{"paper_id":"81ec6108-37a0-4836-896d-b6f83fb68e83","body_text":"Abstract\nPurpose\nThere 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.\nMethods\nIn 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.\nResults\nWomen 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.\nConclusion\nChronic 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.\nSimilar content being viewed by others\nReferences\nCiavattini A, Delli Carpini G, Clemente N, Moriconi L, Gentili C, Di Giuseppe J. Growth trend of small uterine fibroids and human chorionic gonadotropin serum levels in early pregnancy: an observational study. Fertil steril. 2016;105(5):1255–1260.\nCiavattini A, Clemente N, Delli Carpini G, Di Giuseppe J, Giannubilo SR, Tranquilli AL. Number and size of uterine fibroids and obstetric outcomes. J Matern Fetal Neonatal Med. 2015;28(4):484–488.\nStewart EA, Laughlin-Tommaso SK, Catherino WH, Lalitkumar S, Gupta D, Vollenhoven B. Uterine fibroids. Nat Rev Dis primers. 2016;2:16043.\nDownes E, Sikirica V, Gilabert-Estelles J, et al. The burden of uterine fibroids in five European countries. Eur J Obstet Gynecol Reprod Biol. 2010;152(1):96–102.\nCarls GS, Lee DW, Ozminkowski RJ, Wang S, Gibson TB, Stewart E. What are the total costs of surgical treatment for uterine fibroids? J Womens Health (Larchmt). 2008;17(7):1119–1132.\nIslam MS, Greco S, Janjusevic M, et al. Growth factors and pathogenesis. Best Pract Res Clin Obstet Gynaecol. 2016;34:25–36.\nOkolo S. Incidence, aetiology and epidemiology of uterine fibroids. Best Pract Res Clin Obstet Gynaecol. 2008;22(4):571–588.\nTakeda T, Sakata M, Isobe A, et al. Relationship between metabolic syndrome and uterine leiomyomas: a case-control study. Gynecol Obstet Invest. 2008;66(1):14–17.\nWise LA, Laughlin-Tommaso SK. Epidemiology of uterine fibroids: from menarche to menopause. Clin Obstet Gynecol. 2016;59(1):2–24.\nYang Y, He Y, Zeng Q, Li S. Association of body size and body fat distribution with uterine fibroids among Chinese women. J Womens Health (Larchmt). 2014;23(7):619–626.\nSato F, Nishi M, Kudo R, Miyake H. Body fat distribution and uterine leiomyomas. J Epidemiol. 1998;8(3):176–180.\nSamadi AR, Lee NC, Flanders WD, Boring JR, III Parris EB. Risk factors for self-reported uterine fibroids: a case-control study. Am J Public Health. 1996;86(6):858–862.\nStolk RP, Meijer R, Mali WP, Grobbee DE, van der Graaf Y; Secondary Manifestations of Arterial Disease Study G. Ultrasound measurements of intraabdominal fat estimate the metabolic syndrome better than do measurements of waist circumference. Am J Clin Nutr. 2003;77(4):857–860.\nKim SK, Kim HJ, Hur KY, et al. Visceral fat thickness measured by ultrasonography can estimate not only visceral obesity but also risks of cardiovascular and metabolic diseases. Am J Clin Nutr. 2004;79(4):593–599.\nAaltonen T, Amerio S, Amidei D, et al. Observation of the production of a W boson in association with a single charm quark. Phys Rev Lett. 2013;110(7):071801.\nSadlonova J, Kostal M, Smahelova A, Hendl J, Starkova J, Nachtigal P. Selected metabolic parameters and the risk for uterine fibroids. Int J Gynaecol Obstet. 2008;102(1):50–54.\nAksoy Y, Sivri N, Karaoz B, Sayin C, Yetkin E. Carotid intima-media thickness: a new marker of patients with uterine leiomyoma. Eur J Obstet Gynecol Reprod Biol. 2014;175:54–57.\nHoldsworth-Carson SJ, Zaitseva M, Vollenhoven BJ, Rogers PA. Clonality of smooth muscle and fibroblast cell populations isolated from human fibroid and myometrial tissues. Mol Hum Reprod. 2014;20(3):250–259.\nBennett MR, Sinha S, Owens GK. Vascular smooth muscle cells in atherosclerosis. Circ Res. 2016;118(4):692–702.\nAlpay Z, Saed GM, Diamond MP. Female infertility and free radicals: potential role in adhesions and endometriosis. J Soc Gynecol Investig. 2006;13(6):390–398.\nFletcher NM, Saed MG, Abu-Soud HM, Al-Hendy A, Diamond MP, Saed GM. Uterine fibroids are characterized by an impaired antioxidant cellular system: potential role of hypoxia in the pathophysiology of uterine fibroids. J Assist Reprod Genet. 2013;30(7):969–974.\nCiavattini A, Di Giuseppe J, Clemente N, et al. Thickness of preperitoneal fat as a predictor of malignancy in overweight and obese women with endometrial polyps. Oncol Lett. 2016;11(3):2278–2282.\nSuzuki R, Watanabe S, Hirai Y, et al. Abdominal wall fat index, estimated by ultrasonography, for assessment of the ratio of visceral fat to subcutaneous fat in the abdomen. Am J Med. 1993;95(3):309–314.\nYagi K. Lipid peroxides and related radicals in clinical medicine. Adv Exp Med Biol. 1994;366:1–15.\nSwinburn BA, Sacks G, Hall KD, et al. The global obesity pandemic: shaped by global drivers and local environments. Lancet. 2011;378(9793):804–814.\nBazzocchi A, Filonzi G, Ponti F, Albisinni U, Guglielmi G, Battista G. Ultrasound: which role in body composition? Eur J Radiol. 2016;85(8):1469–1480.\nFasshauer M, Bluher M. Adipokines in health and disease. Trends Pharmacol Sci. 2015;36(7):461–470.\nFlood A, Strayer L, Schairer C, Schatzkin A. Diabetes and risk of incident colorectal cancer in a prospective cohort of women. Cancer Causes Control. 2010;21(8):1277–1284.\nLee CH, Woo YC, Wang Y, Yeung CY, Xu A, Lam KS. Obesity, adipokines and cancer: an update. Clin Endocrinol (Oxf). 2015;83(2):147–156.\nNair S, Al-Hendy A. Adipocytes enhance the proliferation of human leiomyoma cells via TNF-alpha proinflammatory cytokine. Reprod Sci. 2011;18(12):1186–1192.\nWan F, Qin X, Zhang G, et al. Oxidized low-density lipoprotein is associated with advanced-stage prostate cancer. Tumour Biol. 2015;36(5):3573–3582.\nSuzuki K, Ito Y, Wakai K, et al. Serum oxidized low-density lipoprotein levels and risk of colorectal cancer: a case-control study nested in the Japan Collaborative Cohort Study. Cancer Epidemiol Biomarkers Prev. 2004;13(11 Pt 1):1781–1787.\nHalliwell B, Gutteridge JMC. Free Radicals in Biology and Medicine. 5th ed. Oxford, United Kingdom: Oxford University Press; 2015.\nWalter MF, Jacob RF, Jeffers B, et al. Serum levels of thiobarbituric acid reactive substances predict cardiovascular events in patients with stable coronary artery disease: a longitudinal analysis of the PREVENT study. J Am Coll Cardiol. 2004;44(10):1996–2002.\nTal R, Segars JH. The role of angiogenic factors in fibroid pathogenesis: potential implications for future therapy. Hum Reprod Update. 2014;20(2):194–216.\nCelletti FL, Waugh JM, Amabile PG, Brendolan A, Hilfiker PR, Dake MD. Vascular endothelial growth factor enhances atherosclerotic plaque progression. Nat Med. 2001;7(4):425–429.\nRicci C, Ferri N. Naturally occurring PDGF receptor inhibitors with potential anti-atherosclerotic properties. Vascul Pharmacol. 2015;70:1–7.\nPanutsopulos D, Papalambros E, Sigala F, Zafiropoulos A, Arvanitis DL, Spandidos DA. Protein and mRNA expression levels of VEGF-A and TGF-beta1 in different types of human coronary atherosclerotic lesions. Int J Mol Med. 2005;15(4):603–610.\nMas A, Stone L, O’Connor PM, et al. Developmental exposure to endocrine disruptors expands murine myometrial stem cell compartment as a prerequisite to leiomyoma tumorigenesis [published online October 14, 2016]. Stem Cells. 2016.\nMesquita FS, Dyer SN, Heinrich DA, Bulun SE, Marsh EE, Nowak RA. Reactive oxygen species mediate mitogenic growth factor signaling pathways in human leiomyoma smooth muscle cells. Biol Reprod. 2010;82(2):341–351.\nAuthor information\nAuthors and Affiliations\nCorresponding author\nRights and permissions\nAbout this article\nCite this article\nVignini, A., Sabbatinelli, J., Clemente, N. et al. Preperitoneal Fat Thicknesses, Lipid Profile, and Oxidative Status in Women With Uterine Fibroids. Reprod. Sci. 24, 1419–1425 (2017). https://doi.org/10.1177/1933719116689598\nPublished:\nIssue date:\nDOI: https://doi.org/10.1177/1933719116689598","source_license":"CC0","license_restricted":false}