Cortisol, the Cortisol-Dehydroepiandrosterone Ratio, and Pro-Inflammatory Cytokines in Patients with Current Major Depressive Disorder Comorbid with Borderline Personality Disorder

Kahl, Kai G.; Bens, Susanne; Ziegler, Kristin; Rudolf, Sebastian; Dibbelt, L.; Kordon, Andreas; Schweiger, Ulrich

doi:10.1016/j.biopsych.2005.08.001

Cited by 86 publications

(56 citation statements)

References 32 publications

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“…The peripheral levels of IL-6, TNF-α, and IL-1β are increased in patients with depression [13][14][15][16][17] , and antidepressant treatments reverse this effect [18][19][20] . These consistent results demonstrate that IL-6, TNF-α, and IL-1β are putative biomarkers for depression.…”

Section: Infl Ammatory Biomarkers Of Depressionmentioning

confidence: 99%

Inflammation: a mechanism of depression?

Han

2014

Neurosci. Bull.

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In recent decades, major depression has become more prevalent and research has shown that immune activation and cytokine production may be involved. This review is mainly focused on the contribution of infl ammation to depression. We fi rst briefl y introduce the infl ammatory biomarkers of depression, then discuss the sources of cytokines in the brain, and fi nally describe the neuroimmunological mechanisms underlying the association between infl ammation and depression.Keywords: depression; infl ammation; cytokines; hypothalamic-pituitary-adrenal axis; 5-HT; neuroplasticity ·Review· IntroductionThe prevalence of major depression has increased dramatically over the past few decades [1] , and women are nearly twice as likely as men to develop depressive disorder [2] . Depression is classified as a brain disorder, but its symptomatology includes some behaviors that also occur during chronic infl ammatory stress [3] . Research has shown that immune activation and the production of cytokines may be involved in depression [4] , so this relationship has received much attention. In fact, three causal pathways have been proposed: depression to inflammation, inflammation to depression, and a bidirectional relationship [5] . In this review, we focus on the impact of inflammation on depression and the underlying mechanisms. Cytokines are small cell-signaling proteins that mediate and regulate immune responses and inflammation, and can be divided into two categories:the pro-inflammatory cytokines interleukin (IL)-1 β, IL-6, IL-8, and tumor necrosis factor (TNF)-α, and the anti-inflammatory cytokines IL-1Rα, IL-4, IL-10, and transforming growth factor (TGF)-β1. Generally, t he proinfl ammatory cytokines promote systemic infl ammation and are essential for the initiation of an infl ammatory response to disease [6] , while the anti-inflammatory cytokines antagonize these actions to reduce inflammation and promote healing [6,7] . Moreover, some cytokines play dual roles [8] . In the central nervous system (CNS), the cellular source, function, and mechanisms of action of cytokines differ from those in the periphery. In the following, we briefl y introduce the current research on infl ammatory biomarkers of depression. Infl ammatory Biomarkers of DepressionSo far, there are neither universally accepted or defi nitive biomarkers of depression [9] , nor effective methods to assess the severity, endophenotypes, or response to treatment [10] .However, sufficient evidence has suggested changes in the circulating levels of cytokines in depressed patients, which can be reversed by antidepressant treatments [11,12] .So, many studies have aimed to clarify the neurobiological changes in depression and to establish inflammatory biomarkers. The peripheral levels of IL-6, TNF-α, and IL-1β are increased in patients with depression [13][14][15][16][17] , and antidepressant treatments reverse this effect [18][19][20] . These consistent results demonstrate that IL-6, TNF-α, and IL-1β are putative biomarkers for depression. However, due to the he...

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Section: Infl Ammatory Biomarkers Of Depressionmentioning

confidence: 99%

Inflammation: a mechanism of depression?

Han

2014

Neurosci. Bull.

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“…Dysregulation of the HPA system has been demonstrated in several studies to result in hypercortisolism, imbalance of pro-and anti-inflammatory cytokines, and lowered feedback sensitivity, with or without major depressive disorder (Kahl 2006;Purnell 2009). Reasons for this phenomenon were not well elucidated, although increased cortisol in people with borderline personality disorder might result from their recurrent state of severe inner stress and tension.…”

Section: Borderline Personality Disordermentioning

confidence: 99%

Metabolic syndrome in psychiatry: advances in understanding and management

Ho¹,

Zhang²,

Mak³

et al. 2014

Adv. psychiatr. treat

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SummaryMetabolic syndrome comprises a number of cardiovascular risk factors that increase morbidity and mortality. The increase in incidence of the syndrome among psychiatric patients has been unanimously demonstrated in recent studies and it has become one of the greatest challenges in psychiatric practice. Besides the use of psychotropic drugs, factors such as genetic polymorphisms, inflammation, endocrinopathies and unhealthy lifestyle contribute to the association between metabolic syndrome and a number of psychiatric disorders. In this article, we review the current diagnostic criteria for metabolic syndrome and propose clinically useful guidelines for psychiatrists to identify and monitor patients who may have the syndrome. We also outline the relationship between metabolic syndrome and individual psychiatric disorders, and discuss advances in pharmacological treatment for the syndrome, such as metformin.LEARNING OBJECTIVES•Be familiar with the definition of metabolic syndrome and its parameters of measurement.•Appreciate how individual psychiatric disorders contribute to metabolic syndrome and vice versa.•Develop a framework for the prevention, screening and management of metabolic syndrome in psychiatric patients.

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“…12 Therefore, according to this model, the presence of depressive symptoms in RA may be more than a psychological reaction to the pain and functional disability related to the disease and may represent a dimension of the chronic inflammation status of RA; in this case, depressive symptoms would be in fact related to cytokine release itself. [12][13][14][15][16] In order to epidemiologically survey these hypotheses, AbdelNasser et al and Bagnato et al compared the prevalence of depressive symptoms in RA and osteoarthritis (OA), another chronic rheumatic disease that causes pain and functional disability. 7,11 Differently from RA, OA is essentially degenerative and non-inflammatory.…”

Section: Introductionmentioning

confidence: 99%

Depressive symptoms in rheumatoid arthritis

Mella

Bértolo

Dalgalarrondo

2010

Rev. Bras. Psiquiatr.

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Objective: To determine the prevalence of depressive and anxiety symptoms in patients with rheumatoid arthritis (a chronic inflammatory disease) in comparison to a control group with osteoarthritis (a chronic non-inflammatory degenerative disease) and to identify the sociodemographic and clinical variables associated with depressive symptoms in these patients. Method: Sixty-two rheumatoid arthritis patients and 60 osteoarthritis patients participated in the study. Sociodemographic and clinical data were collected and the Hospital Anxiety and Depression Scale and the Disability Index of the Health Assessment Questionnaire were applied. Results: The prevalence of depressive symptoms was of 53.2% in rheumatoid arthritis and 28.3% in osteoarthritis (p = 0.005). The prevalence of anxiety symptoms was of 48.4% in rheumatoid arthritis and 50.0% in osteoarthritis (p = 0.859). The mean (and standard deviation) scores in the Disability Index of the Health Assessment Questionnaire were 1.4 (0.8) in rheumatoid arthritis and 1.4 (0.6) in osteoarthritis (p = 0.864). Rheumatoid arthritis patients with depressive symptoms had lower education and higher disease activity and functional disability. Conclusion: Although these two rheumatic diseases are similar in terms of the pain and functional disability that they cause, a significantly higher prevalence of depressive symptoms was found in rheumatoid arthritis patients. This difference might be explained by the hypothesis of a neuroimmunobiological mechanism related to cytokines in inflammatory diseases, which has been considered as a candidate to the development of depressive symptoms. Descriptors

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Cortisol, the Cortisol-Dehydroepiandrosterone Ratio, and Pro-Inflammatory Cytokines in Patients with Current Major Depressive Disorder Comorbid with Borderline Personality Disorder

Cited by 86 publications

References 32 publications

Inflammation: a mechanism of depression?

Inflammation: a mechanism of depression?

Metabolic syndrome in psychiatry: advances in understanding and management

Depressive symptoms in rheumatoid arthritis

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