Publications by Year: 2002

2002
Christodoulacos G, Panoulis C, Botsis D, Rizos D, Kassanos D, Creatsas G. Transvaginal sonographic monitoring of the uterine effects of raloxifene and a continuous combined replacement therapy in postmenopausal women. Maturitas. 2002;42(1):77 - 84.Abstract
Objective: To study the effect of 17β-estradiol+norethisterone acetate and raloxifene on the endometrium and uterine volume in postmenopausal women. Methods: Patients were randomly assigned to 17β-estradiol 2 mg+norethisterone acetate 1mg (E2+NETA) daily (n=90) or raloxifene HCl 60 mg (Evista) daily (n=43). Transvaginal sonography was done at baseline and at 6, 12 and 18 months, and at 6 and 12 months in-patients treated with E2+NETA and EVISTA respectively. Patients were asked to record bleeding-spotting episodes. Whenever required patients were referred for hysteroscopy±biopsy of the endometrium. Results: Patients under E2+NETA had a higher bleeding-spotting incidence (48.6%) compared with EVISTA (7.7%). Endometrial thickness increased significantly under E2+NETA as compared with baseline; however, at end point thickness reverted to baseline values. Evista had a non-stimulatory effect on the endometrium. Changes in uterine volume were not statistically significant. Conclusions: Both treatment regimens provided comparable uterine safety. However, raloxifene exhibited a more favorable safety profile on the uterus as expressed in the bleeding-spotting incidence and the effect on endometrial thickness and uterine volume. Transvaginal sonography appears to be a dependable method for monitoring the effect of treatment on the uterus. © 2002 Elsevier Science Ireland Ltd. All rights reserved.
Rizos D, Hassiakos D, Grigori-Kostaraki P, Sarandakou A, Botsis D, Salamalekis E. Maternal serum leptin concentration during the second trimester of pregnancy: Association with fetal chromosomal abnormalities. Prenatal Diagnosis. 2002;22(3):221 - 225.Abstract
Recent studies suggest that leptin, the product of the obese gene, is produced by the placenta during pregnancy. The present study addressed the question whether second trimester maternal serum leptin could be altered by fetal Down syndrome or Edwards syndrome. Maternal serum leptin concentrations were measured in 18 pregnancies complicated with Down syndrome, six pregnancies complicated with Edwards syndrome and 183 uncomplicated pregnancies during the second trimester of pregnancy. The present results demonstrate that leptin concentrations in uncomplicated pregnancies slightly decrease from the 16th week of pregnancy, reaching a minimum of 18.8 ng/ml around the 20th week, and then rapidly increase to 28.2 ng/ml by the 24th week. Leptin correlation with maternal body weight decreases from r=0.695 at 16-17 week of gestation to r=0.544 at < 22 weeks of gestation. There was no significant difference between the mean MoMs of Down syndrome- (0.926) or Edwards syndrome- (0.960) affected pregnancies and normal pregnancies (1.002). A weak correlation (r=0.18, p<0.02) was observed between corrected leptin MoMs and human chorionic gonadotrophin (hCG) MoMs in normal pregnancies. It is assumed that around the 20th week of pregnancy placental leptin production is activated or at least is accelerated and it is added to the amount of leptin produced by maternal adipose tissue. Fetal Down syndrome or Edwards syndrome does not seem to alter maternal leptin concentration and therefore leptin cannot be used as a marker for these chromosomal abnormalities in the early second trimester of pregnancy. Copyright © 2002 John Wiley & Sons, Ltd.
Giannaki G, Sarandakou A, Rizos D, Xyni K, Protonotariou E, Phocas I. Mucin-like carcinoma-associated antigen in paired serum and breast milk samples of lactating mothers and sera of their neonates in the early postpartum period. European Journal of Obstetrics Gynecology and Reproductive Biology. 2002;105(2):120 - 123.Abstract
Objective: To evaluate postpartum MCH changes in the early postpartum period, and to examine whether neonatal MCA is related to that in maternal serum (MS) or milk. Study design: MCA was measured by EIA on the second and fifth postpartum day in serum and BM from 30 lactating women and their single term neonates. Sera from 20 healthy women (controls), were also analyzed. Results: All neonatal antigen concentrations were below the cut-off level for MCA (11ng/ml). MS MCA was significantly increased compared with that in controls (P<0.00001), while antigen values in BM were highly elevated (P<0.00001), with a significant increase (P<0.0003) from the second to the fifth postpartum day. A strong correlation was found between the second and fifth day postpartum samples in MS, neonatal serum and BM MCA concentrations (rs=0.94, P<0.00001; rs=0.75, P<0.00001 and rs=0.69, P<0.0001, respectively). A significant correlation was also found in MCA values on the fifth postpartum day between neonatal serum and BM (rs=0.54, P<0.02). Conclusions: From these findings one may speculate on some ripening process in milk production and a possible transition of MCA from the neonatal gastro-intestinal tract into circulation. © 2002 Elsevier Science Ireland Ltd. All rights reserved.
Giannaki G, Rizos D, Xyni K, Sarandakou A, Phocas I, Creatsas G. sCD31/sPECAM-1 levels in breast milk and sera of mother-infant pairs in the early postpartum period. Early Human Development. 2002;67(1-2):61 - 68.Abstract
Immunomediators seem to have a central role in the immune system of both human milk and newborn infants. CD31/PECAM-1 is an adhesion molecule, member of Ig gene superfamily, mediating cell-cell adhesion in both homophilic and heterophilic ways. Levels of the soluble form of PECAM-1 (sPECAM-1) were evaluated on the 2nd and 5th day postpartum in breast milk and serum paired samples from 20 lactating women as well as in time-matched serum from their single, term, healthy neonates. Concentrations of sPECAM-1 in breast milk (median, range) on both the 2nd (2.05 ng/ml, 0.0-7.2) and 5th day postpartum (0.89 ng/ml, 0.0-3.6) were about 10 and 20 times lower than those (mean ± SD) in controls (healthy adults) (19.83 ± 5.17, p < 7 × 10-8), showing a significant fall from the 2nd to the 5th day postpartum (p < 0.0005). Maternal serum sPECAM-1 values (mean ± SD) were significantly lower on the 2nd day postpartum (14.21 ± 5.15 ng/ml) than those in controls (p < 0.002), but reached control values on the 5th day postpartum after a significant rise (p < 0.0075). Neonatal serum sPECAM-1 values with no significant difference between the 2nd (14.4 ± 4.11 ng/ml) and 5th day of life (14.54 ± 4.99 ng/ml) were significantly lower than those in controls (p < 0.002). Values of sPECAM-1 in milk and sera of lactating mothers and their neonates on the 2nd day postpartum depended on the mode of delivery, being significantly lower after caesarean section (p < 0.034, p < 0.0075 and p < 0.035, respectively). In conclusion, our findings in the early postpartum period demonstrate that: (a) sPECAM-1 is present in human milk in low and decreasing concentrations; (b) the shedding of sPECAM-1 is an established component of the neonatal immune system from birth, though in lower concentrations than in adults, possibly reflecting its immaturity; and (c) the mode of delivery has a significant effect on sPECAM-1 values in milk and sera of lactating mothers and their neonates; the lower values after caesarean section may reveal a deranged endothelial homeostasis. © 2002 Elsevier Science Ireland Ltd. All rights reserved.