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.

Previous Gestational Diabetes Mellitus (pGDM) is a common condition and has been associated with future development of Type 2 Diabetes Mellitus (T2DM) and Metabolic Syndrome (MS) in women affected. The pathogenesis and risk factors implicated in the development of these conditions later in the lives of women with pGDM are not as yet fully understood. Research has recently focused on a group of substances produced mainly by adipose tissue called adipokines, this group including, among others, adiponectin, leptin, Retinol-Binding Protein-4 (RBP-4), and resistin. These substances as well as other inflammatory mediators (CRP, IL-6, PAI-1, TNF-α) seem to play an important role in glucose tolerance and insulin sensitivity dysregulation in women with pGDM. We summarize the data available on the role of these molecules.

Presentation of uterine prolapse is a rare event in a pregnant woman, which can be pre-existent or else manifest in the course of pregnancy. Complications resulting from prolapse of the uterus in pregnancy vary from minor cervical infection to spontaneous abortion, and include preterm labor and maternal and fetal mortality as well as acute urinary retention and urinary tract infection. Moreover, affected women may be at particular risk of dystocia during labor that could necessitate emergency intervention for delivery. Recommendations regarding the management of this infrequent but potentially harmful condition are scarce and outdated. This review will examine the causative factors of uterine prolapse and the antepartum, intrapartum and puerperal complications that may arise from this condition as well as therapeutic options available to the obstetrician. While early recognition and appropriate prenatal management of uterine prolapse during pregnancy is imperative, implementation of conservative treatment modalities throughout pregnancy, these applied in accordance with the severity of the uterus prolapse and the patient's preference, may be sufficient to achieve uneventful pregnancy and normal, spontaneous delivery.