scholarly journals Cost variation analysis among different antidepressant drugs used to treat major depressive disorder

2020 ◽  
Vol 6 (2) ◽  
pp. 51-54
2019 ◽  
Vol 23 (2) ◽  
pp. 88-95
Author(s):  
Antoine Yrondi ◽  
Laura M Fiori ◽  
Benicio N Frey ◽  
Raymond W Lam ◽  
Glenda M MacQueen ◽  
...  

Abstract Introduction Antidepressant drugs are effective therapies for major depressive disorder; however, they are frequently associated with side effects. Although there is some evidence for a relationship between genetic variation and side effects, little is known regarding the role of dynamic molecular factors as moderators of side effects. The aim of this study was to assess microRNA (miRNA) changes associated with side effects during escitalopram treatment and their downstream effects on target gene expression. Methods A total 160 patients with major depressive disorder from the CAN-BIND-1 cohort were included. Side effects were assessed with the Toronto Side Effect Scale after 2 weeks of treatment with escitalopram. We assessed the relationship between side effects and changes in peripheral expression of miRNAs between baseline and week 2. For miRNA whose expression changed, we used target prediction algorithms to identify putative messenger RNA (mRNA) targets and assessed their expression. Results Nausea was experienced by 42.5% of patients. We identified 45 miRNAs whose expression changed on initiation of escitalopram treatment, of which 10 displayed a negative association with intensity of nausea (miR15b-5p, miR17-5p, miR20a-5p, miR20b-5p, miR103a-3p, miR103b, miR106a-5p, miR182-5p, miR185-5p, and miR660-5p). Additionally, we found negative associations between 4 microRNAs (miR20a-5p, miR106a-5p, miR185-5p, miR660-5p) and mRNA targets. The expression of the miR185-5p target, CAMK2δ was significantly decreased [log 2 mean = −0.048 (0.233)] between weeks 0 and 2 (P = .01)]. Conclusions We identified an overexpression of miR185-5p during escitalopram treatment of major depressive disorder, which was negatively associated with intensity of nausea, and identified a potential mRNA target that may mediate this effect.


2013 ◽  
Vol 16 (10) ◽  
pp. 2195-2208 ◽  
Author(s):  
Teresa A. Victor ◽  
Maura L. Furey ◽  
Stephen J. Fromm ◽  
Arne Öhman ◽  
Wayne C. Drevets

Abstract An emerging hypothesis regarding the mechanisms underlying antidepressant pharmacotherapy suggests that these agents benefit depressed patients by reversing negative emotional processing biases (Harmer, 2008). Neuropsychological indices and functional neuroimaging measures of the amygdala response show that antidepressant drugs shift implicit and explicit processing biases away from the negative valence and toward the positive valence. However, few studies have explored such biases in regions extensively connected with the amygdala, such as the pregenual anterior cingulate cortex (pgACC) area, where pre-treatment activity consistently has predicted clinical outcome during antidepressant treatment. We used functional magnetic resonance imaging (fMRI) to investigate changes in haemodynamic response patterns to positive vs. negative stimuli in patients with major depressive disorder (MDD) under antidepressant treatment. Participants with MDD (n = 10) underwent fMRI before and after 8 wk sertraline treatment; healthy controls (n = 10) were imaged across an equivalent interval. A backward masking task was used to elicit non-conscious neural responses to sad, happy and neutral face expressions. Haemodynamic responses to emotional face stimuli were compared between conditions and groups in the pgACC. The response to masked-sad vs. masked-happy faces (SN-HN) in pgACC in the depressed subjects was higher in the pre-treatment condition than in the post-treatment condition and this difference was significantly greater than the corresponding change across time in the controls. The treatment-associated difference was attributable to an attenuated response to sad faces and an enhanced response to happy faces. Pre-treatment pgACC responses to SN-HN correlated positively with clinical improvement during treatment. The pgACC participates with the amygdala in processing the salience of emotional stimuli. Treatment-associated functional changes in this limbic network may influence the non-conscious processing of such stimuli by reversing the negative processing bias extant in MDD.


2021 ◽  
Vol 10 (8) ◽  
pp. 1706
Author(s):  
Anna Mosiołek ◽  
Aleksandra Pięta ◽  
Sławomir Jakima ◽  
Natalia Zborowska ◽  
Jadwiga Mosiołek ◽  
...  

Major depressive disorder (MDD) is one of the most prevalent mental illness and a leading cause of disability worldwide. Despite a range of effective treatments, more than 30% of patients do not achieve remission as a result of conventional therapy. In these circumstances the identification of novel drug targets and pathogenic factors becomes essential for selecting more efficacious and personalized treatment. Increasing evidence has implicated the role of inflammation in the pathophysiology of depression, revealing potential new pathways and treatment options. Moreover, convergent evidence indicates that MDD is related to disturbed neurogenesis and suggests a possible role of neurotrophic factors in recovery of function in patients. Although the influence of antidepressants on inflammatory cytokines balance was widely reported in various studies, the exact correlation between drugs used and specific cytokines and neurotrophins serum levels often remains inconsistent. Available data suggest anti-inflammatory properties of selective serotonin reuptake inhibitors (SSRIs), selective serotonin and noradrenaline inhibitors (SNRIs), and tricyclic antidepressants (TCAs) as a possible additional mechanism of reduction of depressive symptoms. In this review, we outline emerging data regarding the influence of different antidepressant drugs on a wide array of peripheral biomarkers such as interleukin (IL)-1ß, IL-2, IL-5, IL-6, IL-8, IL-10, C-reactive protein (CRP), or interferon (IFN)-γ. Presented results indicate anti-inflammatory effect for selected drugs or lack of such effect. Research in this field is insufficient to define the role of inflammatory markers as a predictor of treatment response in MDD.


2021 ◽  
Vol 12 ◽  
Author(s):  
Jane A. Foster ◽  
Glen B. Baker ◽  
Serdar M. Dursun

Major depressive disorder (MDD) is a prominent cause of disability worldwide. Current antidepressant drugs produce full remission in only about one-third of MDD patients and there are no biomarkers to guide physicians in selecting the best treatment for individuals. There is an urgency to learn more about the etiology of MDD and to identify new targets that will lead to improved therapy and hopefully aid in predicting and preventing MDD. There has been extensive interest in the roles of the immune system and the gut microbiome in MDD and in how these systems interact. Gut microbes can contribute to the nature of immune responses, and a chronic inflammatory state may lead to increased responsiveness to stress and to development of MDD. The gut microbiome-immune system-brain axis is bidirectional, is sensitive to stress and is important in development of stress-related disorders such as MDD. Communication between the gut and brain involves the enteric nervous system (ENS), the autonomic nervous system (ANS), neuroendocrine signaling systems and the immune system, and all of these can interact with the gut microbiota. Preclinical studies and preliminary clinical investigations have reported improved mood with administration of probiotics and prebiotics, but large, carefully controlled clinical trials are now necessary to evaluate their effectiveness in treating MDD. The roles that several gut microbe-derived molecules such as neurotransmitters, short chain fatty acids and tryptophan play in MDD are reviewed briefly. Challenges and potential future directions associated with studying this important axis as it relates to MDD are discussed.


Author(s):  
Johanna Seifert ◽  
Fabienne Führmann ◽  
Matthias A. Reinhard ◽  
Rolf R. Engel ◽  
Xueqiong Bernegger ◽  
...  

AbstractData on drug prescription for outpatients with major depressive disorder (MDD) suggest women are more likely to be treated with psychotropic drugs, while data on sex differences regarding pharmacological treatment of psychiatric inpatients are currently not available. Drug utilization data from the program “Drug Safety in Psychiatry” (German: Arzneimittelsicherheit in der Psychiatrie, AMSP) of 44,418 psychiatric inpatients with MDD were analyzed for sex differences between 2001 and 2017. Sex differences were analyzed using relative risks (RR) and 95% confidence intervals (95% CI). Time trends were analyzed by comparing the first (2001–2003) with the last time period (2015–2017). In general, men and women were equally likely to use psychotropic drugs. Monotherapy was more common in men. Women were more likely to utilize ≥ 4 psychotropic drugs. Antidepressant drugs (ADDs) were the most prescribed drug class. Men had a higher utilization of noradrenergic and specific serotonergic antidepressants (RR 1.15; 95% CI 1.12–1.19), especially mirtazapine (RR 1.16; 95% CI 1.12–1.19), but also of other ADDs such as bupropion (RR 1.50; 95% CI 1.35–1.68). Males had a slightly higher utilization of second-generation antipsychotic drugs (RR 1.06; 95% CI 1.03–1.09) and were less often treated with low-potency first-generation antipsychotic drugs (RR 0.86; 95% CI 0.83–0.90). Tranquilizing (e.g., benzodiazepines; RR 0.89; 95% CI 0.86–0.92) and hypnotic drugs (e.g., Z-drugs; RR 0.85; 95% CI 0.81–0.89) were less utilized in the treatment of male patients. Not all sex differences were stable over time. More sex differences were detectable in 2015–2017 than in 2001–2003. Findings suggest that certain psychotropic drugs are preferred in the treatment of men vs. women, however, sex differences found in this study are not as large as in ambulatory settings. To make evidence-based sex-specific recommendations in the treatment of MDD, differences in drug response and tolerability need to be further researched.


Author(s):  
André F. Carvalho ◽  
Gilberto S. Alves ◽  
Cristiano A. Köhler ◽  
Roger S. McIntyre

Major depressive disorder (MDD) is a chronic and disabling illness often associated with elevated rates of non-recovery and substantial psychosocial burden. Cognitive impairment is a common residual manifestations of MDD. Overactivation of the hypothalamic–pituitary–adrenal axis, along with immune–inflammatory imbalances, a decrease in neurotrophin signaling, and an increase in oxidative and nitrosative stress, leads to neuroprogression and cognitive deterioration in MDD. “Cognitive remission” has been proposed as a novel treatment target for MDD. Cognitive remediation therapy has provided encouraging results for the management of cognitive deficits in MDD. The effects of standard antidepressant drugs on MDD-related cognitive dysfunction are often suboptimal, which calls for the development of novel agents with the potential to target cognitive impairments in MDD. The incorporation of biobehavioral strategies (e.g., exercise) and multimodal treatment approaches (e.g., cognitive training, antidepressant therapy, and neuromodulation) is more likely to generate therapeutic benefit.


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