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Schizophr Bull. 2015 Sep;41(5):1162-70. doi: 10.1093/schbul/sbv028. Epub 2015 Mar 31.

Cortisol and Inflammatory Biomarkers Predict Poor Treatment Response in First Episode Psychosis.

Author information

1
Department of Psychological Medicine, King's College London, Institute of Psychiatry, Psychology and Neuroscience, London, UK; National Institute for Health Research Mental Health Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London, London, UK; valeria.mondelli@kcl.ac.uk.
2
National Institute for Health Research Mental Health Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London, London, UK; Department of Psychosis Studies, King's College London, Institute of Psychiatry, Psychology and Neuroscience, London, UK;
3
Department of Psychological Medicine, King's College London, Institute of Psychiatry, Psychology and Neuroscience, London, UK;
4
Department of Psychosis Studies, King's College London, Institute of Psychiatry, Psychology and Neuroscience, London, UK;
5
Department of Psychological Medicine, King's College London, Institute of Psychiatry, Psychology and Neuroscience, London, UK; National Institute for Health Research Mental Health Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London, London, UK;
6
Department of Health Services and Population Research, King's College London, Institute of Psychiatry, Psychology and Neuroscience, London, UK.

Abstract

BACKGROUND:

Cortisol and inflammatory markers have been increasingly reported as abnormal at psychosis onset. The main aim of our study was to investigate the ability of these biomarkers to predict treatment response at 12 weeks follow-up in first episode psychosis.

METHODS:

In a longitudinal study, we collected saliva and blood samples in 68 first episode psychosis patients (and 57 controls) at baseline and assessed response to clinician-led antipsychotic treatment after 12 weeks. Moreover, we repeated biological measurements in 39 patients at the same time we assessed the response. Saliva samples were collected at multiple time points during the day to measure diurnal cortisol levels and cortisol awakening response (CAR); interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor-α, and interferon-γ (IFN-γ) levels were analyzed from serum samples. Patients were divided into Non-Responders (n = 38) and Responders (n = 30) according to the Remission symptom criteria of the Schizophrenia Working Group Consensus.

RESULTS:

At first onset, Non-Responders had markedly lower CAR (d = 0.6, P = .03) and higher IL-6 and IFN-γ levels (respectively, d = 1.0, P = .003 and d = 0.9, P = .02) when compared with Responders. After 12 weeks, Non-Responders show persistent lower CAR (P = .01), and higher IL-6 (P = .04) and IFN-γ (P = .05) when compared with Responders. Comparison with controls show that these abnormalities are present in both patients groups, but are more evident in Non-Responders.

CONCLUSIONS:

Cortisol and inflammatory biomarkers at the onset of psychosis should be considered as possible predictors of treatment response, as well as potential targets for the development of novel therapeutic agents.

KEYWORDS:

HPA axis; cytokine; inflammation; outcome; schizophrenia; stress

PMID:
25829375
PMCID:
PMC4535637
DOI:
10.1093/schbul/sbv028
[Indexed for MEDLINE]
Free PMC Article

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