The prevalence of premalignant and malignant endometrial polyps is very low. Advanced age, menopause, obesity and diabetes increase the risk of endometrial polyp malignancy.

OBJECTIVE: To investigate maternal serum adiponectin and Ιnterleukin-1beta (IL-1β) levels during the pre-and post-partum periods in pregnant women with and without Gestational Diabetes Mellitus (GDM). DESIGN: Thirty control pregnant Caucasian women without GDM and thirty Body Mass Index (BMI) and age-matched Caucasian women with GDM examined in the outpatient clinic between the 24 th and 26 th week of their pregnancy and on the 3 rd day postpartum underwent anthropometry and had serum blood taken. Both groups, were monitored by a dietitian and had comparable weight gain during pregnancy. Birth weight was also measured. RESULTS: At the 3 rd day postpartum, compared to the 2 nd trimester of pregnancy, women with GDM had lower serum adiponectin levels, lower serum IL-1β levels and lower Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) values. At the 2 nd trimester of pregnancy, women with GDM had lower serum adiponectin levels, higher IL-1β and higher HOMA-IR values compared to women without GDM. At the 3 rd day postpartum, women with GDM had lower serum adiponectin levels, higher IL-1β and higher HOMA-IR values compared to women without GDM. Second trimester serum adiponectin values of women with GDM correlated negatively with birth weight. CONCLUSIONS: Gestational diabetes is a state of insulin resistance associated with altered levels of proinflammatory cytokines, increased IL-1β and decreased adiponectin values. Both of these alterations might be attributed to placental pathology in pregnancies with GDM.

In all subjects, leptin and adiponectin predict negatively and positively anti-oxidation, respectively, while high sensitivity IL-6 predicts positively and negatively pro- and anti-oxidation, respectively. High-sensitivity C-reactive protein is increased and negatively associated with anti-oxidation in pre-pubertal obese boys, suggesting that childhood obesity is associated with aseptic inflammation and oxidative stress.

Acute lung injury (ALI) results in high morbidity and mortality among preterm neonates and efforts have therefore been devoted to both antenatal and postnatal prevention of the disease. ALI is the result of an inflammatory response which is triggered by a variety of different mechanisms. It mostly affects the fetal lung and, in particular, causes damage to the integrity of the lung's alveolar-capillary unit while weakening its cellular linings. Chemotactic activity and inflammatory products, such as proinflammatory cytokines TNF-α, IL-1, IL-6, IL-11, VEGF,TGF-α and TGF-β, provoke serious damage to the capillary endothelium and the alveolar epithelium, resulting in hyaline membrane formation and leakage of protein-rich edema fluid into the alveoli. Chorioamnionitis plays a major part in triggering fetal lung inflammation, while mechanical ventilation, the application of which is frequently necessary in preterm neonates, also causes ALI by inducing proinflammatory cytokines. Many different ventilation-strategies have been developed in order to reduce potential lung injury. Furthermore, tissue injury may occur as a result of injurious oxygen by-products (Reactive Oxygen Species, ROS), secondary to hyperoxia. Knowledge of the inflammatory pathways that connect intra-amniotic inflammation and ALI can lead to the formulation of novel interventional procedures. Future research should concentrate on the pathophysiology of ALI in preterm neonates and οn possible pharmaceutical interventions targeting prevention and/or resolution of ALI.