Associations of Serum Cytokine Receptor Levels with Melancholia, Staging of Illness, Depressive and Manic Phases, and Severity of Depression in Bipolar Disorder

Siwek, Marcin; Sowa-Kućma, Magdalena; Styczeń, Krzysztof; Misztak, Paulina; Nowak, Rafał; Szewczyk, Bernadeta; Dudek, Dominika; Rybakowski, Janusz; Nowak, Gabriel; Maes, Michaël

doi:10.1007/s12035-016-0124-8

Cited by 53 publications

(36 citation statements)

References 35 publications

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“…Recently, it has been reconceptualized as a changing disorder with different clinical manifestations over the course of its development from an at-risk or latent stage to a late or end-stage, thus supporting the assumption that it would benefit from a staging model 1 . Clinical manifestations consistent with staging models include cognitive deterioration and functional decline 2,3 , changes in inflammatory and neuroanatomical biomarkers [3][4][5][6][7][8][9] , less response to treatment 10 , and worse self-reported quality of life (QoL) 11 linked to disorder progression.…”

Section: Introductionmentioning

confidence: 93%

A clinical staging model for bipolar disorder: longitudinal approach

et al. 2020

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Bipolar disorder (BD) has been identified as a life-course illness with different clinical manifestations from an at-risk to a late stage, supporting the assumption that it would benefit from a staging model. In a previous study, we used a clustering approach to stratify 224 patients with a diagnosis of BD into five clusters based on clinical characteristics, functioning, cognition, general health, and health-related quality of life. This study was design to test the construct validity of our previously developed k-means clustering model and to confirm its longitudinal validity over a span of 3 years. Of the 224 patients included at baseline who were used to develop our model, 129 (57.6%) reached the 3-year follow-up. All life domains except mental health-related quality of life (QoL) showed significant worsening in stages (p < 0.001), suggesting construct validity. Furthermore, as patients progressed through stages, functional decline (p < 0.001) and more complex treatment patterns (p = 0.002) were observed. As expected, at 3 years, the majority of patients remained at the same stage (49.6%), or progressed (20.9%) or regressed (23.3%) one stage. Furthermore, 85% of patients who stayed euthymic during that period remained at the same stage or regressed to previous stages, supporting its longitudinal validity. For that reason, this study provides evidence of the construct and longitudinal validity of an empirically developed, comprehensive staging model for patients with BD. Thus, it may help clinicians and researchers to better understand the disorder and, at the same time, to design more accurate and personalized treatment plans.

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Section: Introductionmentioning

confidence: 93%

A clinical staging model for bipolar disorder: longitudinal approach

et al. 2020

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“…During depressive episodes, serum levels of CRP, TNF-α, IL-6, IL-1β, sTNFR1 and CXCL10 are elevated [ 10 , 47 , 51 ]. Increased depression severity is associated with greater elevations of pro-inflammatory cytokines [ 52 ]. During manic episodes, serum levels of IL-6, TNF-α, sTNFR1, IL-RA, CXCL10, CXCL11 and IL-4 are often elevated [ 47 , 51 ].…”

Section: Cytokine Changes Associated With Bipolar Disordermentioning

confidence: 99%

Bipolar Disorder and Immune Dysfunction: Epidemiological Findings, Proposed Pathophysiology and Clinical Implications

2017

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Bipolar disorder (BD) is strongly associated with immune dysfunction. Replicated epidemiological studies have demonstrated that BD has high rates of inflammatory medical comorbidities, including autoimmune disorders, chronic infections, cardiovascular disease and metabolic disorders. Cytokine studies have demonstrated that BD is associated with chronic low-grade inflammation with further increases in pro-inflammatory cytokine levels during mood episodes. Several mechanisms have been identified to explain the bidirectional relationship between BD and immune dysfunction. Key mechanisms include cytokine-induced monoamine changes, increased oxidative stress, pathological microglial over-activation, hypothalamic-pituitary-adrenal (HPA) axis over-activation, alterations of the microbiome-gut-brain axis and sleep-related immune changes. The inflammatory-mood pathway presents several potential novel targets in the treatment of BD. Several proof-of-concept clinical trials have shown a positive effect of anti-inflammatory agents in the treatment of BD; however, further research is needed to determine the clinical utility of these treatments. Immune dysfunction is likely to only play a role in a subset of BD patients and as such, future clinical trials should also strive to identify which specific group(s) of BD patients may benefit from anti-inflammatory treatments.

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“…Recent emergent evidence points to the importance of the etiopathogenetic relationship between activation of immune-inflammatory pathways and psychiatric syndromes, including bipolar disorder (BD) (Berk et al, 2011;Grande et al, 2016;Hamdani et al, 2013;Leon-Caballero et al, 2015;Maes et al, 1995;Rege and Hodgkinson, 2013;Siwek et al, 2016). Available data support a relationship between autoimmunity and BD.…”

Section: Introductionmentioning

confidence: 99%