Preperitoneal Fat Thicknesses, Lipid Profile, and Oxidative Status in Women With Uterine Fibroids

Abstract

There is growing evidence supporting a possible role for metabolic syndrome and its determinants, such as dyslipidemia, in uterine fibroid (UF) pathogenesis. The present study aims to investigate the association between UFs and visceral and subcutaneous fat thickness (SFT), lipid profile, and oxidative and antioxidative status. In this cross-sectional study, 35 patients diagnosed with UFs and 15 women without UFs were enrolled. Clinical history and anthropometric parameters were collected for every woman. Characteristics of UFs, preperitoneal fat thickness (PFT), and SFT were assessed ultrasonically. Lipid profile, glucose, thiobarbituric acid reactive substances (TBARs), and superoxide dismutase (SOD) activity were evaluated on plasma from participants. Women with UFs showed a significantly increased PFT (11.63 ± 3.39 vs 7.01 ± 3.10 mm; P < .001), lower levels of high-density lipoprotein cholesterol (HDL-C; 45.4 ± 8.3 vs 57.2 ± 13.4 mg/dL; P = .017), higher levels of low-density lipoprotein cholesterol (LDL-C; 92.3 ± 21.5 vs 72.0 ± 14.6 mg/dL; P = .007), and oxidized LDL (65.2 ± 20.7 vs 43.0 ± 11.3 U/L; P = .002). In patients, TBARs concentration was significantly higher (9.41 ± 6.49 vs 2.92 ± 1.65 nmol malondialdehyde/100 μg prot; P < .001), whereas SOD activity was lower (1.09 ± 0.19 vs 1.37 ± 0.41 U/μL; P = .005). Preperitoneal fat thickness was positively associated with body mass index, oxidized LDL, and TBARs. At multivariate analysis, PFT and HDL-C maintained a significant correlation with the diagnosis of UFs. Chronic inflammation triggered and sustained by visceral fat could play a determinant role in cell differentiation and proliferation processes, necessary for the development of UFs. Alterations in cholesterol fractions may be explained as a consequence of the increased visceral fat deposits and can reflect an increased risk of subclinical atherosclerosis in patients with UF.