One of the pathogenesis of schizophrenia is dysregulated immunity, especially if it is involved in the occurrence of cognitive impairment. Therefore, it is necessary to explore changes in the inflammatory indicators and their relationship with cognitive functions in patients with schizophrenia. CBC is simple and readily available and accurately reflects the indicators of body inflammation, and it has been investigated using CBC to discover that there is a difference in inflammatory response between schizophrenia and normal individuals (Özdin and Böke, 2018). However, no study has been found on the relationship between CBC and the cognitive deficit of schizophrenia patients. As shown in our results, this study has shown that there is an inflammatory difference between schizophrenics and normal people, and it shows that people with schizophrenia have higher monocyte count, PLR, and MLR, which were associated with clinical symptoms. Furthermore, we assessed cognitive function in schizophrenia using MCCB and found that Hb levels and PLR were associated with global cognitive impairment. As far as we know, these have never been reported.
Exposure to decreasing in maternal hemoglobin during pregnancy were correlated with increased risk for schizophrenia in offspring (Ellman et al., 2012). In adults with schizophrenia, functional near infra-red spectroscopy (fNIRS) studies report decreased oxyhemoglobin levels in prefrontal cortex (Kumar et al., 2017). In this study, we found patients with schizophrenia were with lower Hb levels, which may be explained by poor nutrition in patients with schizophrenia in this study, with the results that we found that there was a tendency for lower BMI in schizophrenia, although there was no significant difference. Iron is a precursor to the synthesis of hemoglobin. Maternal iron deficiency during pregnancy increases the risk of schizophrenia in offspring (Sørensen et al., 2011). And Sussulini et al (2018) reported iron levels of schizophrenic patients were found to be increased after treatment with antipsychotics. Thus, the reduction in Hb levels may be explained by decreased iron levels in patients with schizophrenia. Moreover, worse cognitive function has been found related with lower Hb levels in patients with various types of anemia (Shah et al., 2011; Onem et al., 2010; Zamboni et al., 2006; Hollocks et al., 2012; Sungthong et al., 2002), also, our results showed positive correlations between Hb levels and global cognitive function in patients with schizophrenia, which has never been reported to our knowledge. Collectively, this study provides evidence for the correlation between the Hb level and cognitive deficits in patients with schizophrenia.
As inflammation markers, higher PLR and MLR have been found in schizophrenic patients during relapse period when compared with the control group (Özdin and Böke, 2018), which were consistent with our study. Ribeiro-Santos et al (2014) summarized that microglial activation, monoaminergic imbalance, brain abnormalities and the kynurenine pathway were possible mechanisms underlying cognitive impairment in schizophrenia. Platelet plays an important role in the activation of microglia (García-Culebras et al., 2018), and peripheral monocytes are thought to have many commonalities with microglia (Ruizhi et al., 2018), these may result in increased PLR and MLR in schizophrenia. Moreover, PLR has been found reported to be related to cognitive function in bipolar disorder (Sağlam et al., 2018). Similarly, this study found that increased PLR in patients with schizophrenia was associated with impaired cognitive function, suggesting that inflammation is involved in cognitive impairment in patients with schizophrenia.
We acknowledge that our study has some limitations. First, the performance of subjects in cognitive tasks are related to their education level as we know. Unfortunately, we did not include the effect of education level on cognitive function, although we have ensured that each subject could understand and complete the cognitive tasks. Secondly, considering that the acute stage of schizophrenia is more representative, all the patients we selected were in the acute stage of schizophrenia, which tends to show a poor degree of cooperation. Therefore, only six cognitive tasks were selected in MCCB, although these tasks also reflected cognitive function broadly.
In conclusion, we preliminarily explored the relationship between cognitive function and CBC in patients with schizophrenia, and found that cognitive deficits in patients with schizophrenia was associated with poor nutrition and dysregulated immunity, and hemoglobin and PLR could be used as markers for both. We hope clinicians will pay more attention to the poor nutrition and dysregulated immunity in patients with schizophrenia in the future.