Adequate vitamin D status during pregnancy is crucial to assure normal fetal skeletal growth and to provide the vitamin D needed for infants' stores. To determine the actual situation in Greece, we evaluated serum 25-hydroxyvitamin D (25[OH]D), calcium (Ca), phosphorus (P), alkaline phosphatase (ALP), parathyroid hormone (PTH), osteocalcin (OC), and calcitonin (CT) concentrations in 123 healthy mother-newborn pairs recruited from a public hospital of the sunny Athenian region. Blood samples were obtained from pregnant women at term and their neonates (cord blood). The study was conducted between June 2003 and May 2004. None of the mothers has been prescribed vitamin D supplements. Maternal 25(OH)D levels (16.4 [11-21.1] ng/mL) were significantly lower than umbilical venous blood concentrations (20.4 [13.9-30.4] ng/mL) (P < 0.001). A strong correlation was observed between maternal and infant 25(OH)D concentrations (r = 0.626, P < 0.001). Twenty-four (19.5%) mothers and 10 (8.1%) neonates had 25(OH)D <10 ng/mL. Pregnant women who delivered in summer and autumn reported higher levels of 25(OH)D (18.9 [12.9-23.3] ng/mL) than those who delivered in winter and spring (14.6 [10.1-18.5] ng/mL) (P = 0.006). Mothers with a darker phototype had lower levels of serum 25(OH) D than those with a fair phototype (P = 0.023). Umbilical venous blood Ca, P, OC, and CT levels were significantly higher than maternal venous blood levels (P < 0.001). PTH umbilical levels were lower than maternal levels (P < 0.001). Apparently, the abundant sunlight exposure in Athens is not sufficient to prevent hypovitaminosis D. Pregnant women should be prescribed vitamin D supplementations, and the scientific community should consider vitamin D supplementation of foods.

Gestational diabetes mellitus (GDM) and type 2 diabetes (T2D) share common pathophysiological features, including β-cell dysfunction and insulin resistance. In this study, we investigated the association between GDM and five recently identified T2D susceptibility loci, in a Greek population. We studied 148 women with GDM and 107 non-diabetic unrelated pregnant Greek women, for polymorphisms in the TCF7L2 gene (rs7903146 C/T), the PPARG gene (Pro12Ala), the KCNJ11 gene (E23K), the IRS1 gene (G972R) and in the FOXC2 gene (-512C>T). The T-allele of the TCF7L2 rs7903146 (C/T) polymorphism was found to be significantly associated with an increased risk of GDM [p = 0.0003; odds ratio (OR) 2.04 (95%CI 1.38-3.00)]. Additionally, CT and TT genotypes were significantly overrepresented in women with GDM compared to controls (p = 0.0003 and p = 0.0148, respectively). Analysis of the IRS1 G972R polymorphism showed that the R-allele frequency was increased in women with GDM [(p = 0.009; OR 1.67 (95%CI 1.14-2.47)]. The genotypes and allele frequencies of the other polymorphisms studied did not statistically differ between the GDM and the control women. Thus, our data suggest that the common T2D susceptibility polymorphism of TCF7L2 (rs7903146 C/T) gene, and the G972R polymorphism of the IRS1 gene, seem to predispose to GDM in Greek women.

MET administration lowered LH activity in all PCOS women and in ovulatory responders and also compromised PRL stimulated secretion in the latter cases. These findings were indicative of an effect of MET on pituitary activity.

No abstract

We previously reported increased apoptosis in the maternal circulation during pregnancy, partly accounting for the presence of cell-free fetal DNA in maternal plasma. In the current study, apoptosis was quantitated in 60 peripheral blood samples obtained from 15 women sequentially tested postpartum using the binding of annexin V. FISH with X/Y probes was performed on annexin V-positive cells isolated by MACS in patients with male fetuses to estimate the proportion of fetal cells among the apoptotic cell population. Twenty-four women at the thirty-seventh to thirty-eighth week of gestation and 35 nonpregnant females were used as controls. Apoptosis rate in the thirty-seventh to thirty-eighth week was 12.5% (9.2-14.7%). At 30 minutes, 12 hours, 24 hours, and 48 hours postpartum, it was 25.1% (16.8-28.5%), 12.5% (10.9-14.1%), 6.1% (4.8-7.1%), and 2.3% (1.3-3.0%), respectively. Male apoptotic cells were identified in all cases with male fetuses at 37 to 38 weeks of gestation, and the mean proportion was 9.9% (5.9-13.2%). The proportion of fetal cells 30 minutes after delivery was 14.8% (12.5-25.5%) and 12 hours postpartum 2.1% (0.8-4.1%). Male fetal apoptotic cells were detected in three of eight samples collected 24 hours after delivery from women who delivered males, at frequencies of 0.10%, 0.15%, and 0.25% (mean 0.16%). There were no fetal apoptotic cells 48 hours after delivery. Apoptosis partly accounts for the clearance of fetal cells from the maternal circulation. Because it is a rapid reaction, completed within 2-3 hours, persistence of fetal cells is possibly due to apoptosis-resistant progenitors or to defective regulation of apoptosis, leading to fetal cell microchimerism associated with autoimmune diseases.