Objective:We reviewed the data of the termination of pregnancy (TOP) cases between 2002 and 2010 to evaluate the changes in fetal indications for both early and late TOPs in this period.
Material and Methods:The data of 962 TOP cases were analysed in two groups according to the periods as in 2002-2006 and 2007-2010. The women were also subdivided into two categories according to their gestational age; <23 weeks' gestation (early termination) and ≥23 weeks' gestation (late termination).Results: Four hundred and fifty-eight (47.6%) of TOPs were performed between 2002 and 2006 (Group 1) and 504 (52.3%) were performed between 2007 and 2010 (Group 2). The number of early (<23 weeks) and late (≥23 weeks) terminations were 583 (60.6%) and 379 (39.3%), respectively. The vast majority of anomalies were central nervous sytem malformations (51.8%). They were followed by multiple anomalies (10.2%) and chromosomal anomalies (9.4%). Chromosomal and cardiovascular system anomalies were significantly higher in 2007-2010 in comparison to 2002-2006 (p<0.0001 and p=0.002, respectively). There was no statistically significant difference between the fetal indications that led to early termination compared to those that led to late termination.
Conclusion:The distribution of indications for TOP was influenced by the development in prenatal screening policy, resulting in a significant increase in terminations due to chromosomal and cardiovascular system anomalies. Cultural, educational, religious and legal factors cause differences in the indications for TOP as well as the gestational age that TOPS are performed. Sonuç: Terminasyon endikasyonlarının dağılımı prenatal tarama politikalarındaki gelişimden etkilenmiş, buna bağlı olarak kromozom ve kardiyovaskuler sistem anomalileri nedeniyle yapılan terminasyonların sayısı önemli ölçüde artmıştır. Kültürel, eğitimsel, dini ve yasal faktörler terminasyon yapıldığı gebelik haftasının yanı sıra terminasyon endikasyonlarında da değişikliklere yol açmaktadır. (J Turkish-German Gynecol Assoc 2012; 13: 85-90)
Objectives
To develop a nomogram for fetal left brachiocephalic vein (LBCV) diameters during a healthy pregnancy and to assess LBCV values in fetuses with fetal growth restriction (FGR).
Methods
This prospective observational study included 31 FGR pregnancies and 438 low-risk pregnancies. The low-risk group was used to determine the 5th, mean, and 95th percentiles for the LBCV between 12 and 39 weeks of gestation based on gestational age. On growth charts, LBCV measurements of FGR fetuses were displayed, and those above the gestational age 95th percentile were considered wide vein. Cerebroplacental ratio (CPR) and umbilical artery (UA), middle cerebral artery (MCA), and ductus venosus (DV) Doppler parameters were evaluated in FGR fetuses.
Results
LBCV diameter increased significantly with advancing gestational age. The LBCV diameters were above the 95th percentile in 23 of the 31 FGR fetuses (74.2%). All fetuses (15/15, 100%) with early-onset (EO)-FGR and 8 fetuses (8/16, 50%) with the late-onset (LO)-FGR had LBCV values above the 95th percentile (p<0.01). UA-PI was significantly higher and MCA-PI and CPR were significantly lower in LO-FGR fetuses with LBCV diameters above the 95th percentile (p<0.05).
Conclusions
LBCV diameters of fetuses with FGR were significantly wider than the normal population. In the LO-FGR group, there was a good correlation between LBCV diameter and CPR.
Gillessen‐Kaesbach‐Nishimura syndrome (GIKANIS) is a congenital disease of glycosylation (CDG) linked to the ALG9 gene. GIKANIS is a lethal disorder characterized by atypical facial features, generalized skeletal changes with shortening of the long bones with broad, round metaphyses, round ilia, and deficient ossification of the skull, cervical spine and pubic bones, and visceral abnormalities including polycystic kidneys and congenital cardiac defects. GIKANIS is caused by a homozygous splicing variant (c.1173 + 2 T > A) leading to skipping of exon 10, frameshift, and premature termination codon of the ALG9 gene. To our best knowledge, only two affected families with confirmed molecular analyses have been reported. We present an additional report on two siblings with the same mutation, emphasizing the prenatal ultrasonographic features. Their facial and skeletal manifestations recapitulated those previously reported. Ultrasonography revealed polycystic kidneys and unbalanced atrioventricular septal defect (AVSD) with transposition of the great arteries.
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