Sp1 collagen I A1 polymorphism in women with stress urinary incontinence
Dimos Sioutis, Emmanuel Economou, Irene Lambrinoudaki, Vasilios Tsamadias, Maria Creatsa, Angelos Liapis
International Urogynecology Journal Volume 22, Number 7, 835-839, DOI: 10.1007/s00192-011-1372-9
Introduction and hypothesis: Stress urinary incontinence (SUI) is in part attributed to qualitative and quantitative changes in connective tissue of the urogenital tract. We examined the association of collagen type I a1 (COLIA 1)
Sp1 polymorphism with the risk of SUI. Methods: Forty-five postmenopausal women suffering from urodynamically verified SUI (study group) were compared
to 45 healthy volunteers (control). DNA was extracted from peripheral blood. The genotyping concerning the type 1 a1 collagen gene Sp1 polymorphism was performed with polymerase chain reaction. Results: The polymorphic T allele was overrepresented in the SUI patients (63.2% versus 36.8%, p=0.016). Odds
ratio for SUI in women harboring the T allele was 2.19 (95% CI 1.149–4.176) compared to women with the wildtype genotype.
Conclusions The COLIA1 Sp1 polymorphism is associated
with increased prevalence of stress urinary incontinence in
postmenopausal women.
The implication of second-trimester amniotic fluid TNF-alpha, cytochrome C and cell death nucleosomes in the prediction of preterm labor and/or premature rupture of membranes
K. Puchner, C. Iavazzo, D. Gourgiotis, M. Boutsikou, S. Baka, D. Hassiakos, E. Kouskouni, E. Economou, A. Malamitsi-Puchner, G. Creatsas
Arch Gynecol Obstet DOI 10.1007/s00404-011-1909-7
Aim The multifactorial pathway leading to preterm labor possibly includes the implication of apoptosis. This study aimed to clarify the role of amniotic Xuid apoptotic molecules (TNF-alpha, cytochrome C and cell death nucleosomes)
at midtrimester as possible predictors of preterm labor (PTL) and/or premature rupture of membranes (PROM). Method In this case–control study, comprising 360
women undergoing genetic amniocentesis and out of whom 38 delivered preterm and 18 out of the latter after PROM, the above apoptotic molecules were determined by ELISA. The 38 cases with PTL and 18 cases with PROM were
matched for age with 38 and 18 respective controls delivering at term, and the levels of apoptotic molecules were compared. Results: Cell death nucleosome levels were found to be signiWcantly associated with preterm delivery. SpeciWcally,
for every unit increase in nucleosomes, women were on average 0.2% more likely to deliver preterm (OR: 1.002, CI: 1.0–1.003, p = 0.018). In contrast, such an association was not found concerning the other two apoptotic molecules
(TNF-a and Cytochrome C). Conclusion Second-trimester amniotic Xuid cell death
nucleosomes’ levels are signiWcantly associated with preterm delivery and could possibly serve as predicting markers.
Maternal Serum Levels of TNF-Alpha and IL-6 Long after Delivery in Preeclamptic and Normotensive Pregnant Women
N. Vitoratos, E. Economou, C. Iavazzo, K. Panoulis, G. Creatsas
Mediators Inflamm. 2010;2010:908649. Epub 2010 Dec 28
To evaluate maternal TNF-alpha and IL-6 plasma levels in normotensive pregnant women, women with preeclampsia, and to examine the temporal changes in their levels from theantepartum to the postpartum period correlated with the regression
of preeclampsia. Method. A prospective study was performed in the 2nd Department of Obstetrics and Gynecology, University of Athens. Blood samples were obtained: (1) antepartum at the time of clinical diagnosis of the syndrome, 2. 12-14 weeks postpartum. Results.No statistically significant differences were found in IL-6 levels, whereas a difference was found in TNF-alpha levels between
preeclamptic and controls in antepartum period (0.80 pg/ml versus 0.60 pg/ml, P : .04). Long after delivery, TNF-alpha levels were significantly higher in preeclamptic compared to normotensive controls (0.86 pg/ml versus 0.60 pg/ml, P : .004). No difference was observed in TNF-alpha before and after delivery in both groups. No difference was noticed in IL-6 levels in women of normotensive
group long after delivery compared to that before delivery. Long after delivery IL-6 levels were statistically significant higher in preeclamptic women compared to normal controls (3.53 ± 0.52 pg/ml versus 1.69 ± 0.48 pg/ml, P : .02). Conclusion. Preeclamptic women remain under a status of increased inflammatory stress up to 12-14 weeks postpartum despite the fact that all the other signs of preeclampsia are resolved.
Antepartum and postpartum maternal plasma levels of E-selectin in pre-eclampsia, gestational proteinuria and gestational hypertension
Katerina Papakonstantinou, Emanouel Economou, Dimitris Hasiakos, Nikolaos Vitoratos
J Matern Fetal Neonatal Med. 2011 Aug;24(8):1027-32. doi: 10.3109/14767058.2010.545907
Pathophysiologic features of pre-eclampsia (PE) suggest that generalized endothelial cell damage and dysfunction are the major features of the disease. E-selectin is a cell adhesion molecule and its increased expression indicates endothelial cell activation [1]. In this pilot study, we have investigated alterations of maternal antepartum and postpartum plasma levels of soluble(s) E-selectin
in normotensive pregnant women and women with PE, gestational hypertension (GH) and gestational proteinuria (GP). We further sought to determine whether changes in plasma levels of sEselectin from antepartum to postpartum would correlate with the postpartum regression of PE.
Circulating leptin and ghrelin are differentially influenced by estrogen/progestin therapy and raloxifene
Irene V. Lambrinoudaki, George E. Christodoulakos, Emmanuel V. Economou, Sofia A. Vlachou, Constantinos P. Panoulis, Andreas P. Alexandrou
Maturitas. 2008 Jan 20;59(1):62-71
Background: Leptin and ghrelin are increasingly being recognized as cardiotropic hormones, promoting or inhibiting the atherosclerotic process, respectively. Apoptosis may be one pathway through which the actions of these hormones are mediated. Sex hormones are reported to influence the secretion and action of ghrelin and leptin. Objective: To evaluate (1) the association of circulating ghrelin and leptin with selected markers of receptor-mediated apoptosis and (2) the effect of estrogen monotherapy, low dose estrogen–progestin therapy, tibolone and raloxifene on serum ghrelin and leptin in healthy postmenopausal women.
Methods: Eighty eight postmenopausal women aged 44–62 years were randomly allocated to daily (1) conjugated equine estrogens 0.625 mg (CEE), (2) 17-estradiol 1mg plus norethisterone acetate 0.5 mg (E2/NETA), (3) tibolone 2.5 mg, (4) raloxifene HCl 60 mg or (5) no treatment. Serum markers of apoptosis sFas, Fas-ligand (Fas-L) and caspase-1 were measured at baseline. Serum leptin and ghrelin were measured at baseline and at 3 months. Results: Body Mass Index (BMI) and estradiol levels correlated positively, while FSH correlated negatively with serum leptin (BMI: r = 0.646, p = 0.005, estradiol: r = 0.432, p = 0.001, FSH: r =−0.401, p = 0.002). Insulin levels associated positively with circulating leptin (r = 0.394, p = 0.011) and negatively with circulating ghrelin (r =−0.401, p = 0.009). Serum leptin decreased significantly in E2/NETA group (baseline: 2.882±0.76 ng/ml, 3 months: 2.687±0.66 ng/ml, p = 0.043), while it increased significantly in the raloxifene group (baseline: 2.671±0.54 ng/ml, 3 months: 2.839±0.47 ng/ml). Ghrelin levels decreased significantly only in the raloxifene group (baseline: 1634±592 pg/ml, 3 months: 1408±534 pg/ml). Conclusion: Apoptosis may be a pathway through which leptin exerts a pro-atherogenic effect. Low dose HT may act carioprotectively by decreasing letpin levels in healthy recently menopaused women.
