The fetus may be exposed to increased endogenous or synthetic glucocorticoid (GS) exposure in late gestation. Approximately 7% of pregnant women in Europe and North America are treated with synthetic GSs to promote lung maturation in fetuses at risk of preterm delivery. Maternal steroid treatment before preterm delivery is one of the best documented and most cost effective life saving treatments in prenatal medicine but, in certain circumstances, the price of accelerated lung maturity may be loss of brain cells, increased neurodevelopmental disability, intra-uterine growth restriction (IUGR), and an increased risk of preterm delivery, of programming of post-natal hypertension, and of increased post-natal activity in the hypothalamo-pituitary-adrenal (HPA) axis. Placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is the key enzyme which protects the fetus from overexposure to GSs by their oxidation into inactive derivates. We review the evidence for the metabolism of GSs during pregnancy and how endogenous and synthetic GSs cause other changes in the placenta which affect fetal development.

Gestational diabetes mellitus (GDM) is considered to be one of the most frequent medical complication observed among pregnant women. The role of adipokines in the pathogenesis of GDM remains strictly unknown. Different adipokines have been studied throughout gestation, and they have been proposed as biomarkers of GDM and other pregnancy-related complications; however, there is no biomarker reported for GDM screening at present. The aim of this study was to evaluate serum nesfatin-1 and vaspin levels in GDM and non-GDM women, to characterize the correlation between these adipokines, and to assess the potential role of circulating adipokines in the prediction of risk of gestational diabetes mellitus. Serum concentrations of nesfatin-1 and vaspin were measured in 153 women with GDM, and in 84 patients with uncomplicated pregnancy by enzyme-linked immunosorbent assay (ELISA) kits, according to the manufacturer’s instructions. Circulating levels of nesfatin-1 and vaspin were significantly lower in the GDM group than in the control group. Nesfatin-1 levels were negatively correlated with vaspin levels. The results of this study point out the possible role of nesfatin-1 and vaspin as potential novel biomarkers for the prediction and early diagnosis of GDM. Further studies are necessary to evaluate the influence of nesfatin-1 and vaspin on glucose metabolism in the early stages of GDM.

Intra-uterine growth retardation (IUGR) represents one of the major problems in perinatal medicine. IUGR is one of main causes of perinatal mortality and morbidity. A huge number and variety of established and possible causes of IUGR have been described. There are currently no data about effective treatment of this fetal condition. IUGR has been described to be strictly involved in fetal programming. Fetal programming is the general idea, which tells us how during development of the embryo and fetus significant physiological parameters can be shaped by environmental events. A link between the intra-uterine growth retardation and the risk of developing type 2 diabetes, obesity and cardiovascular disease postnatally has been well documented. The aim of this paper is to present an overview of the current knowledge of IUGR effects on development of hypertension and cardiovascular diseases, impact on insulin secretion and resistance, diabetes mellitus and metabolic syndrome. The influence of intrauterine growth retardation on predisposition to obesity and adipose dysfunction was also described.

of hypertension in pregnancy 757 to 10% of pregnancies in the United States and Europe. Women with chronic HT (1%-5% of the general population) have a higher risk of PE than women without pre existing HT (17%-25% vs 3%-5%, respectively). Furthermore, 7% to 20% of women with chronic HT have poor BP control in pregnancy (excluding those with PE). Significantly elevated BP in pregnancy is a di rect threat to maternal and fetal health and life. According to the World Health Organization (WHO), HT and its complications are among the leading causes of mortality in pregnancy in developed countries (approx. 16%). 9-11 HT promotes low birth weight (LBW), increas es the risk of PE superimposed on chronic HT and preterm birth, may cause placental abrup tion, leads to complications which require pro longed intensive care of a neonate with special ist neonatal treatment, and may cause intrauter ine fetal death. 12,13 PE is the most dangerous maternal complica tion of HT. PE is associated with a particularly high risk of complications harmful to the mother

Objective The aim of the study was to evaluate the levels of adipokines such as adiponectin and leptin as well as soluble intercellular adhesion molecule-1 (sICAM-1) and endogenous NOS inhibitor-asymmetric dimethylarginine (ADMA), as the endothelium dysfunction markers in pregnant women with gestational hypertension (GH). Patients and Methods Adiponectin, leptin, sICAM-1, and ADMA concentrations were measured in a group of 34 patients with GH and in 32 healthy pregnant women between the 24th and 34th week of gestation with ELISA tests. Results The patients with GH compared with healthy ones were characterized by significantly higher BMI (28.09 ± 7.90 vs. 22.34 ± 4.21 kg/m2, p=0.016) and higher concentrations of leptin (45.89 ± 35.91 vs. 24.09 ± 24.40 ng/mL, p=0.006). sICAM-1 levels were also higher in the GH group but without the statistical significance (264.51 ± 50.99 vs. 232.56 ± 43.3 ng/ml, p=0.057). There were no significant differences between groups in adiponectin (8.79 ± 8.67 vs. 7.90 ± 3.71 μg/mL, p=0.46, NS) and ADMA (0.57 ± 0.26 vs. 0.60 ± 0.24 μmol/L, p=0.68, NS) levels. The significant correlation between leptin levels and BMI value was observed only in patients with GH (R = 0.56, p=0.02). Conclusions The higher levels of leptin in pregnant women with gestational hypertension may be suggestive of the role of leptin in GH development. As the patients in the GH group had higher BMI, hyperleptinemia may link obesity with gestational hypertension. The significance of leptin as the predictive marker of GH development could be implied. It could be postulated that the higher levels of sICAM-1 in the GH patients, although not statistically significant, could reflect some impairment of the endothelium function occurring in GH regardless of BMI. The comparable adiponectin levels in GH and healthy pregnant patients and the lack of its correlation with BMI may indicate the occurrence of a protective mechanism in pregnancy maintaining its concentration and preserving from the consequences of the decrease in its levels in overweight and obese patients. Since ADMA levels were similar in GH and healthy pregnant women, ADMA seems not to be involved in GH pathogenesis, suggesting that NO synthesis is not impaired in this pregnancy complication. As the data on the gestational hypertension pathogenesis and its correlations with adipokines and markers of the endothelium dysfunction are limited, further studies on this issue are warranted.

Tests for thrombophilia should be carried out in women with adverse pregnancy outcomes in their history, who are planning pregnancy, to start anticoagulant prophylaxis. Our study supports the thesis that tests for thrombophilia should be carried out in women with a history of adverse pregnancy outcomes and who are planning a pregnancy to start anticoagulant prophylaxis.

Prevention of preeclampsia (PE) remains one of the most significant problems in perinatal medicine. Due to the possible unpredictable course of hypertension in pregnancy, primarily PE and the high complication rate for the mother and fetus/newborn, it is urgent to offer pregnant women in high-risk groups effective methods of preventing the PE development or delaying its appearance. In addition, due to the association of PE with an increased risk of developing cardiovascular diseases (CVD) in later life, effective preeclampsia prevention could also be important in reducing their incidence. Ideal PE prophylaxis should target the pathogenetic changes leading to the development of PE and be safe for the mother and fetus, inexpensive and freely available. Currently, the only recognized method of PE prevention recommended by many institutions around the world is the use of a small dose of acetylsalicylic acid in pregnant women with risk factors. Unfortunately, some cases of PE are diagnosed in women without recognized risk factors and in those in whom prophylaxis with acetylsalicylic acid is not adequate. Hence, new drugs which would target pathogenetic elements in the development of preeclampsia are studied. Vitamin D (Vit D) seems to be a promising agent due to its beneficial effect on placental implantation, the immune system, and angiogenic factors. Studies published so far emphasize the relationship of its deficiency with the development of PE, but the data on the benefits of its supplementation to reduce the risk of PE are inconclusive. In the light of current research, the key issue is determining the protective concentration of Vit D in a pregnant woman. The study aims to present the possibility of using Vit D to prevent PE, emphasizing its impact on the pathogenetic elements of preeclampsia development.

Nitric oxide (NO) is a key molecule involved in a variety of biological functions throughout the whole body. Many studies have been devoted to establish the role of NO in perinatal medicine and the different findings have promoted the clinical use of NO donors as new pharmacological tools. NO regulates the vascular tone and blood flow by activating soluble guanylate cyclase in the vascular smooth muscles. NO is essential for leukocyte adhesion and platelet aggregation, and it controls mitochondrial oxygen consumption. Abnormalities in vascular NO production and transport result in endothelial dysfunction with various cardiovascular disorders such as hypertension, atherosclerosis and angiogenesis-associated disorders. The NO system has important roles in mammalian reproductive physiology, especially in the utero-placental system. It has been shown to participate in the extravillous trophoblast invasion of decidua and myometrium, in regulation of vascular reactivity of utero-placental and fetal-placental circulations, in prevention of platelet and neutrophil aggregation and adhesion in the intervillous space, and in trophoblast apoptosis. The aim of this review is to present the theoretical background and significance of NO in normal and preeclamptic pregnancy as well as to consider how NO donors could be useful in clinical practice.