PB2270 THE RELATIONSHIP BETWEEN OXIDATIVE STRESS MARKERS, AGE, NEUTROPHIL‐TO‐LYMPHOCYTE RATION AND OBESITY

Background:Obesity is a complex metabolic disease associated with an excessive accumulation of white adipose tissue (WAT). WAT secretes adipokines, which in turn generate reactive oxygen species (ROS) or decrease the total antioxidant capacity (TAC), and pro‐inflammatory cytokines (TNF‐alpha, IL1, IL6), leading to obesity‐induced inflammation.Aims:To evaluate oxidative stress via ROS and TAC measurement and evaluate obesity‐induced inflammation via the neutrophil‐to‐lymphocyte ratio (NLR) in obese patients.Methods:We evaluated oxidative stress and NLR in obese subjects vs. non‐obese controls. Patients were divided by age, sex, and degree of obesity. Obesity was diagnosed according to the WHO criteria, based on the body mass index (BMI). Oxidative stress was evaluated using a CR3000 analyzer via the FORT (Free Oxygen Radical Testing for ROS quantification) and FORD (Free Oxygen Radical Defence for TAC measurement) assays. NLR was evaluated as a marker of chronic inflammation (normal values: 0.78‐3.53). Statistical analysis of data was conducted using the student T‐test and a p‐value < 0.05 was considered significant. The study was approved by the Ethics Committee of the University of Medicine and Pharmacy of Craiova (approval no. 40/27.03.2018) and written informed consent was collected from all subjects involved.Results:The study group involved 85 obese patients (mean age 61.85 ± 10.60 years, age range 24‐82): 17 males (20.00%, mean age 62.65 ± 8.90 years, age range 43‐77) and 68 females (80.00%, mean age 61.65 ± 10.97 years, age range 24‐82). The control group included 30 non‐obese subjects (mean age 44.60 ± 18.45 years, age range 18‐85). Mean BMI was 36.44 ± 3.63 kg/m2 in obese subjects (men: 35.35 ± 3.41 kg/m2, women: 36.71 ± 3.63 kg/m2) vs. 24.56 ± 1.76 kg/m2 in controls (p‐value < 0.0001). Stratification in obesity classes was: 38 patients (44.70%) ‐ class I obesity, 31 patients (36.47%) ‐ class II obesity, 16 patients (18.83%) – class III obesity. FORT values were increased in obese patients vs. controls (3.09 ± 0.36 mmol/L vs. 2.03 ± 0.14 mmol/L, p‐value<0.001). FORD values were decreased in obese patients vs. controls (0.69 ± 0.15 mmol/L vs. 1.27 ± 0.13 mmol/L, p‐value<0.001). We did not record significant differences in terms of NLR in obese subjects vs. controls (2.46 ± 0.96 vs. 2.31 ± 0.26, p = 0.4036). In obese subjects, we found positive correlations between FORT and BMI (r s  = 0.38407, p = 0.00028), NLR (r s  = 0.06771, p = 0.5381) and age (r s  = 0.06781, p = 0.53748). Negative correlations were recorded between FORD and BMI (rs = ‐0.35083, p = 0.001), age (rs = ‐0.04698, p = 0.66942) and NLR (rs = ‐0.06732, p = 0.54045)Summary/Conclusion:In our study group, ROS levels were increased and TAC was decreased in obese patients as compared to healthy controls. ROS levels and TAC correlated with BMI, but not in a significant manner with age or NLR.