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Published on: November 21, 2013
Pro-/antiinflammatory dysregulation in early psychosis: results from a 1-year follow-up study
Borja García-Bueno1, Miquel Bioque1, Karina S MacDowell1
1Department of Pharmacology, Faculty of Medicine, Complutense University, Instituto de Investigación Sanitaria -IIS- Hospital 12 de Octubre (i+12), Madrid, Spain (Drs García-Bueno, MacDowell, and Leza); Unitat d'Esquizofrènia Clínic, Hospital Clínic, University of Barcelona, IDIBAPS, Barcelona, Spain (Drs Bioque and Bernardo); Department of Preventive Medicine and Public Health, University of Zaragoza, Zaragoza, Spain (Dr Santabárbara); Hospital Universitario, Alava, EHU/UPV and National Distance Education University, Vitoria, Spain (Drs Martínez-Cengotitabengoa and González-Pinto); Child and Adolescent Psychiatry Department IIS Gregorio Marañón (IISGM), Hospital General Universitario Gregorio Marañón, Madrid, Spain (Drs Moreno and Parellada); Department of Psychiatry, Faculty of Medicine, University of Oviedo, Oviedo, Spain (Drs Sáiz and Bobes); Department of Pharmacology, Faculty of Medicine, University of Cádiz, Cádiz, Spain (Drs Berrocoso and Micó); Department of Pharmacology, Faculty of Medicine, University of Barcelona, Barcelona, Spain (Dr Gassó); Hospital Clínico Universitario, Zaragoza, Spain (Dr Fe Barcones).
Background:
Previous studies indicated a systemic deregulation of the pro-/antiinflammatory balance in subjects after 6 months of a first psychotic episode. This disruption was reexamined 12 months after diagnosis to identify potential risk/protective factors and associations with symptom severity.
Methods:
Eighty-five subjects were followed during 12 months and the determination of the same pro-/antiinflammatory mediators was carried out in plasma and peripheral blood mononuclear cells. Multivariate logistic regression analyses were used to identify risk/protective factors. Multiple linear regression models were performed to detect the change of each biological marker during follow-up in relation to clinical characteristics and confounding factors.
Results:
This study suggests a more severe systemic pro-/antiinflammatory deregulation than in earlier pathological stages in first psychotic episode, because not only were intracellular components of the inflammatory response increased but also the majority of soluble elements. Nitrite plasma levels and cyclooxygenase-2 expression in peripheral blood mononuclear cells are reliable potential risk factors and 15d-prostaglandin-J2 plasma levels a protection biomarker. An interesting relationship exists between antipsychotic dose and the levels of prostaglandin-E2 (inverse) and 15d-prostaglandin-J2 (direct). An inverse relationship between the Global Assessment of Functioning scale and lipid peroxidation is also present.
Conclusions:
Summing up, pro-/antiinflammatory mediators can be used as risk/protection biomarkers. The inverse association between oxidative/nitrosative damage and the Global Assessment of Functioning scale, and the possibility that one of the targets of antipsychotics could be the restoration of the pro-/antiinflammatory balance support the use of antiinflammatory drugs as coadjuvant to antipsychotics.
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