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Eur Neuropsychopharmacol. 2015 Oct;25(10):1532-43. doi: 10.1016/j.euroneuro.2015.06.007. Epub 2015 Jun 20.

Inflammation and clinical response to treatment in depression: A meta-analysis.

Author information

1
Affective Disorders Research Group, Centre for Affective Disorders, Psychological Medicine, Institute of Psychiatry, King׳s College London, London, UK. Electronic address: Becci.strawbridge@kcl.ac.uk.
2
Affective Disorders Research Group, Centre for Affective Disorders, Psychological Medicine, Institute of Psychiatry, King׳s College London, London, UK.
3
Social, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, King׳s College London, London, UK; Department of Child & Adolescent Psychiatry, Institute of Psychiatry, King׳s College London, London, UK.
4
Affective Disorders Research Group, Centre for Affective Disorders, Psychological Medicine, Institute of Psychiatry, King׳s College London, London, UK; Psychiatric University Clinic, University of Chile, Santiago, Chile.
5
Affective Disorders Research Group, Centre for Affective Disorders, Psychological Medicine, Institute of Psychiatry, King׳s College London, London, UK; National Institute for Health Research (NIHR) Biomedical Research Centre for Mental Health at South London and Maudsley NHS Foundation Trust and Institute of Psychiatry, King׳s College London, London, UK.

Abstract

The depressive state has been characterised as one of elevated inflammation, which holds promise for better understanding treatment-resistance in affective disorders as well as for future developments in treatment stratification. Aiming to investigate alterations in the inflammatory profiles of individuals with depression as putative biomarkers for clinical response, we conducted meta-analyses examining data from 35 studies that investigated inflammation before and after treatment in depressed patients together with a measure of clinical response. There were sufficient data to analyse IL-6, TNFα and CRP. Levels of IL-6 decreased with antidepressant treatment regardless of outcome, whereas persistently elevated TNFα was associated with prospectively determined treatment resistance. Treatment non-responders tended to have higher baseline inflammation, using a composite measure of inflammatory markers. Our findings suggest that elevated levels of inflammation are contributory to treatment resistance. Combining inflammatory biomarkers might prove a useful tool to improve diagnosis and detection of treatment refractoriness, and targeting persistent inflammation in treatment-resistant depression may offer a potential target for the development of novel intervention strategies.

KEYWORDS:

Biological markers; Depression; Depressive disorder; Inflammation; Treatment-resistant

PMID:
26169573
DOI:
10.1016/j.euroneuro.2015.06.007
[Indexed for MEDLINE]

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