To investigate the pregnancy outcome of fetuses affected with trisomy 18, we analyzed 63 cases diagnosed at our hospital from January 1993 to December 2004. Twenty-nine were males and 34 were females. Fifty-eight were prenatally diagnosed, and in 16 (27.6%) of them intrauterine fetal death (IUFD) occurred between 28 weeks and 41 weeks gestation (34.6 +/- 3.9 weeks, Mean +/- SD). Ten (17.2%) fetuses died during labor and their age ranged from 30 weeks to 40 weeks of gestation. The total number of cases ending in fetal demise was 26 (44.8%) and the mean gestational age at the time of fetal demise was 35.0 +/- 3.6 weeks (Mean +/- SD). All liveborn infants (n = 36) were born after 31 weeks gestation. In our study the preterm birth ratio for trisomy 18 is 34.8%, which is much higher than the ratio for the general population. Females are more likely than males to be long-term survivors. These data are helpful in the counseling of parents faced with the difficult decision of whether or not to continue a pregnancy with a fetus affected with trisomy 18.

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Effects of GnRH on free cytosolic Ca2+ concentrations ([Ca2+]i) were examined in individual first trimester human cytotrophoblast and syncytiotrophoblast cells by fura-2 microspectrofluorimetry. GnRH (10(-6) M) did not affect [Ca2+]i in cytotrophoblasts on days 2-9 of culture, with 50 cells tested each day. GnRH (10(-6) M) did not affect [Ca2+]i on days 2-3, but increased [Ca2+]i in 15% of culture-derived syncytiotrophoblasts on day 4 (8 of 52 cells) and in 48% on days 5-9 of culture (158 of 332 cells). Culture-derived syncytiotrophoblasts originated from four first trimester placentae. GnRH increased [Ca2+]i in a preliminary trial using syncytiotrophoblasts derived directly from a single first trimester placenta and cultured for 3 days (13 of 33 cells). Culture-derived first trimester syncytiotrophoblast cells that responded to 10(-6) M GnRH (28 of 63 cells) on day 6 also responded to GnRH at 10(-7) M (26 of 28 of the above cells), 10(-8) M (24 of 28 cells, 10(-9) M (22 of 28 cells), and 10(-10) M (3 of 28 cells). No cells responded to GnRH below a concentration of 10(-10) M. Desensitization of syncytiotrophoblasts by continuous GnRH perifusion (10(-6) M) and blockade of GnRH by competitive antagonism with Nal-Glu-GnRH (10(-6) M) suggested that effects of GnRH were receptor specific. The results provide direct evidence supporting the contention that the intracellular signaling resultant from GnRH receptor-ligand interactions in syncytiotrophoblasts may be at least partially mediated by transient increases in [Ca2+]i.