focus on gingival and circulating cytokines
    (Academic Press Inc Elsevier Science, 2016) de Oliveira Solis, Ana Cristina; Marques, Andrea Horvath; Dominguez, Wagner Vasques; de Almeida Prado, Euthymia Brandao [UNIFESP]; Pannuti, Claudio Mendes; Moreira Lotufo, Roberto Fraga; Lotufo-Neto, Francisco
    An imbalance in stimulated cytokine production is associated with the etiopathogenesis of numerous diseases such as major depressive disorder (MDD) and periodontal disease. Increased cytokine levels have been reported in the gingival crevicular fluid (GCF) of patients with MDD. Thirty-six outpatients with MDD participated in this study. Each outpatient was age-matched (+/- 3 years) with a healthy control (n = 36). The patients were controlled for race and smoking habits. Unstimulated and stimulated interleukin 6 (IL-6), interleukin 1 beta (IL-1 beta), and interferon-gamma (INF-gamma) production in whole blood culture (WBC) and IL-6 and IL-1 beta levels in the GCF were evaluated. Circulating levels of IL-6 and IL-1 beta (unstimulated) as well as GCF IL-1 beta were modestly lower in MDD patients, compared to the levels in age-matched controls (Mann-Whitney, p = 0.002, 0.0075, ANCOVA, p = 0.025, respectively). In the unstimulated group, there was no correlation between the levels of circulating IL-6 and GCF IL-6 (r = 0.07, p = 0.67), and between the levels of circulating IL-1 beta and the IL-1 beta level in the CGF (r = -0.08, p = 0.63). In the LPS stimulation group, there was no correlation between the levels of circulating levels of IL-6 and GCF IL-6 (r = 0.02, p= 0.91) or between the circulating IL-1 beta and GCF IL-1 beta (r = 0.13, p= 0.42). We observed modest immunosuppression in MDD patients (evaluated by no stimulation whole blood culture [WBC]), especially in patients with melancholic depression, chronic depression, and severe depression. (C) 2015 Elsevier Inc. All rights reserved.
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    Gene expression in blood of children and adolescents: MOediation between childhood maltreatment and major depressive disorder
    (Pergamon-Elsevier Science Ltd, 2017) Spindola, Leticia Maria [UNIFESP]; Pan, Pedro Mario [UNIFESP]; Moretti, Patricia Natalia [UNIFESP]; Ota, Vanessa Kiyomi [UNIFESP]; Santoro, Marcos Leite [UNIFESP]; Cogo-Moreira, Hugo [UNIFESP]; Gadelha, Ary [UNIFESP]; Salum, Giovanni; Manfro, Gisele Gus; Mari, Jair Jesus [UNIFESP]; Brentani, Helena; Grassi-Oliveira, Rodrigo; Brietzke, Elisa [UNIFESP]; Miguel, Euripedes Constantino; Rohde, Luis Augusto; Sato, Joao Ricardo; Bressan, Rodrigo Affonseca [UNIFESP]; Belangero, Sintia Iole [UNIFESP]
    Investigating major depressive disorder (MDD) in childhood and adolescence can help reveal the relative contributions of genetic and environmental factors to MDD, since early stages of disease have less influence of illness exposure. Thus, we investigated the mRNA expression of 12 genes related to the hypothalamic pituitary adrenal (HPA) axis, inflammation, neurodevelopment and neurotransmission in the blood of children and adolescents with MDD and tested whether a history of childhood maltreatment (CM) affects MDD through gene expression. Whole-blood mRNA levels of 12 genes were compared among 20 children and adolescents with MDD diagnosis (MDD group), 49 participants without MDD diagnosis but with high levels of depressive symptoms (DS group), and 61 healthy controls (HC group). The differentially expressed genes were inserted in a mediation model in which CM, MDD, and gene expression were, respectively, the independent variable, outcome, and intermediary variable. NR3C1, TNF, TNFR1 and IL1B were expressed at significantly lower levels in the MDD group than in the other groups. CM history did not exert a significant direct effect on MDD. However, an indirect effect of the aggregate expression of the 4 genes mediated the relationship between CM and MDD. In the largest study investigating gene expression in children with MDD, we demonstrated that NR3C1, TNF, TNFR1 and IL1B expression levels are related to MDD and conjunctly mediate the effect of CM history on the risk of developing MDD. This supports a role of glucocorticoids and inflammation as potential effectors of environmental stress in MDD. (C) 2017 Elsevier Ltd. All rights reserved.
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    Impact of 5-HTTLPR and BDNF polymorphisms on response to sertraline versus transcranial direct current stimulation: Implications for the serotonergic system
    (Elsevier B.V., 2013-11-01) Brunoni, A. R.; Kemp, A. H.; Shiozawa, P.; Cordeiro, Q.; Valiengo, L. C. L.; Goulart, A. C.; Coprerski, B. [UNIFESP]; Lotufo, P. A.; Brunoni, D. [UNIFESP]; Perez, A. B. A. [UNIFESP]; Fregni, F.; Bensenor, I. M.; Universidade de São Paulo (USP); Fac Ciencias Med Santa Casa de Misericordia Sao P; Univ Sydney; Universidade Federal de São Paulo (UNIFESP); Harvard Univ
    Transcranial direct current stimulation (tDCS) has been intensively investigated as a non-pharmacological treatment for major depressive disorder (MDD). While many studies have examined the genetic predictors of antidepressant medications, this issue remains to be investigated for tDCS. in the current study, we evaluated whether the BDNF Val66Met and the 5-HTT (5-HTTLPR) polymorphisms were associated with tDCS antidepressant response. We used data from a factorial trial that evaluated the efficacy of tDCS and sertraline and enrolled 120 moderate-to-severe, antidepressant-free participants. in the present study, we used analyses of variance to evaluate whether the BDNF (Val/Val vs. Met-carries) and 5-HTTLPR alleles (long/long vs short-carriers) were predictors of tDCS (active/sham) and sertraline (sertraline/placebo) response. Analyses were conducted on the polymorphisms separately and also on their interaction. Genotype frequencies were in Hardy-Weinberg equilibrium. BDNF polymorphism was not associated with treatment response. We found that 5-HTTLPR predicted tDCS effects as long/long homozygotes displayed a larger improvement comparing active vs. sham tDCS, while short-allele carriers did not. A dose-response relationship between active-sham differences with the long allele was also suggested. These results strengthen the role of the serotonergic system in the tDCS antidepressant effects and expand previous findings that reported that tDCS mechanisms of action partially involve serotonergic receptors. Therefore, we hypothesize that tDCS is a neuromodulation technique that acts over depression through the modulation of serotonergic system and that tDCS top-down antidepressant effects might not be optimal in brain networks with a hyperactive amygdala inducing bottom-up effects, such as occurs in short-carriers. (C) 2013 Elsevier B.V. and ECNP. All rights reserved.
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    Inflamed moods: A review of the interactions between inflammation and mood disorders
    (Elsevier B.V., 2014-08-04) Rosenblat, Joshua D.; Cha, Danielle S.; Mansur, Rodrigo B. [UNIFESP]; McIntyre, Roger S.; Univ Toronto; Univ Western Ontario; Universidade Federal de São Paulo (UNIFESP)
    Mood disorders have been recognized by the World Health Organization (WHO) as the leading cause of disability worldwide. Notwithstanding the established efficacy of conventional mood agents, many treated individuals continue to remain treatment refractory and/or exhibit clinically significant residual symptoms, cognitive dysfunction, and psychosocial impairment. Therefore, a priority research and clinical agenda is to identify pathophysiological mechanisms subserving mood disorders to improve therapeutic efficacy.During the past decade, inflammation has been revisited as an important etiologic factor of mood disorders. Therefore, the purpose of this synthetic review is threefold: 1) to review the evidence for an association between inflammation and mood disorders, 2) to discuss potential pathophysiologic mechanisms that may explain this association and 3) to present novel therapeutic options currently being investigated that target the inflammatory-mood pathway.Accumulating evidence implicates inflammation as a critical mediator in the pathophysiology of mood disorders. Indeed, elevated levels of pro-inflammatory cytokines have been repeatedly demonstrated in both major depressive disorder (MDD) and bipolar disorder (BD) patients. Further, the induction of a pro-inflammatory state in healthy or medically ill subjects induces 'sickness behavior' resembling depressive symptomatology.Potential mechanisms involved include, but are not limited to, direct effects of pro-inflammatory cytokines on monoamine levels, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, pathologic microglial cell activation, impaired neuroplasticity and structural and functional brain changes.Anti-inflammatory agents, such as acetyl-salicylic acid (ASA), celecoxib, anti-TNF-alpha agents, minocycline, curcumin and omega-3 fatty acids, are being investigated for use in mood disorders. Current evidence shows improved outcomes in mood disorder patients when anti-inflammatory agents are used as an adjunct to conventional therapy; however, further research is needed to establish the therapeutic benefit and appropriate dosage. (C) 2014 Elsevier Inc. All rights reserved.
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    Is there a metabolic-mood syndrome? A review of the relationship between obesity and mood disorders
    (Elsevier B.V., 2015-05-01) Mansur, Rodrigo B. [UNIFESP]; Brietzke, Elisa [UNIFESP]; McIntyre, Roger S.; Univ Toronto; Universidade Federal de São Paulo (UNIFESP)
    Obesity and mood disorders are highly prevalent and co-morbid. Epidemiological studies have highlighted the public health relevance of this association, insofar as both conditions and its co-occurrence are associated with a staggering illness-associated burden. Accumulating evidence indicates that obesity and mood disorders are intrinsically linked and share a series of clinical, neurobiological, genetic and environmental factors. the relationship of these conditions has been described as convergent and bidirectional; and some authors have attempted to describe a specific subtype of mood disorders characterized by a higher incidence of obesity and metabolic problems. However, the nature of this association remains poorly understood. There are significant inconsistencies in the studies evaluating metabolic and mood disorders; and, as a result, several questions persist about the validity and the generalizability of the findings. An important limitation in this area of research is the noteworthy phenotypic and pathophysiological heterogeneity of metabolic and mood disorders. Although clinically useful, categorical classifications in both conditions have limited heuristic value and its use hinders a more comprehensive understanding of the association between metabolic and mood disorders. A recent trend in psychiatry is to move toward a domain specific approach, wherein psychopathology constructs are agnostic to DSM-defined diagnostic categories and, instead, there is an effort to categorize domains based on pathogenic substrates, as proposed by the National Institute of Mental Health (NIMH) Research Domain Criteria Project (RDoC). Moreover, the substrates subserving psychopathology seems to be unspecific and extend into other medical illnesses that share in common brain consequences, which includes metabolic disorders. Overall, accumulating evidence indicates that there is a consistent association of multiple abnormalities in neuropsychological constructs, as well as correspondent brain abnormalities, with broad-based metabolic dysfunction, suggesting, therefore, that the existence of a metabolic-mood syndrome is possible. Nonetheless, empirical evidence is necessary to support and develop this concept. Future research should focus on dimensional constructs and employ integrative, multidisciplinary and multimodal approaches. (C) 2015 Elsevier B.V. All rights reserved.
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    Lack of association of indoleamine 2,3-dioxygenase polymorphisms with interferon-alpha-related depression in hepatitis C
    (Elsevier B.V., 2011-10-01) Almeida, Amanda Cristina Galvão Oliveira de [UNIFESP]; Quarantini, Lucas de Castro [UNIFESP]; Sampaio, Aline Santos [UNIFESP]; Lyra, André Castro; Parise, Carmen Livia [UNIFESP]; Paraná, Raymundo; Oliveira, Irismar Reis de; Koenen, Karestan C; Miranda-Scippa, Ângela Marisa de Aquino [UNIFESP]; Guindalini, Camila [UNIFESP]; Universidade Federal da Bahia (UFBA); Universidade Federal de São Paulo (UNIFESP); Harvard Univ
    Background: Major depression is a frequent adverse effect of interferon-alpha (IFN-alpha) therapy. Although the indoleamine 2,3-dioxygenase (IDO) enzyme seems to be involved in the pathophysiology of IFN-alpha-induced depression, no pharmacogenetic study has investigated Whether variation in the IDO gene modifies vulnerability to this adverse effect.Methods: A cross-sectional study assessing 277 hepatitis C patients recruited in two specialized outpatient clinics of Brazil. They were interviewed with the Mini International Neuropsychiatric Interview (MINI) approximately 1 month after the end of IFN-alpha plus ribavirin therapy. Genomic DNA of individuals was extracted from venous blood. Three IDO single-nucleotide polymorphisms (SNPs) were genotyped (rs3824259; rs10089084 and rs35099072).Results: MINI indicated that 21.3% of the sample met criteria for a major depressive episode during the course of IFN-alpha therapy. No association with the diagnosis of a major depressive episode during the course of IFN-alpha therapy was observed genotype or allele-wise (p > 0.05). Current major depression and/or current anxiety disorder was significantly associated with IFN-alpha-related depression (p < 0.005). However, gender, age, route of infection, result of the antiviral treatment, past history of substance use disorders, depression or any other psychiatric disorder showed no association with IFN-a-related depression (p > 0.05).Conclusions: Our results suggest no influence of the variants in the IDO gene and the diagnosis of interferon-alpha-related depression in the Brazilian population. Interferon-alpha-related depression may impose persistent psychopathology on at least 15% of the depressed patients even 2 years after antiviral therapy termination. the cross-sectional design is a limitation of our study, predisposing memory bias. Prospective pharmacogenetic studies are warranted to continue investigation of the impact of IDO polymorphisms on the development of IFN-alpha-induced depression. (C) 2011 Elsevier Inc. All rights reserved.
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    Liraglutide promotes improvements in objective measures of cognitive dysfunction in individuals with mood disorders: A pilot, open-label study
    (Elsevier Science Bv, 2017) Mansur, Rodrigo Barbachan [UNIFESP]; Ahmed, Juhie; Cha, Danielle S.; Woldeyohannes, Hanna O.; Subramaniapillai, Mehala; Lovshin, Julie; Lee, Jung G.; Lee, Jae-Hon; Brietzke, Elisa [UNIFESP]; Reininghaus, Eva Z.; Sim, Kang; Vinberg, Maj; Rasgon, Natalie; Hajek, Tomas; McIntyre, Roger S.
    Background: There is a paucity of treatments that are capable of reliably and robustly improving cognitive function in adults with mood disorders. Glucagon-like peptide-1 is synthesized centrally and its receptors are abundantly expressed in neural circuits subserving cognitive function. We aimed to determine the effects of liraglutide, a GLP-1 receptor (GLP-1 R) agonist, on objective measures of cognition in adults with a depressive or bipolar disorder. Methods: In this 4-week, pilot, open-label, domain-based study (e.g. cognition), we recruited 19 individuals with major depressive disorder (MDD) or bipolar disorder (BD) and an impairment in executive function. defined as a below-average performance in the Trail Making Test-B (TMTB). Liraglutide 1.8 mg/day was added as an adjunct to existing pharmacotherapy. Results: Participants had significant increases from baseline to week 4 in the TMTB standard score (age am education corrected) (Cohen's d=0.64, p=0.009) and in a composite Z-score comprising multiple cognitive tests (i.e. Digit Symbol Substitution Test, Rey Auditory Verbal Learning Test, Stroop test) (Cohen's d=0.77, p < 0.001). Neither changes in mood rating scales nor metabolic parameters were associated with changes in cognitive performance (all p > 0.05)
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    A randomized, double-blind, placebo-controlled, crossover trial evaluating the effect of intranasal insulin on cognition and mood in individuals with treatment-resistant major depressive disorder
    (Elsevier Science Bv, 2017) Cha, Danielle S.; Best, Michael W.; Bowie, Christopher R.; Gallaugher, Laura Ashley; Woldeyohannes, Hanna O.; Soczynska, Joanna K.; Lewis, Gary; MacQueen, Glenda; Sahakian, Barbara J.; Kennedy, Sidney H.; Lui, Jane P.; Mansur, Rodrigo B. [UNIFESP]; McIntyre, Roger S.
    Background: Cognitive dysfunction in major depressive disorder (MDD) is identified as a primary therapeutic target
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    The role of oxidative and nitrosative stress in accelerated aging and major depressive disorder
    (Pergamon-Elsevier Science Ltd, 2016) Maurya, Pawan Kumar [UNIFESP]; Noto, Cristiano [UNIFESP]; Rizzo, Lucas B. [UNIFESP]; Rios, Adiel C. [UNIFESP]; Nunes, Sandra O. V.; Barbosa, Decio Sabbatini; Sethi, Sumit [UNIFESP]; Zeni, Maiara [UNIFESP]; Mansur, Rodrigo B.; Maes, Michael; Brietzke, Elisa [UNIFESP]
    Major depressive disorder (MDD) affects millions of individuals and is highly comorbid with many age-associated diseases such as diabetes mellitus, immune-inflammatory dysregulation and cardiovascular diseases. Oxidative/nitrosative stress plays a fundamental role in aging, as well as in the pathogenesis of neurodegenerative/neuropsychiatric disorders including MDD. In this review, we critically review the evidence for an involvement of oxidative/nitrosative stress in acceleration of aging process in MDD. There are evidence of the association between MDD and changes in molecular mechanisms involved in aging. There is a significant association between telomere length, enzymatic antioxidant activities (SOD, CAT, GPx), glutathione (GSH), lipid peroxidation (MDA), nuclear factor kappa B, inflammatory cytokines with MDD. Major depression also is characterized by significantly lower concentration of antioxidants (zinc, coenzyme Q10, PON1). Since, aging and MDD share a common biological base in their pathophysiology, the potential therapeutic use of antioxidants and anti-aging molecules in MDD could be promising. (C) 2015 Elsevier Inc. All rights reserved.
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    Selfish brain and selfish immune system interplay: A theoretical framework for metabolic comorbidities of mood disorders
    (Pergamon-Elsevier Science Ltd, 2017) Yamagata, Ana Sayuri [UNIFESP]; Mansur, Rodrigo Barbachan [UNIFESP]; Rizzo, Lucas Bortolotto [UNIFESP]; Rosenstock, Tatiana; McIntyre, Roger S.; Brietzke, Elisa [UNIFESP]
    According to the "selfish brain" theory, the brain regulates its own energy supply influencing the peripheral metabolism and food intake according to its needs. The immune system has been likewise "selfish" due to independent energy consumption