Bio

Bio


My clinical interest in pregnancies complicated with birth defects has led my underlying research interests in genomic abnormalities in the human trophoblast carrying to faulty placentation. The latter began with initial work during K12 and KO8 funding. I took a great interest in the human placenta as it carries potential advantages over other tissues sources: first, this highly metabolically active organ is the potential source of many transcripts. Second, the placenta forms at a very early stage of embryonic development, potentially allowing detection of primary alterations as compared to secondary changes that may mask the underlying causal phenomena. Finally, studying early placentation may provide targets for development of novel molecular approaches, such as up-regulate or down-regulate genes, the protein products of which could potentially serve as molecular surrogates for diagnosis and treatment of pregnancy complication such as miscarriages, pre-eclampsia, pregnancy induced hypertension and intrauterine growth retardation. This work has led to the first Trisomy 21, Trisomy 18, trisomy 13 cell lines established from human placentas making it possible to apply gene editing in the early stages of human trophoblast development.

As my primary clinical responsibility involves treating patients needing medical care and support through their high risk pregnancies, I am interested in factors that may impact outcomes, such as prenatal screening and diagnosis, maternal heart conditions, labor and delivery management, and safety approaches for the second stage of labor. In investigating length of labor and approaches to shorten the second stage, I have found methods of improving perinatal outcomes in diverse maternal populations.

With regards to my interest in fetal medicine, I have worked in collaboration with other specialists such as radiologists and pediatric cardiologists utilizing imagining studies to assess and determine successful perinatal care and fetal survival.

Clinical Focus


  • High Risk Obstetrics
  • Obstetrics and Gynecology
  • Genetics
  • Maternal Cardiac Conditions

Administrative Appointments


  • Global Health ACOG/ US.Gov Fellow Associate, ACOG (2017 - Present)
  • Diversity Communication Advisory Board (CAB) member, Stanford University SOM (2016 - Present)
  • Office of the Dean for Faculty Development and Diversity (OFDD) Liasion, Stanford University SOM (2015 - Present)

Honors & Awards


  • Peter A. Grannum, M.D Memorial Award". Excellence in Teaching, Yale University (2001-04)
  • "Lysosomal Diseases and Brain Scholar Award", Children's Gaucher Research Foundation (2008)
  • Outstanding Faculty Award in Medical Student Teaching, UCSF (2009)
  • March of Dimes Scholar, "Reproductive Scientist Development Award", NIH/NICHD/ MOD (2011-13)
  • Outstanding Faculty Award in Medical Student Teaching, UCSF (2012)
  • Outstanding Faculty Teaching Award, UCSF (2015)
  • Academy for Leadership and Development Scholar, SMFM (2016)
  • Stanford Leadership Development Program Scholar, Stanford University/Stanford Heath care System (2018-19)

Boards, Advisory Committees, Professional Organizations


  • OBGYN, American Board of Obstetrics and Gynecology (2007 - Present)
  • Medical Geneticist, American Board of Medical genetics and Genomics (2011 - Present)
  • Maternal-Fetal-Medicine specialist, American Board of Obstetrics and Gynecology (2013 - Present)

Professional Education


  • Board Certification: Clinical Genetics, American Board of Medical Genetics and Genomics (2011)
  • Fellowship, University of California, at San Francisco (UCSF), Diagnostic Imagine (2006)
  • Board Certification: Obstetrics and Gynecology, American Board of Obstetrics and Gynecology (2007)
  • Residency: Yale School Of Medicine Office of Student Affairs (2004) CT
  • Internship: Yale School Of Medicine Office of Student Affairs (2004) CT
  • Board Certification: Maternal and Fetal Medicine, American Board of Obstetrics and Gynecology (2013)
  • Fellowship: University of California San Francisco (2008) CA
  • Medical Education: Central University of Venezuela (1997) Venezuela

Community and International Work


  • Utilization of Obstetrics Simulation to decrease Adverse Perinatal Outcomes

    Topic

    global women's health education

    Partnering Organization(s)

    GOMOSGOFAR

    Populations Served

    LIMS

    Location

    International

    Ongoing Project

    Yes

    Opportunities for Student Involvement

    Yes

Publications

All Publications


  • Chronic antepartum maternal hyperoxygenation in a case of severe fetal Ebstein's anomaly with circular shunt physiology. Annals of pediatric cardiology Arunamata, A., Axelrod, D. M., Bianco, K., Balasubramanian, S., Quirin, A., Tacy, T. A. ; 10 (3): 284?87

    Abstract

    Perinatal mortality remains high among fetuses diagnosed with Ebstein's anomaly of the tricuspid valve. The subgroup of patients with pulmonary valve regurgitation is at particularly high risk. In the setting of pulmonary valve regurgitation, early constriction of the ductus arteriosus may be a novel perinatal management strategy to reduce systemic steal resulting from circular shunt physiology. We report the use of chronic antepartum maternal oxygen therapy for constriction of the fetal ductus arteriosus and modulation of fetal pulmonary vascular resistance in a late presentation of Ebstein's anomaly with severe tricuspid valve regurgitation, reversal of flow in the ductus arteriosus, and continuous pulmonary valve regurgitation.

    View details for PubMedID 28928616

  • Perinatal Outcomes in Women With Cardiac Arrhythmia. Lee, J., Sie, L., Sherwin, E. B., Girsen, A. I., Tolani, A. T., Miller, H. E., Panelli, D. M., Do, S. C., Khandelwal, A., Bianco, K. SPRINGER HEIDELBERG. 2020: 161A
  • Changes in pregnancy-related serum biomarkers early in gestation are associated with later development of preeclampsia. PloS one Hao, S., You, J., Chen, L., Zhao, H., Huang, Y., Zheng, L., Tian, L., Maric, I., Liu, X., Li, T., Bianco, Y. K., Winn, V. D., Aghaeepour, N., Gaudilliere, B., Angst, M. S., Zhou, X., Li, Y. M., Mo, L., Wong, R. J., Shaw, G. M., Stevenson, D. K., Cohen, H. J., Mcelhinney, D. B., Sylvester, K. G., Ling, X. B. 2020; 15 (3): e0230000

    Abstract

    Placental protein expression plays a crucial role during pregnancy. We hypothesized that: (1) circulating levels of pregnancy-associated, placenta-related proteins throughout gestation reflect the temporal progression of the uncomplicated, full-term pregnancy, and can effectively estimate gestational ages (GAs); and (2) preeclampsia (PE) is associated with disruptions in these protein levels early in gestation; and can identify impending PE. We also compared gestational profiles of proteins in the human and mouse, using pregnant heme oxygenase-1 (HO-1) heterozygote (Het) mice, a mouse model reflecting PE-like symptoms.Serum levels of placenta-related proteins-leptin (LEP), chorionic somatomammotropin hormone like 1 (CSHL1), elabela (ELA), activin A, soluble fms-like tyrosine kinase 1 (sFlt-1), and placental growth factor (PlGF)-were quantified by ELISA in blood serially collected throughout human pregnancies (20 normal subjects with 66 samples, and 20 subjects who developed PE with 61 samples). Multivariate analysis was performed to estimate the GA in normal pregnancy. Mean-squared errors of GA estimations were used to identify impending PE. The human protein profiles were then compared with those in the pregnant HO-1 Het mice.An elastic net-based gestational dating model was developed (R2 = 0.76) and validated (R2 = 0.61) using serum levels of the 6 proteins measured at various GAs from women with normal uncomplicated pregnancies. In women who developed PE, the model was not (R2 = -0.17) associated with GA. Deviations from the model estimations were observed in women who developed PE (P = 0.01). The model developed with 5 proteins (ELA excluded) performed similarly from sera from normal human (R2 = 0.68) and WT mouse (R2 = 0.85) pregnancies. Disruptions of this model were observed in both human PE-associated (R2 = 0.27) and mouse HO-1 Het (R2 = 0.30) pregnancies. LEP outperformed sFlt-1 and PlGF in differentiating impending PE at early human and late mouse GAs.Serum placenta-related protein profiles are temporally regulated throughout normal pregnancies and significantly disrupted in women who develop PE. LEP changes earlier than the well-established biomarkers (sFlt-1 and PlGF). There may be evidence of a causative action of HO-1 deficiency in LEP upregulation in a PE-like murine model.

    View details for DOI 10.1371/journal.pone.0230000

    View details for PubMedID 32126118

  • Trisomy 21 is Associated with Caspase-2 Upregulation in Cytotrophoblasts at the Maternal-Fetal Interface REPRODUCTIVE SCIENCES Leon-Martinez, D., Robinson, J. F., Zdravkovic, T., Genbacev, O., Gormley, M., Mcmaster, M., Fisher, S. J., Bianco, K. 2020; 27 (1): 100?109

    Abstract

    Impaired placentation is implicated in poor perinatal outcomes associated with Trisomy 21. Earlier studies revealed abnormal cytotrophoblast differentiation along the invasive pathway as a contributing mechanism. To further elucidate the causes, we evaluated Caspase-2 expression at the protein level (immunolocalization and immunoblot) in samples from Trisomy 21 (n = 9) and euploid (n = 4) age-matched placentas. Apoptosis was investigated via the TUNEL assay. An immunolocalization approach was used to characterize Caspase-3, Fas (CD95), and Fas ligand in the same samples. Caspase-2 was significantly overexpressed in Trisomy 21 placentas, with the highest expression in villous cores and invasive cytotrophoblasts. Immunolocalization showed that Caspase-3 had a similar expression pattern as Caspase-2. Using the TUNEL approach, we observed high variability in the number of apoptotic cells in biopsies from different regions of the same placenta and among different placentas. However, Trisomy 21 placentas had more apoptotic cells, specifically in cell columns and basal plates. Furthermore, Caspase-2 co-immunolocalized with Fas (CD95) and FasL in TUNEL-positive extravillous cytotrophoblasts, but not in villous cores. These results help explain the higher levels of apoptosis among placental cells of Trisomy 21 pregnancies in molecular terms. Specifically, the co-expression of Caspase-2 and Caspase-3 with other regulators of the apoptotic process in TUNEL-positive cells suggests these molecules may cooperate in launching the observed apoptosis. Among trophoblasts, only the invasive subpopulation showed this pattern, which could help explain the higher rates of adverse outcomes in these pregnancies. In future experiments, this relationship will be further examined at a functional level in cultured human trophoblasts.

    View details for DOI 10.1007/s43032-019-00002-x

    View details for Web of Science ID 000525433300011

    View details for PubMedID 32046398

  • Contraception uptake among women with cardiovascular disease: The impact of a multidisciplinary team care approach Miller, H. E., Sie, L., Lee, C. J., Panelli, D. M., Sherwin, E. B., Noon, B., Girsen, A., Bianco, K. MOSBY-ELSEVIER. 2020: S707?S708
  • Maternal Outcomes in Planned and Unplanned Pregnancies in Women with Cardiac Disease. Do, S. C., Tolani, A. T., Sie, L., Girsen, A. I., Lee, C. J., Sherwin, E., Panelli, D. M., El-Sayed, Y. Y., Khandelwal, A., Blumenfeld, Y. J., Bianco, K. SAGE PUBLICATIONS INC. 2019: 323A
  • A Multidisciplinary Approach to Care of Pregnant Patients with History of Open Heart Surgery. Do, S. C., Lee, C. J., Sie, L., Tolani, A. T., Sherwin, E., Girsen, A. I., El-Sayed, Y. Y., Khandelwal, A., Bianco, K., Blumenfeld, Y. J. SAGE PUBLICATIONS INC. 2019: 323A?324A
  • Care of the pregnant cardiac patient e the importance of a multidisciplinary approach Tolani, A. T., Do, S. C., Blumenfeld, Y. J., Sie, L., Girsen, A. I., Lee, C. J., Sherwin, E. B., Tsur, A., El-Sayed, Y. Y., Khandelwal, A., Bianco, K. MOSBY-ELSEVIER. 2019: S536
  • Outcomes of women with primary and secondary pulmonary hypertension during pregnancy Blumenfeld, Y. J., Girsen, A. I., Druzin, M. L., Lyell, D. J., Bianco, K. Y., Herrero, T., Bentley, J., Seckel, E., Zamanian, R. T., El-Sayed, Y. Y. MOSBY-ELSEVIER. 2019: S405
  • Hospital variations in the use of forceps assisted delivery - results from a state-wide analysis Bentley, J., Lee, H., Lyell, D., El-Sayed, Y., Ness, A., Bianco, K., Spiegel, A., Blumenfeld, Y. MOSBY-ELSEVIER. 2018: S344
  • Maternal morbidity after forceps vs vacuum assisted delivery - Outcomes from a large state-wide cohort Bentley, J., Lyell, D., El-Sayed, Y., Ness, A., Foeller, M., Bianco, K., Spiegel, A., Martin, B., Do, S., Blumenfeld, Y. MOSBY-ELSEVIER. 2018: S345
  • Fetal intolerance to labor in pregnancies complicated by marginal and eccentric cord insertion Young-Lin, N., Lutz, A., Leon-Martinez, D., Ye, C., Torosis, M., Jazayeri, Y., Pugh, B., Bianco, K. MOSBY-ELSEVIER. 2018: S285
  • Neonatal outcomes after operative vaginal delivery - are forceps or vacuum safer? Bentley, J. P., Lee, H., Lyell, D., El-Sayed, Y., Ness, A., Bianco, K., Yeaton-Massey, A., Blumenfeld, Y. MOSBY-ELSEVIER. 2018: S343?S344
  • Placental transcriptomes in the common aneuploidies reveal critical regions on the trisomic chromosomes and genome-wide effects PRENATAL DIAGNOSIS Bianco, K., Gormley, M., Farrell, J., Zhou, Y., Oliverio, O., Tilden, H., McMaster, M., Fisher, S. J. 2016; 36 (9): 812-822

    Abstract

    Chromosomal aberrations are frequently associated with birth defects and pregnancy losses. Trisomy 13, Trisomy 18 and Trisomy 21 are the most common, clinically relevant fetal aneusomies. This study used a transcriptomics approach to identify the molecular signatures at the maternal-fetal interface in each aneuploidy.We profiled placental gene expression (13-22?weeks) in T13 (n?=?4), T18 (n?=?4) and T21 (n?=?8), and in euploid pregnancies (n?=?4).We found differentially expressed transcripts (?2-fold) in T21 (n?=?160), T18 (n?=?80) and T13 (n?=?125). The majority were upregulated and most of the misexpressed genes were not located on the relevant trisomic chromosome, suggesting genome-wide dysregulation. A smaller number of the differentially expressed transcripts were encoded on the trisomic chromosome, suggesting gene dosage. In T21, <10% of the genes were transcribed from the Down syndrome critical region (21q21-22), which contributes to the clinical phenotype. In T13, 15% of the upregulated genes were on the affected chromosome (13q11-14), and in T18, the percentage increased to 24% (18q11-22 region).The trisomic placental (and possibly fetal) phenotypes are driven by the combined effects of genome-wide phenomena and increased gene dosage from the trisomic chromosome. 2016 John Wiley & Sons, Ltd.

    View details for DOI 10.1002/pd.4862

    View details for Web of Science ID 000384096800002

    View details for PubMedID 27328057

    View details for PubMedCentralID PMC5104283

  • Integrative analysis of 111 reference human epigenomes. Nature Kundaje, A., Meuleman, W., Ernst, J., Bilenky, M., Yen, A., Heravi-Moussavi, A., Kheradpour, P., Zhang, Z., Wang, J., Ziller, M. J., Amin, V., Whitaker, J. W., Schultz, M. D., Ward, L. D., Sarkar, A., Quon, G., Sandstrom, R. S., Eaton, M. L., Wu, Y., Pfenning, A. R., Wang, X., Claussnitzer, M., Liu, Y., Coarfa, C., Harris, R. A., Shoresh, N., Epstein, C. B., Gjoneska, E., Leung, D., Xie, W., Hawkins, R. D., Lister, R., Hong, C., Gascard, P., Mungall, A. J., Moore, R., Chuah, E., Tam, A., Canfield, T. K., Hansen, R. S., Kaul, R., Sabo, P. J., Bansal, M. S., Carles, A., Dixon, J. R., Farh, K., Feizi, S., Karlic, R., Kim, A., Kulkarni, A., Li, D., Lowdon, R., Elliott, G., Mercer, T. R., Neph, S. J., Onuchic, V., Polak, P., Rajagopal, N., Ray, P., Sallari, R. C., Siebenthall, K. T., Sinnott-Armstrong, N. A., Stevens, M., Thurman, R. E., Wu, J., Zhang, B., Zhou, X., Beaudet, A. E., Boyer, L. A., De Jager, P. L., Farnham, P. J., Fisher, S. J., Haussler, D., Jones, S. J., Li, W., Marra, M. A., McManus, M. T., Sunyaev, S., Thomson, J. A., Tlsty, T. D., Tsai, L., Wang, W., Waterland, R. A., Zhang, M. Q., Chadwick, L. H., Bernstein, B. E., Costello, J. F., Ecker, J. R., Hirst, M., Meissner, A., Milosavljevic, A., Ren, B., Stamatoyannopoulos, J. A., Wang, T., Kellis, M. 2015; 518 (7539): 317-330

    Abstract

    The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.

    View details for DOI 10.1038/nature14248

    View details for PubMedID 25693563

    View details for PubMedCentralID PMC4530010

  • Pregnancy complications are increased among women with cardiomyopathy compared to those with other cardiac diseases Bianco, K., Harris, I., Henry, D., Killion, M., Bosco, V., Thiet, M., Gonzalez, J. MOSBY-ELSEVIER. 2015: S68?S69
  • Congenital Heart Disease and Perinatal Outcomes. Henry, D., Clay, J., Gonzalez, J. M., Harris, I. S., Tilden, H., Bianco, K. SAGE PUBLICATIONS INC. 2014: 148A
  • Reversal of gene dysregulation in cultured cytotrophoblasts reveals possible causes of preeclampsia JOURNAL OF CLINICAL INVESTIGATION Zhou, Y., Gormley, M. J., Hunkapiller, N. M., Kapidzic, M., Stolyarov, Y., Feng, V., Nishida, M., Drake, P. M., Bianco, K., Wang, F., McMaster, M. T., Fisher, S. J. 2013; 123 (7): 2862?72

    Abstract

    During human pregnancy, a subset of placental cytotrophoblasts (CTBs) differentiates into cells that aggressively invade the uterus and its vasculature, anchoring the progeny and rerouting maternal blood to the placenta. In preeclampsia (PE), CTB invasion is limited, reducing placental perfusion and/or creating intermittent flow. This syndrome, affecting 4%-8% of pregnancies, entails maternal vascular alterations (e.g., high blood pressure, proteinuria, and edema) and, in some patients, fetal growth restriction. The only cure is removal of the faulty placenta, i.e., delivery. Previously, we showed that defective CTB differentiation contributes to the placental component of PE, but the causes were unknown. Here, we cultured CTBs isolated from PE and control placentas for 48 hours, enabling differentiation and invasion. In various severe forms of PE, transcriptomics revealed common aberrations in CTB gene expression immediately after isolation, including upregulation of SEMA3B, which resolved in culture. The addition of SEMA3B to normal CTBs inhibited invasion and recreated aspects of the PE phenotype. Additionally, SEMA3B downregulated VEGF signaling through the PI3K/AKT and GSK3 pathways, effects that were observed in PE CTBs. We propose that, in severe PE, the in vivo environment dysregulates CTB gene expression; the autocrine actions of the upregulated molecules (including SEMA3B) impair CTB differentiation, invasion and signaling; and patient-specific factors determine the signs.

    View details for DOI 10.1172/JCI66966

    View details for Web of Science ID 000321316700016

    View details for PubMedID 23934129

    View details for PubMedCentralID PMC3999620

  • Genomic profiles in common aneuploidies: a combination of dose effects and whole genome misregulation Bianco, K., Gormley, M., Tilden, H., McMaster, M., Fisher, S. MOSBY-ELSEVIER. 2013: S30
  • Human Placenta Undergoes Global DNA Methylation Modification during Normal Gestation Houshdaran, S., Goldfien, G. A., Bianco, K. SAGE PUBLICATIONS INC. 2012: 383A?384A
  • Genomic imprinting in offspring conceived with assisted reproductive technology 31st Annual Scientific Meeting of the Society-of-Maternal-Fetal-Medicine (SMFM) Norton, M., Haston, K., Reijo-Pera, R., Chueh, J., Blumenfeld, Y., Bianco, K., Zlatnik, M. MOSBY-ELSEVIER. 2011: S284?S285
  • Stem Cells in Hepatic Regeneration After Injury ADVANCES IN WOUND CARE, VOL 1 Kuscuoglu, U., Bianco, K., Sylvester, K. G., Sen, C. K. 2010; 1: 526?31
  • Effect of estradiol on oocyte development INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS Bianco, K., Mahutte, N. G., Arici, A., Sakkas, D., Taylor, H. S. 2009; 104 (3): 230?32

    Abstract

    To determine whether elevated serum estradiol (E(2)) concentrations in oocyte donors affect assisted reproduction outcome.In a retrospective cohort study of 58 consecutive oocyte donation cycles, donors were stratified into 2 groups according to E(2) concentration, group 1 (n=32; E(2)2000 pg/mL [range, 2062-6957 pg/mL]). Data were analyzed using the t test and chi(2) test.Donors in group 1 produced significantly less oocytes than donors in group 2 (19.3+/-1.7 vs 12.0+/-1.4; P<0.001), and recipients of oocytes from group 1 had significantly fewer numbers of embryos available for transfer (10.4+/-1.1 vs 6.4+/-0.8; P=0.003). However, the mean number (3.3) of embryos transferred and the pregnancy rate were the same in both groups.Elevated estradiol concentration in oocyte donors did not affect pregnancy outcome, suggesting that estradiol levels in donors do not affect oocyte development.

    View details for DOI 10.1016/j.ijgo.2008.10.015

    View details for Web of Science ID 000264255600015

    View details for PubMedID 19056082

    View details for PubMedCentralID PMC3107851

  • Operative vaginal delivery: Now or later? Cheng, Y. W., Bianco, K., Shaffer, B. L., Lyell, D., Caughey, A. B. MOSBY-ELSEVIER. 2007: S97
  • Fetal cerebellar hemorrhage in parvovirus-associated non-immune hydrops fetalis JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE Glenn, O. A., Bianco, K., Barkovich, A., Callen, P. W., Parer, J. T. 2007; 20 (10): 769?72

    Abstract

    We report two cases of fetal cerebellar hemorrhage in the setting of parvovirus-associated hydrops fetalis and fetal blood transfusion. In both cases, the cerebellar hemorrhage was diagnosed by fetal magnetic resonance imaging after intrauterine blood transfusion. To our knowledge, this is the first report of fetal cerebellar hemorrhage in the setting of parvovirus-associated hydrops fetalis, and may be the result of cerebrovascular changes both during and after the transfusion.

    View details for DOI 10.1080/14767050701580960

    View details for Web of Science ID 000250402500011

    View details for PubMedID 17763280

  • Second-trimester ductus venosus measurement and adverse perinatal outcome in fetuses with congenital heart disease JOURNAL OF ULTRASOUND IN MEDICINE Bianco, K., Small, M., Julien, S., Kershaw, T., Michon, M., Copel, J. 2006; 25 (8): 979?82

    Abstract

    The purpose of this study was to determine whether Doppler velocimetry of the ductus venosus (DV) predicts adverse perinatal outcome in congenital heart disease (CHD).We conducted a retrospective cohort study of all pregnant women undergoing fetal echocardiography for CHD in a single perinatal center during a 2-year period. We compared outcomes for fetuses having a diagnosis of CHD in the second trimester and abnormal DV Doppler velocimetric findings with those having CHD and normal DV Doppler findings. Karyotype, gestational age at delivery, fetal loss rate, and rate of termination were assessed. The referral value for an abnormal DV pulsatility index was above the 95th percentile for gestational age. Statistical analysis included the t test, Fisher exact test, and chi(2) test.The incidence of CHD in our population was 7%. There were 98 patients with CHD; of those, 31 had DV measurement. A total of 9 patients had an abnormal DV. Three of this group (33%) had intrauterine fetal death or perinatal death. In patients with CHD and normal DV measurements, 83% had living children versus 33% in the group with an abnormal DV (P < .05). There was no statistically significant difference in the rate of aneuploidy between the normal DV (15%) and abnormal DV (20%) groups (P = .65). The mean gestational age at delivery was similar between the normal (37.63 weeks) and abnormal (38.33 weeks) DV groups (P = .71). There was no difference in the rate of pregnancy termination.Abnormal second-trimester DV measurements are predictive of adverse perinatal outcome in patients with CHD, independent of karyotype or gestational age at delivery. This information may have a role in the counseling of parents with CHD.

    View details for DOI 10.7863/jum.2006.25.8.979

    View details for Web of Science ID 000239445000005

    View details for PubMedID 16870891

  • History of miscarriage and increased incidence of fetal aneuploidy in subsequent pregnancy OBSTETRICS AND GYNECOLOGY Bianco, K., Caughey, A. B., Shaffer, B. L., Davis, R., Norton, M. E. 2006; 107 (5): 1098?1102

    Abstract

    The purpose of this study was to examine the association between history of spontaneous abortion and aneuploidy in a subsequent pregnancy.This was a retrospective cohort study of women who underwent fetal karyotype analysis with amniocentesis or chorionic villus sampling at a single prenatal diagnosis center. Information on spontaneous abortions, parity, maternal age, ethnicity, type of prenatal diagnosis, and karyotype was assessed. Univariable and multivariable analyses were conducted.A total of 46,939 women were included in our analysis. Women with no prior spontaneous abortions had a 1.39% risk for any aneuploidy. In women with one prior spontaneous abortion, this risk increased to 1.67%; for women with 2 previous spontaneous abortions, the risk increased to 1.84%; and for those women who had had 3 or more prior spontaneous abortions, the risk increased further to 2.18% (P < .007). When controlling for maternal age, parity, ethnicity, and mode of prenatal diagnosis and compared with women with no prior spontaneous abortions, women with one prior spontaneous abortion (adjusted odds ratio [AOR] 1.21, 95% confidence interval [CI] 1.01-1.47) or 3 or more prior spontaneous abortions (AOR 1.51, 95% CI 1.02-2.25) had a statistically significant increase in aneuploidy in a subsequent pregnancy. Women with 2 prior spontaneous abortions had an AOR of 1.26 for aneuploidy, but the 95% CI contained unity.An increased risk of karyotypic abnormality identified at the time of prenatal diagnosis is demonstrated in patients with an increasing number of spontaneous abortions. This study provides information regarding this risk among women presenting for prenatal diagnosis. According to our data, for a woman with an a priori risk of 1 in 300 for Down syndrome, 3 prior spontaneous abortions would increase that risk by 47% to 1 in 204. These results should be confirmed in low-risk populations.

    View details for DOI 10.1097/01.AOG.0000215560.86673.22

    View details for Web of Science ID 000241296500019

    View details for PubMedID 16648416

  • Second trimester ductus venosus measurements as a predictor of adverse perinatal outcome in congenital heart disease Bianco, K., Small, M., Browne, N., Julien, S., Kershaw, T., Michon, M., Copel, J. MOSBY, INC. 2004: S173
  • Elevated estradiol levels in oocyte donation cycles do not impair ART outcomes for the recipients. Bianco, K., Mahutte, N. G., Arici, A., Duleba, A. J., Taylor, H. S., Sakkas, D. ELSEVIER SCIENCE INC. 2003: S165

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