Women with polycystic ovary syndrome are more likely to suffer from obesity, insulin resistance, and chronic low-grade inflammation. In fact, the excessive activation of monocytes exacerbates oxidative stress and inflammation. However, high-density lipoprotein cholesterol neutralizes the pro-inflammatory and pro-oxidant effects of monocytes. The aim of this study is to investigate whether monocyte counts to high-density lipoprotein cholesterol ratio can predict the inflammatory condition in patients with polycystic ovary syndrome. In this cross-sectional study, a total of 124 women (61 of them with polycystic ovary syndrome and 63 age-matched healthy volunteers) were included in the study population. Obese polycystic ovary syndrome patients (n = 30) with a body mass index of ≥25 kg/m2 and lean polycystic ovary syndrome patients (n = 31) with a body mass index of < 25 kg/m2 were compared to age-and body mass index-matched healthy subjects (30 obese and 33 non-obese). The monocyte counts to high density lipoprotein cholesterol values in women with polycystic ovary syndrome were significantly higher than in control subjects (p = 0.0018). Moreover, a regression analysis revealed that body mass index, the homeostasis model assessment of insulin resistance and the high sensitivity C-reactive protein levels were confounding factors that affected the monocyte counts to high density lipoprotein cholesterol values. Additionally, a univariate and multivariate logistic regression analysis demonstrated that the increased monocyte counts to high density lipoprotein cholesterol values were more sensitive than the other known risk factors (such as increased body mass index, homeostasis model assessment of insulin resistance and high sensitive C-reactive protein levels) in the prediction of the inflammation in patients with polycystic ovary syndrome. The present study demonstrated that the monocyte count to high density lipoprotein cholesterol may be a novel and useful predictor of the presence of polycystic ovary syndrome.

BACKGROUND: there has been an increased incidence of macrosomic newborns in the world and most of the macrosomic newborns are born from non-GDM pregnant women. The objective of this study was to determine the frequency and the associated risk factors of fetal macrosomia in non-GDM pregnant women. METHODS: a total 4246 consequtive pregnant women who had no GDM was included the study population. Data was collected from hospital database of Bal?kesir State Hospital between January 2014 and January 2015. Statistical analysis was carried out using the independent samples t-test and chi-squared test. Logistic regression analysis was used to determine the relationships between associated risk factors and the presence of fetal macrosomia. In this analysis, fetal macrosomia was taken as the dependent variable and associated risk factors were taken as independent variables. Results are shown as odds ratios (ORs) (95% CI) in the logistic regression analysis. RESULTS: 366 of the 4246 pregnant women were diagnosed with fetal macrosomia (8.6%). Compared the control women, a statistically significant correlation between fetal macrosomia and pre-pregnancy body mass index (BMI), gestational weight gain (GWG), parity, advanced maternal age, and male fetal sex was found. Maternal BMI, and GWG were the two risk factors most strongly associated with macrosomia. CONCLUSION: the prevalance of fetal macrosomia is rising among Turkish women. High pre-pregnancy BMI and GWG represent main modifiable risk factors for macrosomia and need more attention from health care providers.

Introduction: Preeclampsia is a systemic inflammatory disorder and a major cause of maternal and fetal mortality. Fractalkine (CX3CL1) is a member of the chemokine family with multiple functions in the organization of the immune system. It is up-regulated in inflammatory disorders. During inflammation, fractalkine enhances tissue destruction and inflammatory cell invasion. We aimed to investigate the alteration of fractalkine in the placental tissues of pregnant women with preeclampsia and the correlation of this alteration with clinicopathological variables. Materials and methods: Alteration of fractalkine in placental tissue specimens was determined immunohistochemically in 84 pregnant women: 33 women with mild preeclampsia, 19 women with severe preeclampsia, and 30 women with normal pregnancy. Preeclampsia was diagnosed using current guidelines of the American College of Obstetricians and Gynecologists. Results: Pregnant women with mild and severe preeclampsia revealed significantly higher fractalkine expression in syncytiotrophoblast cells than in the normotensive group (p = .0051 and .0001, respectively). The expression of fractalkine in preeclampsia was positively correlated with clinical parameters including the presence of intrauterine growth restriction, systolic and diastolic blood pressure, and 24-h urine protein, whereas it was negatively correlated with plasma albumin levels and placental weight. Additionally, the pathological changes in the placenta-including the presence of syncytiotrophoblast basement membrane thickening, increased number of syncytial knots, and vascularization of terminal villi were significantly correlated with fractalkine expression in pregnant women with preeclampsia. Conclusions: Overexpression of fractalkine in pregnant women with preeclampsia, as well as the correlation between fractalkine expression and poor pregnancy outcomes and placental histopathological changes may be associated with the underlying mechanisms of preeclampsia.

Fetal vascular malperfusion is associated with poor perinatal outcomes in women with preeclampsia and gestational diabetes mellitus. The aim of this study was to determine the association between fetal vascular malperfusion score and syncytiotrophoblast basement membrane thickness and clinicopathological variables, such as developing preeclampsia in women with gestational diabetes mellitus.

Gonadotropin-releasing hormone agonist triggering with concomitant administration of low doses of human chorionic gonadotropin or a freeze-all strategy in high responders