Distributional Characterization of CBC-Derived Inflammatory Indices in Hospitalized Patients with Schizophrenia

Background: Increasing evidence suggests that schizophrenia may be associated with peripheral immune–inflammatory alterations, although the distributional characteristics and heterogeneity of routinely available complete blood count (CBC)-derived inflammatory indices in real-world psychiatric inpatient settings remain insufficiently characterized. The present study aimed to descriptively evaluate the distributional properties of CBC-derived inflammatory markers in hospitalized patients with schizophrenia using an exploratory panel-based analytical framework. Methods: We conducted a retrospective cross-sectional analysis using anonymized CBC laboratory panels obtained from hospitalized patients with schizophrenia at a tertiary psychiatric center. Following panel reconstruction and quality control procedures, 858 structurally valid CBC panels were included in the analyses. Primary inflammatory indices included neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), platelet-to-lymphocyte ratio (PLR), and systemic immune–inflammation index (SII). Descriptive distributional analyses, threshold-based prevalence estimation, Spearman correlation analyses, and exploratory unsupervised clustering procedures were performed to evaluate inflammatory variability and internal distributional patterns within the dataset. Results: Median NLR was 2.51 (IQR: 1.95–3.55), median MLR was 0.25 (IQR: 0.19–0.31), median PLR was 124.10 (IQR: 100.40–163.94), and median SII was 686.96 (IQR: 484.81–1045.85). Threshold-based analyses demonstrated substantial variability in inflammatory burden distributions, with 35.9% of panels showing NLR > 3 and 27.0% demonstrating SII > 1000. Correlation analyses revealed strong positive associations among NLR, PLR, and SII, whereas RDW-CV and MPV demonstrated weaker and more heterogeneous relationships with the principal inflammatory indices. Exploratory clustering analyses generated two distributional clusters, including a smaller cluster exhibiting relatively higher NLR, MLR, PLR, SII, WBC, and platelet values than the remaining panels. Female panels demonstrated significantly higher PLR and SII distributions following false discovery rate (FDR) correction. Conclusions: The present findings suggest that CBC-derived inflammatory indices demonstrate substantial distributional variability within this panel-based schizophrenia dataset. Although the exploratory design, absence of patient-level linkage, and lack of clinical confounder adjustment substantially limit biological interpretation, routinely available hematological inflammatory markers may still provide a pragmatic framework for descriptive characterization of inflammatory variability patterns in real-world psychiatric populations. Future patient-level longitudinal studies integrating clinical, pharmacological, and molecular variables will be necessary to determine the potential clinical relevance of inflammatory heterogeneity in schizophrenia.