Increased Neutrophil/Lymphocyte Ratio in Patients with Depression is Correlated with the Severity of Depression and Cardiovascular Risk Factors

OBJECTIVE: Chronic inflammation is associated with cardiovascular (CV) risk factors and psychiatric disorders. The neutrophil to lymphocyte ratio (NLR) has been investigated as a new biomarker for systemic inflammatory response. The aim of the study is to investigate the relation of NLR with severity of depression and CV risk factors. METHODS: The study population consisted of 256 patients with depressive disorder. Patients were evaluated with the Hamilton Rating Scale for Depression (HAM-D). Patients were classified into four groups according to their HAM-D score such as mild, moderate, severe, and very severe depression. Patients were also evaluated in terms of CV risk factors. RESULTS: Patients with higher HAM-D score had significantly higher NLR levels compared to patients with lower HAM-D score. Correlation analysis revealed that severity of depression was associated with NLR in depressive patients (r=0.333, p<0.001). Patients with one or more CV risk factors have significantly higher NLR levels. Correlation analysis revealed that CV risk factors were associated with NLR in depressive patients (r=0.132, p=0.034). In logistic regression analyses, NLR levels were an independent predictor of severe or very severe depression (odds ratio: 3.02, 95% confidence interval: 1.867-4.884, p<0.001). A NLR of 1.57 or higher predicted severe or very severe depression with a sensitivity of 61.4% and specificity of 61.2%. CONCLUSION: Higher HAM-D scores are associated with higher NLR levels in depressive patients. NLR more than 1.57 was an independent predictor of severe or very severe depression. A simple, cheap white blood cell count may give an idea about the severity of depression.

Chemokine and Chemokine Receptor Polymorphisms in Bipolar Disorder

OBJECTIVE: Bipolar disorder (BD) is a debilitating psychiatric disease with unknown etiology. Recent studies have shown inflammation as a potential contributing factor of BD pathogenesis. However, potential associations between chemokine and chemokine receptor polymorphisms and BD have been fundamentally understudied. To identify participation of chemokines in BD pathogenesis, we examined genetic variants of several chemokine and chemokine receptor genes. METHODS: The study population comprised 200 patients with BD and 195 age- and sex-matched healthy controls. Genotyping of monocyte chemotactic protein 1 (MCP-1) A2518G, CCR2 V64I, CCR5 Δ32, CCR5 A55029G, stromal cell-derived factor 1 (SDF-1) 3'A, and CXCR4 C138T polymorphisms was performed using polymerase chain reaction and restriction enzyme digestion. RESULTS: We found that CCR5-Δ32 II and CXCR4-C138T C+ genotype frequencies contributed to an increased risk for BD. However, no statistical significance could be obtained with these genotypes after Bonferroni correction. A significant asssociation was only found with MCP-1 GG and G+ genotypes, which were markedly more prevalent in patients with BD and these genotypes seemed to significantly increase the risk for BD even after Bonferroni correction. CONCLUSION: Our findings indicate an association between genetic variants of certain chemokine and chemokine receptor (especially MCP-1) genes and BD. The exact mechanisms by which these variants contribute to BD pathogenesis and their clinical implications need to be further investigated.