Many hypotheses have been proposed about development of bipolar disorder including inflammatory processes due to the external and endogenous factors. There are strong evidences that immunological dysfunction is present in bipolar disorder. In the pathophysiology of bipolar disorder, there are many data that support the inflammatory hypothesis.

In this study, to clarify the etiology of bipolar disorder, based on the inflammatory process hypothesis, it is aimed to measure and evaluate serum 15d-PGJ2 and PPARγ, anti-inflammatory cytokine IL-4 levels in patients with bipolar disorder.

This study was performed at Ankara Numune Training and Research Hospital. Ninety-five patients are included in the study that were in their mania or remission periods and meet the DSM-V criteria for bipolar disorder. Forty-four healthy volunteers are included in the study as well. Serum IL-4, 15d-PGJ2, PPARγ levels are measured in both groups. Young Mania Scale, Hamilton Depression Scale, demographic data form were given to patient group.

In our study, 15d-PGJ2, PPARγ levels were found statistically significantly lower in patients with bipolar disorder compared to healthy controls.

There are differences in anti-inflammatory prostaglandin levels in patients with bipolar disorder who are in their mania period when compared to healthy controls and patients in their remission period. This does not show any significance according to smoking and gender. This implies that inflammation markers could be a good candidate to determine trait markers, which will provide an insight for preventing patient from mania period or prognosis after the diagnosis of bipolar disorder.

The authors have not supplied their declaration of competing interest.