Neutrophil-lymphocyte Ratio and C-reactive Protein Level in Patients with Major Depressive Disorder Before and After Pharmacotherapy

Abstract

Neutrophil-lymphocyte ratio (NLR) and C-reactive protein (CRP) level are useful biomarkers of inflammation. This study aimed to assess NLR and CRP level in patients with major depressive disorder before and after pharmacotherapy to determine whether NLR or CRP could be used as biomarkers of severity of major depression and whether there was any sex difference. Patients with major depression who received no pharmacotherapy 1 month prior to the study were included. Their haemoglobin, total white blood cell count, neutrophil and lymphocyte counts, NLR, and CRP levels were evaluated at baseline and 12 weeks post pharmacotherapy, as were the Montgomery Asberg Rating Scale for Depression, the Scale for Impact of Suicidality Management and Assessment and Planning of Care (SIS-MAP), and the Clinical Global Impression Scale - Severity. 24 male and 26 female patients were included. At 12 weeks after pharmacotherapy, males had a higher haemoglobin level (p = 0.025), higher total white blood cell count (p = 0.018), and lower percentage of neutrophils (p = 0.019) than females. There was no sex difference in NLR or CRP. From baseline to 12 weeks, males had no significant change in any blood parameter, but females had a significantly greater increase in the percentage of neutrophils (p = 0.0001) and decrease in the percentage of lymphocytes (p = 0.012), resulting in a significantly increased NLR (p = 0.001). Both males and females had significant improvement on all 3 scales (p < 0.001). At 12 weeks, in males, the increase in NLR positively correlated with CRP as well as the Montgomery-Asberg Depression Rating Scale and the SIS-MAP, but not the Clinical Global Impression-Severity Scale. In females, the increase in NLR did not correlate with CRP or any of the scales. In female patients, the NLR increased in response to antidepressant therapy while CRP remained unchanged. This indicated that inflammation has a role in the pathogenesis of major depression.