Pub Date : 2014-11-01DOI: 10.1017/S0965539515000091
C. Ogilvie
The possibility of prenatal screening for genetic disorders was raised as early as the mid-1950s, and with the introduction in 1966 of amniocentesis for sampling fetal material, it became possible to identify pregnancies with trisomy 21 (Down syndrome), the most common prenatal genetic abnormality. The fetal cells in the amniotic fluid could be cultured, then harvested, followed by chromosome spreading on microscope slides. These chromosome spreads, each representing the chromosomes from a single cell nucleus, could be stained, visualised by light microscopy and counted to establish the chromosome number. However, diagnosis of Down syndrome was expensive, and in the early days of amniocentesis, there was an associated risk of miscarriage; most countries therefore recommended this procedure only for women who were identified as having a raised risk of chromosome abnormality. As it is well established that raised maternal age increases the risk of Down syndrome, amniocentesis was first offered only to women above an age cut-off (usually 35). However, although the risk to an individual woman of having a Down syndrome pregnancy is greater in this age group, the majority of Down syndrome babies are born to younger women, due to the preponderance of pregnancies in the younger group.
{"title":"FREE FETAL DNA AS A SCREENING TEST FOR ANEUPLOIDY – DOES IT ADD UP?","authors":"C. Ogilvie","doi":"10.1017/S0965539515000091","DOIUrl":"https://doi.org/10.1017/S0965539515000091","url":null,"abstract":"The possibility of prenatal screening for genetic disorders was raised as early as the mid-1950s, and with the introduction in 1966 of amniocentesis for sampling fetal material, it became possible to identify pregnancies with trisomy 21 (Down syndrome), the most common prenatal genetic abnormality. The fetal cells in the amniotic fluid could be cultured, then harvested, followed by chromosome spreading on microscope slides. These chromosome spreads, each representing the chromosomes from a single cell nucleus, could be stained, visualised by light microscopy and counted to establish the chromosome number. However, diagnosis of Down syndrome was expensive, and in the early days of amniocentesis, there was an associated risk of miscarriage; most countries therefore recommended this procedure only for women who were identified as having a raised risk of chromosome abnormality. As it is well established that raised maternal age increases the risk of Down syndrome, amniocentesis was first offered only to women above an age cut-off (usually 35). However, although the risk to an individual woman of having a Down syndrome pregnancy is greater in this age group, the majority of Down syndrome babies are born to younger women, due to the preponderance of pregnancies in the younger group.","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"339-348"},"PeriodicalIF":0.0,"publicationDate":"2014-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539515000091","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56979713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-05-01DOI: 10.1017/S0965539514000102
M. Bartsota, Nicolas Judd, J. Carvalho
{"title":"WHEN, HOW AND WHERE TO DELIVER THE FETUS WITH MAJOR CONGENITAL HEART DISEASE","authors":"M. Bartsota, Nicolas Judd, J. Carvalho","doi":"10.1017/S0965539514000102","DOIUrl":"https://doi.org/10.1017/S0965539514000102","url":null,"abstract":"","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"79-94"},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539514000102","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56978815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-05-01DOI: 10.1017/S0965539515000017
O. Kay, A. Hughes, G. Saade, P. Bennett, V. Terzidou, S. Thornton
{"title":"Recent advances in the prevention and treatment of preterm labour: Oxytocin antagonists and the silicone (Arabin) pessary","authors":"O. Kay, A. Hughes, G. Saade, P. Bennett, V. Terzidou, S. Thornton","doi":"10.1017/S0965539515000017","DOIUrl":"https://doi.org/10.1017/S0965539515000017","url":null,"abstract":"","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"134-145"},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539515000017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56979164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-05-01DOI: 10.1017/S0965539514000114
S. Worton, C. Sibley, A. Heazell
Fetal growth restriction (FGR) is defined as the failure of a fetus to attain its full genetic growth potential. It is a leading cause of stillbirth, prematurity, cerebral palsy and perinatal mortality. Small size at birth increases surviving infants’ lifelong risk of adverse health outcomes associated with the metabolic syndrome. The pathophysiology of abnormal fetal growth is extremely complex and incompletely understood, with a plethora of genetic, signalling and metabolic candidates under investigation, many of which may result in abnormal structure and function of the placenta. In contrast to, or maybe because of, the underlying complexities of FGR, the strategies clinicians have for identifying and managing this outcome are conspicuously limited. Current clinical practice is restricted to identifying pregnancies at risk of FGR, and when FGR is detected, using intensive monitoring to guide the timing of delivery to optimise fetal outcomes. Abnormal Doppler indices in the umbilical artery are strongly associated with poor perinatal outcomes and are currently the “gold standard” for clinical surveillance of the growth-restricted fetus.
{"title":"UNDERSTANDING THE PLACENTAL AETIOLOGY OF FETAL GROWTH RESTRICTION; COULD THIS LEAD TO PERSONALIZED MANAGEMENT STRATEGIES?","authors":"S. Worton, C. Sibley, A. Heazell","doi":"10.1017/S0965539514000114","DOIUrl":"https://doi.org/10.1017/S0965539514000114","url":null,"abstract":"Fetal growth restriction (FGR) is defined as the failure of a fetus to attain its full genetic growth potential. It is a leading cause of stillbirth, prematurity, cerebral palsy and perinatal mortality. Small size at birth increases surviving infants’ lifelong risk of adverse health outcomes associated with the metabolic syndrome. The pathophysiology of abnormal fetal growth is extremely complex and incompletely understood, with a plethora of genetic, signalling and metabolic candidates under investigation, many of which may result in abnormal structure and function of the placenta. In contrast to, or maybe because of, the underlying complexities of FGR, the strategies clinicians have for identifying and managing this outcome are conspicuously limited. Current clinical practice is restricted to identifying pregnancies at risk of FGR, and when FGR is detected, using intensive monitoring to guide the timing of delivery to optimise fetal outcomes. Abnormal Doppler indices in the umbilical artery are strongly associated with poor perinatal outcomes and are currently the “gold standard” for clinical surveillance of the growth-restricted fetus.","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"95-116"},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539514000114","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56978909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-05-01DOI: 10.1017/S0965539514000138
B. Hutchinson, R. Palma-Dias, S. Walker
Congenital cytomegalovirus (CMV) infection is now the commonest infective cause of neurological handicap. Arguably, there is no other single contributor to developmental disability where a greater opportunity, and imperative, exists to improve outcomes than CMV. CMV is the most common intrauterine infection and congenital CMV is the leading non-inherited cause of sensorineural deafness. The public health impact of CMV is significant: the overall birth prevalence of congenital CMV is estimated at 0.64%, with 11% of live born infants displaying symptoms.
{"title":"UNIVERSAL CYTOMEGALOVIRUS SCREENING: TIME FOR REAPPRAISAL?","authors":"B. Hutchinson, R. Palma-Dias, S. Walker","doi":"10.1017/S0965539514000138","DOIUrl":"https://doi.org/10.1017/S0965539514000138","url":null,"abstract":"Congenital cytomegalovirus (CMV) infection is now the commonest infective cause of neurological handicap. Arguably, there is no other single contributor to developmental disability where a greater opportunity, and imperative, exists to improve outcomes than CMV. CMV is the most common intrauterine infection and congenital CMV is the leading non-inherited cause of sensorineural deafness. The public health impact of CMV is significant: the overall birth prevalence of congenital CMV is estimated at 0.64%, with 11% of live born infants displaying symptoms.","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"117-133"},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539514000138","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56978980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-02-01DOI: 10.1017/S0965539514000059
M. Chandiramani, P. Bennett, Richard Brown, Yun S. Lee, D. MacIntyre
{"title":"VAGINAL MICROBIOME-PREGNANT HOST INTERACTIONS DETERMINE A SIGNIFICANT PROPORTION OF PRETERM LABOUR","authors":"M. Chandiramani, P. Bennett, Richard Brown, Yun S. Lee, D. MacIntyre","doi":"10.1017/S0965539514000059","DOIUrl":"https://doi.org/10.1017/S0965539514000059","url":null,"abstract":"","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"73-78"},"PeriodicalIF":0.0,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539514000059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56978365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-02-01DOI: 10.1017/S0965539514000047
D. Hui, J. Barrett
{"title":"MODE OF DELIVERY IN TERM AND PRETERM TWINS: A REVIEW","authors":"D. Hui, J. Barrett","doi":"10.1017/S0965539514000047","DOIUrl":"https://doi.org/10.1017/S0965539514000047","url":null,"abstract":"","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539514000047","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56978795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-02-01DOI: 10.1017/S0965539514000084
J. Espinoza
{"title":"THE ROLE OF SPATIO-TEMPORAL IMAGING CORRELATION (STIC) IN THE PRENATAL DIAGNOSIS OF CONGENITAL HEART DEFECTS","authors":"J. Espinoza","doi":"10.1017/S0965539514000084","DOIUrl":"https://doi.org/10.1017/S0965539514000084","url":null,"abstract":"","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"59 1","pages":"59-72"},"PeriodicalIF":0.0,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539514000084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56978869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-02-01DOI: 10.1017/S0965539514000060
Ichchha Madan, M. Redman, Richard Bronsteen, R. Bahado-Singh, L. F. Gonçalves
{"title":"THE GENETIC SONOGRAM","authors":"Ichchha Madan, M. Redman, Richard Bronsteen, R. Bahado-Singh, L. F. Gonçalves","doi":"10.1017/S0965539514000060","DOIUrl":"https://doi.org/10.1017/S0965539514000060","url":null,"abstract":"","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"12-41"},"PeriodicalIF":0.0,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539514000060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56978496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-02-01DOI: 10.1017/S0965539514000096
J. Espinoza
Endothelial cell proliferation and survival require continuous low levels of vascular endothelial growth factor (VEGF). The bioavailability of this angiogenic factor appears to be regulated by anti-angiogenic factors, including the soluble form of VEGF receptor 1 (sFlt-1) in the non-pregnant and pregnant states. During pregnancy a VEGF antagonist (sFlt-1) and other anti-angiogenic factors, including soluble endoglin (s-Eng), are produced by the human placenta and released into the maternal circulation; an excess of these anti-angiogenic factors can lead into angiogenic imbalances and pregnancy complications. This is important because regulation of VEGF action on angiogenic balances appears to be essential for a successful pregnancy.
{"title":"ANGIOGENIC IMBALANCES IN THE PATHOGENESIS OF PREGNANCY COMPLICATIONS","authors":"J. Espinoza","doi":"10.1017/S0965539514000096","DOIUrl":"https://doi.org/10.1017/S0965539514000096","url":null,"abstract":"Endothelial cell proliferation and survival require continuous low levels of vascular endothelial growth factor (VEGF). The bioavailability of this angiogenic factor appears to be regulated by anti-angiogenic factors, including the soluble form of VEGF receptor 1 (sFlt-1) in the non-pregnant and pregnant states. During pregnancy a VEGF antagonist (sFlt-1) and other anti-angiogenic factors, including soluble endoglin (s-Eng), are produced by the human placenta and released into the maternal circulation; an excess of these anti-angiogenic factors can lead into angiogenic imbalances and pregnancy complications. This is important because regulation of VEGF action on angiogenic balances appears to be essential for a successful pregnancy.","PeriodicalId":89369,"journal":{"name":"Fetal and maternal medicine review","volume":"25 1","pages":"42-58"},"PeriodicalIF":0.0,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0965539514000096","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56979121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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