Mean platelet volume in bipolar disorder: the search for an ideal biomarker

The pathophysiology of bipolar disorder (BD) remains a mystery. In this context, interest in the role of the immune and inflammatory systems in BD has been increasing. We aimed to compare the routine hemogram values of BD patients with those of the participants in the healthy control group, to assess the inflammation levels of the two groups. Mean platelet volume (MPV) can be obtained as routine hemogram parameters and may aid in the detection of systemic inflammation.

This study was conducted with BD (manic episode) inpatients (n=132) and healthy controls (n=135). Abnormally distributed variables (ie, neutrophil-lymphocyte ratio [NLR], platelet-lymphocyte ratio [PLR], neutrophils, lymphocytes, hemoglobin, hematocrit [HCT], mean corpuscular volume [MCV], mean corpuscular hemoglobin [MCH], mean corpuscular hemoglobin concentration [MCHC], red cell distribution width [RDW], MPV, and plateletcrit [PCT]) were compared using the Mann-Whitney U-test. Student's t-test was used to compare the mean ages and white blood cell, red blood cell, and platelet counts of the patients with BD against those of the participants in the control group.

The comparisons revealed that while the mean WBC and the median NLR, PLR, neutrophil, lymphocyte, MPV, and PCT values were significantly higher in the patients with BD (P<0.05), the median hemoglobin, RBC, HCT, and MCHC values were significantly higher in the control group (P<0.05).

Comparisons of hemogram values of patients with BD against those of the healthy control group revealed that inflammatory cells (absolute neutrophil count, platelet count, PCT, and MPV) and ratios (NLR, PLR) seem to be altered during manic episodes. These findings support the hypothesis that inflammatory activation occurs in BD during manic episodes. In addition to NLR and PLR, MPV may be useful in the detection of this activation. The most significant limitation in the study is that smokers were not excluded in both groups. The development of new preventive and therapeutic options can be facilitated through the understanding of this mechanism because through this mechanism, inflammation may pathologically affect brain function, as well as inducing and/or perpetuating BD.