Metabolic-inflammatory status as predictor of clinical outcome at 1-year follow-up in patients with first episode psychosis.


Journal

Psychoneuroendocrinology
ISSN: 1873-3360
Titre abrégé: Psychoneuroendocrinology
Pays: England
ID NLM: 7612148

Informations de publication

Date de publication:
01 2019
Historique:
received: 21 04 2018
revised: 31 07 2018
accepted: 07 09 2018
pubmed: 23 9 2018
medline: 1 6 2019
entrez: 23 9 2018
Statut: ppublish

Résumé

Metabolic abnormalities and peripheral inflammation have been increasingly reported in patients at the onset of psychosis and associated with important physical health disorders and increased mortality. However, the impact of an abnormal metabolic-inflammatory status on the psychiatric outcome of these patients has not yet been investigated. The aims of this study were 1) to explore whether, in a sample of patients at their first episode of psychosis (FEP), an overall metabolic-inflammatory status may be measured, by combining metabolic and inflammatory variables in metabolic-inflammatory factors; 2) to explore the association between these factors and clinical outcome at 1-year follow-up (FU), in terms of symptoms severity and treatment response. In this longitudinal study we recruited 42 FEP patients and 46 healthy controls (HC) matched with patients for age, gender and ethnicity. At baseline (T1) we measured high sensitivity C-reactive protein (hsCRP) as biomarker of inflammation, and body mass index (BMI), lipid profile and gluco-metabolic parameters (glycated hemoglobin (HbA1c) and fasting glucose) as metabolic variables. A principal component analysis (PCA) was then used to reduce the dimensionality of the dataset accounting for both inflammation and metabolic status. In FEP patients, we assessed symptoms severity at T1 and at 1-year FU (T2) as well as treatment response to antipsychotics at T2. at T1, FEP showed higher HbA1c (p = 0.034), triglycerides (TG) (p = 0.045) and BMI (p = 0.026) than HC. PCA identified 3 factors: factor 1 accounting for hsCRP, TG and BMI, factor 2 accounting for LDL and cholesterol, and factor 3 accounting for fasting glucose and HbA1c. Factor 1 was associated with T1 negative symptoms severity (p = 0.021) and predicted T2 positive (p = 0.004) and overall symptoms severity (0.001), as well as general psychopathology (p < 0.001) and T2 treatment response (p = 0.007). In this sample of FEP patients, inflammation and metabolism, closely correlated at the onset of psychosis, proved to play a key role as predictors of the clinical course of psychosis when combined in a single factor. These findings offer an important potential target for early screening and interventions.

Sections du résumé

BACKGROUND
Metabolic abnormalities and peripheral inflammation have been increasingly reported in patients at the onset of psychosis and associated with important physical health disorders and increased mortality. However, the impact of an abnormal metabolic-inflammatory status on the psychiatric outcome of these patients has not yet been investigated.
OBJECTIVES
The aims of this study were 1) to explore whether, in a sample of patients at their first episode of psychosis (FEP), an overall metabolic-inflammatory status may be measured, by combining metabolic and inflammatory variables in metabolic-inflammatory factors; 2) to explore the association between these factors and clinical outcome at 1-year follow-up (FU), in terms of symptoms severity and treatment response.
METHODS
In this longitudinal study we recruited 42 FEP patients and 46 healthy controls (HC) matched with patients for age, gender and ethnicity. At baseline (T1) we measured high sensitivity C-reactive protein (hsCRP) as biomarker of inflammation, and body mass index (BMI), lipid profile and gluco-metabolic parameters (glycated hemoglobin (HbA1c) and fasting glucose) as metabolic variables. A principal component analysis (PCA) was then used to reduce the dimensionality of the dataset accounting for both inflammation and metabolic status. In FEP patients, we assessed symptoms severity at T1 and at 1-year FU (T2) as well as treatment response to antipsychotics at T2.
RESULTS
at T1, FEP showed higher HbA1c (p = 0.034), triglycerides (TG) (p = 0.045) and BMI (p = 0.026) than HC. PCA identified 3 factors: factor 1 accounting for hsCRP, TG and BMI, factor 2 accounting for LDL and cholesterol, and factor 3 accounting for fasting glucose and HbA1c. Factor 1 was associated with T1 negative symptoms severity (p = 0.021) and predicted T2 positive (p = 0.004) and overall symptoms severity (0.001), as well as general psychopathology (p < 0.001) and T2 treatment response (p = 0.007).
CONCLUSION
In this sample of FEP patients, inflammation and metabolism, closely correlated at the onset of psychosis, proved to play a key role as predictors of the clinical course of psychosis when combined in a single factor. These findings offer an important potential target for early screening and interventions.

Identifiants

pubmed: 30243054
pii: S0306-4530(18)30398-6
doi: 10.1016/j.psyneuen.2018.09.005
pii:
doi:

Substances chimiques

Antipsychotic Agents 0
Biomarkers 0
Blood Glucose 0
Glycated Hemoglobin A 0
Triglycerides 0
hemoglobin A1c protein, human 0
C-Reactive Protein 9007-41-4
Cholesterol 97C5T2UQ7J

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

145-153

Subventions

Organisme : Medical Research Council
ID : MR/J002739/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/M008436/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N029488/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : G108/603
Pays : United Kingdom
Organisme : MRF
ID : MRF_C0439
Pays : United Kingdom

Informations de copyright

Copyright © 2018 Elsevier Ltd. All rights reserved.

Auteurs

Maria Antonietta Nettis (MA)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychological Medicine, London, UK; National Institute for Health and Research Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London, UK. Electronic address: maria.nettis@kcl.ac.uk.

Giulio Pergola (G)

Group of Psychiatric Neuroscience, Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari 'Aldo Moro', Bari, Italy.

Anna Kolliakou (A)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychosis Studies, London, UK.

Jennifer O'Connor (J)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychosis Studies, London, UK.

Stefania Bonaccorso (S)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychosis Studies, London, UK.

Anthony David (A)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychosis Studies, London, UK.

Fiona Gaughran (F)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychosis Studies, London, UK; National Psychosis Service, South London and Maudsley NHS Foundation Trust, London, UK.

Marta Di Forti (M)

Institute of Psychiatry Psychology and Neuroscience, King's College London, Department of Social Genetic and Developmental Psychiatry (SGDP), London, UK.

Robin M Murray (RM)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychosis Studies, London, UK; Department of Psychiatry, Experimental Biomedicine and Clinical Neuroscience (BIONEC), University of Palermo, Palermo, Italy.

Tiago Reis Marques (TR)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychosis Studies, London, UK.

Giuseppe Blasi (G)

Group of Psychiatric Neuroscience, Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari 'Aldo Moro', Bari, Italy.

Alessandro Bertolino (A)

Group of Psychiatric Neuroscience, Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari 'Aldo Moro', Bari, Italy.

Carmine M Pariante (CM)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychological Medicine, London, UK; National Institute for Health and Research Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London, UK.

Paola Dazzan (P)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychosis Studies, London, UK.

Valeria Mondelli (V)

Institute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychological Medicine, London, UK; National Institute for Health and Research Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London, UK.

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Classifications MeSH