Abstract
OBJECTIVE: Lipoprotein-associated phospholipase A2 (Lp-PLA2) which is believed to play a role in atherosclerotic inflammatory process due to its function in hydrolysis of phospholipids and release of pro-inflammatory products, is considered as a novel biomarker for vascular risk. In this study we aimed to investigate the alterations in Lp-PLA2 and its relationship with other cardiovascular risk factors in patients with testosterone deficiency. MATERIAL AND METHODS: Forty hypogonadic male and 30 healthy male aged between 18-50 years were enrolled in this study. Height-weight, waist-to-hip circumference, body mass index (BMI) blood pressure, and body fat measurements were performed in all subjects. Blood glucose, albumin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, high sensitive C-reactive protein (hs-CRP), apo-A1, apo-B, fibrinogen, insulin, total testosterone, sex hormone binding globulin (SHBG), small dense low-density lipoprotein (sd-LDL), paraoxonase 1, oxidized low-density lipoprotein (ox-LDL) and Lp-PLA 2 values were measured. Free and bioavailable testosterone levels were calculated. Data management was carried out with the statistical program SAS Version 9.2. Statistical evaluations were performed using Analysis of Variance (ANOVA), Kruskal-Wallis test, Wilcoxon test, correlation analysis and chi-square analysis. P values <0.05 were considered statistically significant. RESULTS: In patients with hypogonadism, significant increase in Lp-PLA2 levels were accompanied with risk factors of atherosclerosis, such as increase in total cholesterol, apo-B, sd-LDL, weight, BMI, body fat percentage, and decrease in paraoxonase 1 levels. Although the differences were not significant, similarly ox-LDL, hs-CRP, triglyceride, LDL-cholesterol levels were found to be higher in patients with hypogonadism compared to the control group. The mean level of Lp-PLA2 was the highest when compared with the group of secondary hypogonadism with the lowest testosterone level. CONLUSION: Our study has demonstrated that the testosterone deficiency increases cardiovascular risk via its effects on lipid metabolism and Lp-PLA2 can be used to assess this risk.