Effects of electroconvulsive therapy in the systemic inflammatory balance of patients with severe mental disorder.

Abstract

There is a great interest in the role of the immune system and the inflammatory balance as key mechanisms involved in the pathophysiology of severe mental disorders. Previous studies have indicated that electroconvulsive therapy (ECT) produces changes in certain inflammatory mediators or in the immune system response. This study aimed to explore the effects of ECT on the nuclear transcription factor κB (NFκB) pathway, a main regulatory pathway of the inflammatory/immune response. Thirty subjects with a severe mental disorder receiving treatment with ECT in our center were included. Thirteen systemic biomarkers related to the NFκB pathway were analyzed right before and 2 h after a single ECT session. An ECT session significantly decreased the expression of NFκB (P = 0.035) and of the inducible nitric oxide synthase (P = 0.012), and the plasma levels of nitrites (P = 0.027), prostaglandin E2 (P = 0.049), and 15-deoxy-PGJ2 (P < 0.001). Decrease in plasmatic levels of nitrites was greater in females than in males (P = 0.021). A positive correlation between the ECT stimulus load and changes in the expression of NFkB was found (P = 0.036). Thiobarbituric acid reactive substance levels were decreased in treatment responders and increased in non-responders (P = 0.047). Our study shows the effects that a single session of ECT produces on a canonical regulatory pathway of the inflammatory/innate immune system and the inflammatory balance. These biomarkers could be useful as treatment response targets and could help to clarify the biological basis of ECT action. These findings warrant greater attention in future investigations and in the translational significance of these data.