Placenta accreta is now the chief cause of postpartum hemorrhage resulting in maternal and neonatal morbidity. Prenatal diagnosis decreases blood loss at delivery and intra and post-partum complications. Ultrasound is critical for diagnosis and MRI is a complementary tool when the diagnosis is uncertain. Peripartum hysterectomy has been the standard of therapy but conservative management is increasingly being used. The etiology of accreta is due to a deficiency of maternal decidua resulting in placental invasion into the uterine myometrium. The molecular basis for the development of invasive placentation is yet to be elucidated but may involve abnormal paracrine/autocrine signaling between the deficient maternal decidua and the trophoblastic tissue. The interaction of hormones such as Relaxin which is abundant in maternal decidua and INSL4, an insulin like peptide found in placental trophoblastic tissue may play role in the formation of placenta accreta.

Most adnexal masses are benign and ultrasound characteristics can help guide the assessment of asymptomatic ovarian masses. When surgical management is chosen, laparoscopy can be safely performed in pregnancy. Ovarian torsion is a complication for persistent masses in pregnancy.

This study aimed to determine whether poor glycemic control in early pregnancy is associated with an increased risk of congenital heart disease (CHD) for infants of women with preexisting diabetes. A retrospective review examined two tertiary care centers of diabetic pregnancies that recorded early hemoglobin A1c (HbA1c) values (<20 weeks). The incidence of prenatally diagnosed CHD was calculated and stratified by HbA1c level. Poor glycemic control was defined as an HbA1c level of 8.5 % or higher. Fetal echocardiography was used to identify fetuses that resulted in infants with suspected CHD. Neonatal echocardiograms and pathology reports were reviewed for confirmation of the diagnosis. Of 535 patients, 30 (5.6 %) delivered an infant with confirmed CHD. Among the patients with poor glycemic control, 8.3 % (n = 17) delivered an infant with CHD, whereas 3.9 % (n = 13) of those with an HbA1c level lower than 8.5 % delivered an infant with CHD (p = 0.03). Poor glycemic control in early pregnancy is associated with an increased risk of CHD in offspring. The incidence of CHD in patients with adequate glycemic control still is sufficiently high to justify routine fetal echocardiography for all gravidas with preexisting diabetes regardless of HbA1c level.

A persistent ovarian mass in pregnancy does not confer an increased risk of adverse pregnancy outcomes.

This study was designed to show whether placental relaxin (RLN), its receptor (RXFP1), or insulin-like peptide 4 (INSL4) might have altered expression in patients with placenta accreta. The baseline expression of their genes through gestation (n ¼ 34) was quantitated in the placental basal plate (BP) and villous trophoblast (TR), and compared to their expression in placenta accreta (n ¼ 6). The proteins were also immunolocalized and quantitated in the accreta tissues. The messenger RNAs (mRNAs) of matrix metalloproteinase 9, -2, and tissue inhibitors of matrix metalloproteinase (TIMP)-1 were also measured. Results demonstrated that the BP and TR expressed low levels of RLN/RXFP1 and INSL4 through gestation. In accreta, increased RLN gene and protein in BP were associated with antepartum bleeding whereas INSL4 expression decreased throughout the TR. There were no changes in mRNAs for MMPs, but TIMP-1 was increased only in the invasive TR.

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We describe a patient with trisomy 8 mosaicism followed through a sixth pregnancy and discuss issues in phenotypic and genotypic variability, the risk for neoplasia, and reproductive risks. Am. J. Med. Genet. 75:382-385, 1998.

Placental UDP-glucuronosyltransferase (UGT) enzymes have critical roles in hormone, nutrient, chemical balance and fetal exposure during pregnancy. Placental UGT1A isoforms were profiled and differences between preeclamptic (PE) and non-PE placental UGT expression determined. In third trimester villous placenta, UGT1A1, 1A4, 1A6 and 1A9 were expressed and active in all specimens (n = 10), but UGT1A3, 1A5, 1A7, 1A8 and 1A10 were absent. The UGT1A activities were comparable to human liver microsomes per milligram, but placental microsome yields were only 2 % of liver (1 mg/g of tissue vs. 45 mg/g of tissue). For successful PCR, placental collection and processing within 60 min from delivery, including DNAse and ≥300 ng of RNA in reverse transcription were essential and snap freezing in liquid nitrogen immediately was the best preservation method. Although UGT1A6 mRNA was lower in PE (P < 0.001), there were no other significant effects on UGT mRNA, protein or activities. A more comprehensive tissue sample set is required for confirmation of PE interactions with UGT. Placental UGT1A enzyme expression patterns are similar to the liver and a detoxicative role for placental UGT1A is inferred.