title: Mediators of chronic inflammation in polycystic ovarian syndrome.
abstract: Polycystic ovarian syndrome (PCOS) is an endocrine disorder affecting 5-10% of reproductive-age women. Hyperandrogenemia, which characterizes the syndrome, stimulates the maturation of adipocytes and favors central obesity. The linking hub between obesity and other metabolic manifestations of the syndrome seems to be chronic low-grade inflammation. We discuss the most reliable current data regarding the role of inflammatory mediators in PCOS, with particular focus on the genetic mechanisms implicated. C-reactive protein levels are 96% higher in PCOS patients than in healthy controls. Patients with the -308A polymorphism of the tumor necrosis factor-α gene have elevated androgens in comparison with carriers of the -308G. Interleukin 18 (IL-18) is elevated in lean patients, with a further rise in the presence of obesity and insulin resistance. Polymorphisms of the IL-1a, IL-1b and IL-6 genes have also been associated with PCOS. Plasminogen activator inhibitor-1 levels are positively associated with the syndrome, and carriers of the 4G allele of the 4G/5G polymorphism are at risk of developing PCOS. Other mediators discussed include adhesion molecules, osteoprotegerin, asymmetric dimethylarginine, homocysteine and advanced glycation end-products. The elucidation of the pathogenetic mechanisms implicated in PCOS and their connection with low-grade inflammation may in the future offer the opportunity for the formulation of novel therapeutic strategies and individualized therapy for these patients.
authors.affiliation: 2nd Department of Obstetrics and Gynecology, Aretaieio Hospital, University of Athens Medical School, Athens, Greece.
authors.forename: E
authors.initials: E
authors.lastname: Deligeoroglou
authors.forename: N
authors.initials: N
authors.lastname: Vrachnis
authors.forename: N
authors.initials: N
authors.lastname: Athanasopoulos
authors.forename: Z
authors.initials: Z
authors.lastname: Iliodromiti
authors.forename: S
authors.initials: S
authors.lastname: Sifakis
authors.forename: S
authors.initials: S
authors.lastname: Iliodromiti
authors.forename: C
authors.initials: C
authors.lastname: Siristatidis
authors.forename: G
authors.initials: G
authors.lastname: Creatsas
mesh_terms: D000273:Adipose Tissue / Q000276:immunology / Q000378:metabolism; D001778:Blood Coagulation Disorders / Q000209:etiology; D015815:Cell Adhesion Molecules / Q000097:blood / Q000378:metabolism; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism*; D011085:Polycystic Ovary Syndrome / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D011110:Polymorphism, Genetic; D012307:Risk Factors; D013923:Thromboembolism / Q000453:epidemiology / Q000209:etiology
chemical_list: D015815:Cell Adhesion Molecules; D018836:Inflammation Mediators