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High-sensitivity C-reactive protein and cyclothymic temperament as predictors of suicidal risk

Published online by Cambridge University Press:  26 August 2025

L. Cavallo*
Affiliation:
Unit of Clinical Psychiatry, Department of Neurosciences/Department of Experimental and Clinical Neurosciences (DIMSC), Polytechnic University of Marche, Ancona, Italy
G. Longo
Affiliation:
Unit of Clinical Psychiatry, Department of Neurosciences/Department of Experimental and Clinical Neurosciences (DIMSC), Polytechnic University of Marche, Ancona, Italy
L. Orsolini
Affiliation:
Unit of Clinical Psychiatry, Department of Neurosciences/Department of Experimental and Clinical Neurosciences (DIMSC), Polytechnic University of Marche, Ancona, Italy
U. Volpe
Affiliation:
Unit of Clinical Psychiatry, Department of Neurosciences/Department of Experimental and Clinical Neurosciences (DIMSC), Polytechnic University of Marche, Ancona, Italy
*
*Corresponding author.

Abstract

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Introduction

An increasing number of studies have investigated the role of inflammation in mood disorders, like an altered C-reactive protein (CRP) hematic level. Some studies have also shown an association between suicidal behavior and increased CRP levels.

Objectives

The objective of this study was to evaluate the association between specific clinical features and high sensitivity CRP (hsCRP) levels with suicidal risk in mood disorders inpatients.

Methods

A naturalistic, observational, cross-sectional study was carried out by retrospectively recruiting 353 adult inpatients affected by severe mental illness (SMI), excluding patients affected by inflammatory pathology, alcohol/substances use disorders or treaded by anti-inflammatory/immunosuppressive therapy. In this sample 241 patients suffering from mood disorders were selected. HsCRP levels were measured at the ward admission. All patients were assessed with subscale 5 of the Mini International Neuropsychiatric Interview (MINI-5-s), TEMPS-M, BPRS, HAM-D21, YMRS, CGI-S, CGI-I, MOCA, MDQ, MSRS.

Results

A logistic regression analysis was performed to ascertain the effects of hsCRP and personality trait on the likelihood of suicidality risk. The logistic regression model was statistically significant, χ2(2) = 32.868, p < 0.001. The model explained 18.7% (Nagelkerke R2) of the variance in subjects with a suicidality risk and correctly classified 76.8% of cases. According to the logistic regression model, suicidality risk is negatively predicted by the total score of the YMRS (exp(B)=0.969, IC95%=0.947-0.993, p=0.01) and hostility subscale of the BPRS (exp(B)=0.905, IC95%=0.819-1.000, p=0.05) while it is positively predicted by the cyclothymic temperament subscale of the TEMPS-M (exp(B)=1.066, IC95%=1.017-1.118, p=0.008) and hsCRP (exp(B)=1.090, IC95%=1.012-1.174, p=0.024).

Conclusions

The study suggests the potential transdiagnostic association between low grade inflammation, temperament and suicidal risk in patients affected by mood disorders. Our preliminary findings could support a routine introduction of hsCRP hematic measurement, due to its relatively low cost, for its possible utility as an early trans-diagnostically biomarker for suicidal risk. The findings could also lead to developing a model to identify subjects who may benefit from a combined anti-inflammatory and psychopharmacological treatment strategy during the acute illness phase. A neuroinflammatory approach could further help stage and subtype mood disorder patients in more homogenous samples and investigate short- and long-term treatment implications, clinical course, and prognosis. Further research studies should consider all illness phases and how specific temperament and chronotype may influence treatment response, illness course, and outcomes.

Disclosure of Interest

None Declared

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Abstract
Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
© The Author(s), 2025. Published by Cambridge University Press on behalf of European Psychiatric Association
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