scholarly journals Effects of Antidepressant Treatment on Peripheral Biomarkers in Patients with Major Depressive Disorder (MDD)

2021 ◽  
Vol 10 (8) ◽  
pp. 1706
Author(s):  
Anna Mosiołek ◽  
Aleksandra Pięta ◽  
Sławomir Jakima ◽  
Natalia Zborowska ◽  
Jadwiga Mosiołek ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Recovery Of Function ◽  
Antidepressant Treatment ◽  
Antidepressant Drugs ◽  
Selective Serotonin ◽  
Major Depressive ◽  
Anti Inflammatory

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.

scholarly journals Effect of Selective Serotonin Reuptake Inhibitors and Immunomodulator on Cytokines Levels: An Alternative Therapy for Patients with Major Depressive Disorder

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
María Eugenia Hernandez ◽  
Danelia Mendieta ◽  
Mayra Pérez-Tapia ◽  
Rafael Bojalil ◽  
Iris Estrada-Garcia ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Serotonin Reuptake Inhibitors ◽  
Selective Serotonin ◽  
Major Depressive ◽  
Anti Inflammatory

Major depressive disorder (MDD) is a psychiatric illness that presents as a deficit of serotonergic neurotransmission in the central nervous system. MDD patients also experience alterations in cortisol and cytokines levels. Treatment with selective serotonin reuptake inhibitors (SSRIs) is the first-line antidepressant regimen for MDD. The aim of this study was to determine the effect of a combination of SSRIs and an immunomodulator—human dialyzable leukocyte extract (hDLE)—on cortisol and cytokines levels. Patients received SSRIs or SSRIs plus hDLE. The proinflammatory cytokines IL-1β, IL-2, and IFN-γ; anti-inflammatory cytokines IL-13 and IL-10; and 24-h urine cortisol were measured at weeks (W) 0, 5, 20, 36, and 52 of treatment. The reduction in cortisol levels in the SSRI-treated group was 30% until W52, in contrast, the combined treatment induced a 54% decrease at W36. The decline in cortisol in patients who were treated with SSRI plus hDLE correlated with reduction of anti-inflammatory cytokines and increases levels of proinflammatory cytokines at the study conclusion. These results suggest that the immune-stimulating activity of hDLE, in combination with SSRIs, restored the pro- and anti-inflammatory cytokine balance and cortisol levels in depressed patients versus those who were given SSRIs alone.

Triiodothyronine (T3) supplementation in major depressive disorder

2015 ◽  
Vol 5 (6) ◽  
pp. 253-259 ◽  
Author(s):  
Anna K. Morin
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Antidepressant Treatment ◽  
Treatment Resistance ◽  
Tricyclic Antidepressant ◽  
Selective Serotonin ◽  
Major Depressive ◽  
Thyroid Abnormalities

Abstract Introduction The use of thyroid hormones to enhance the effects of antidepressants is based on evidence supporting a link between thyroid function and Major Depressive Disorder. Thyroid abnormalities have been found in patients with Major Depressive Disorder and have been correlated with depression severity. Symptoms associated with clinical hypothyroidism include mood disturbances, primarily depression. In addition, an increase in antidepressant treatment resistance has been associated with thyroid abnormalities. This article reviews the existing data regarding triiodothyronine (T3) supplementation of antidepressants in the treatment of major depressive disorder. Methods Medline and EMBASE were searched from 1996 to November 2014 using the key terms triiodothyronine, T3, and treatment-resistant depression. Results T3 may increase serotonergic neurotransmission and has been studied as an add-on agent in patients with unipolar depression with and without thyroid dysfunction to accelerate, enhance, and augment the effects of tricyclic antidepressants and selective serotonin reuptake inhibitors. Discussion Data support the use of T3 augmentation (25-50 μg/d) for the treatment of depressive symptoms in some patient populations without thyroid hormone abnormalities who do not respond to an adequate trial of a tricyclic antidepressant or a selective serotonin reuptake inhibitor. Monitoring for adverse effects and conditions that may be exacerbated by T3 augmentation is recommended.

Sign in / Sign up

Export Citation Format

Share Document