Resistin as an inflammatory marker in patients with schizophrenia treated with clozapine

Abstract

Background: Schizophrenia is associated with excess cardiovascular comorbidity and mortality related to lifestyle factors, such as lack of physical activity, poor diet, and smoking. The prevalence of metabolic syndrome is increased among patients with schizophrenia, with the highest rates among patients on clozapine treatment. Smoking, obesity, physical inactivity, airway inflammation and obstruction, and adipose tissue and inflammatory marker activation are related in systemic inflammation. Low-grade inflammation is also associated with schizophrenia. Adipokine resistin is a biomarker involving several acute and chronic inflammatory states. However, the inflammatory role of resistin is so far inconclusive and studies in schizophrenia are scanty.

Aims: The aim of the present study was to explore the role of serum resistin as an inflammatory marker in patients with schizophrenia on clozapine treatment.

Methods: Associations between serum levels of resistin and some other selected cytokines/adipokines (adiponectin, leptin, adipsin, IL-6, IL-1Ra, TNF-α, hs-CRP) and metabolic markers in 190 patients with schizophrenia on clozapine treatment were studied using a cross-sectional study design.

Results: Among male patients especially, smokers had higher levels of resistin than non-smokers, and among smokers resistin levels were associated with IL-1Ra and hs-CRP levels. In the whole patient group levels of resistin associated with levels of IL-1Ra, and among male patients with low HDL-cholesterol.

Conclusions: Resistin is a biomarker of systemic inflammation associated with smoking among patients with schizophrenia on clozapine treatment. Resistin might have a role as a marker of cardiovascular comorbidity.

Keywords:

• Cytokine
• smoking
• IL-1Ra
• hs-CRP
• IL-6

Disclosure statement

J-P.K. has consulted for Otsuka and received support from Bristol-Myers Squibb, Eli Lilly, Lundbeck and Janssen-Cilag to participate in international congresses. O.K. has consulted for Medivir; received speaker’s fees from Janssen-Cilag, and received support from Otsuka and Lundbeck to participate in international congresses. N.S. has received support from Bristol-Myers Squibb and Janssen-Cilag to participate in international congresses. M.V. has consulted for Astra Zeneca, GlaxoSmithKline, Eli Lilly, and Servier; conducted clinical trials for Bristol-Myers Squibb, Eli Lilly, Lundbeck, Sanofi-Aventis, and Servier; received support from Bristol-Myers Squibb, GlaxoSmithKline, Eli Lilly, Lundbeck, and Servier to participate in international congresses; and received a research grant from GlaxoSmithKline, Lundbeck, and Pfizer. E.L. has worked as a lecturer or chairman in symposia sponsored by pharmaceutical companies Astra-Zeneca, Eli Lilly, Lundbeck, and Servier; served on the national advisory board of Servier; and received support from Astra-Zeneca, Lundbeck, Otsuka and Servier to participate in international congresses.

Funding

This study was financially supported by the Competitive State Research Financing of the Expert Responsibility area of Tampere University Hospital, unit for public health service.