Clinical‐pathological features in placentas of pregnancies with SARS‐CoV‐2 infection and adverse outcome: case series with and without congenital transmission
Objective To correlate clinical outcomes to pathology in SARS‐CoV‐2 infected placentas in stillborn and live‐born infants presenting with fetal distress. Design Retrospective, observational. Setting Nationwide. Population Five stillborn and nine live‐born infants from 13 pregnant women infected with...
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| Vydáno v: | BJOG : an international journal of obstetrics and gynaecology Ročník 129; číslo 8; s. 1361 - 1374 |
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| Hlavní autoři: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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England
Wiley Subscription Services, Inc
01.07.2022
John Wiley and Sons Inc |
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| ISSN: | 1470-0328, 1471-0528, 1471-0528 |
| On-line přístup: | Získat plný text |
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| Abstract | Objective
To correlate clinical outcomes to pathology in SARS‐CoV‐2 infected placentas in stillborn and live‐born infants presenting with fetal distress.
Design
Retrospective, observational.
Setting
Nationwide.
Population
Five stillborn and nine live‐born infants from 13 pregnant women infected with SARS‐CoV‐2 seeking care at seven different maternity units in Sweden.
Methods
Clinical outcomes and placental pathology were studied in 14 cases (one twin pregnancy) of maternal SARS‐CoV‐2 infection with impaired fetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus‐related pathology on the villous capillary endothelium, trophoblast and other cells.
Main outcome measures
Maternal and fetal clinical outcomes and placental pathology in stillborn and live‐born infants.
Results
Reduced fetal movements were reported (77%) and time from onset of maternal COVID‐19 symptoms to signs of fetal distress among live‐born infants was 6 (3–12) days and to diagnosis of stillbirth 11 (2–25) days. Two of the live‐born infants died during the postnatal period. Signs of fetal distress led to emergency caesarean section in all live‐born infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one live‐born neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillositis and trophoblast necrosis were associated with SARS‐CoV‐2 placental infection and congenital transmission.
Conclusions
SARS‐CoV‐2 can cause rapid placental dysfunction with subsequent acute fetal hypoxia leading to intrauterine fetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillositis and trophoblast degeneration.
Tweetable
SARS‐CoV‐2 can cause rapid placental dysfunction and intrauterine fetal compromise.
Linked article: This article is commented on by Yves Ville, pp. 1375 in this issue. To view this minicommentary visit https://doi.org/10.1111/1471-0528.17162.
This article includes Author Insights, a video available at: https://vimeo.com/bjog/authorinsights17132 |
|---|---|
| AbstractList | Objective To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and live-born infants presenting with fetal distress. Design Retrospective, observational. Setting Nationwide. Population Five stillborn and nine live-born infants from 13 pregnant women infected with SARS-CoV-2 seeking care at seven different maternity units in Sweden. Methods Clinical outcomes and placental pathology were studied in 14 cases (one twin pregnancy) of maternal SARS-CoV-2 infection with impaired fetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus-related pathology on the villous capillary endothelium, trophoblast and other cells. Main outcome measures Maternal and fetal clinical outcomes and placental pathology in stillborn and live-born infants. Results Reduced fetal movements were reported (77%) and time from onset of maternal COVID-19 symptoms to signs of fetal distress among live-born infants was 6 (3-12) days and to diagnosis of stillbirth 11 (2-25) days. Two of the live-born infants died during the postnatal period. Signs of fetal distress led to emergency caesarean section in all live-born infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one live-born neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillositis and trophoblast necrosis were associated with SARS-CoV-2 placental infection and congenital transmission. Conclusions SARS-CoV-2 can cause rapid placental dysfunction with subsequent acute fetal hypoxia leading to intrauterine fetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillositis and trophoblast degeneration. To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and live-born infants presenting with fetal distress. Retrospective, observational. Nationwide. Five stillborn and nine live-born infants from 13 pregnant women infected with SARS-CoV-2 seeking care at seven different maternity units in Sweden. Clinical outcomes and placental pathology were studied in 14 cases (one twin pregnancy) of maternal SARS-CoV-2 infection with impaired fetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus-related pathology on the villous capillary endothelium, trophoblast and other cells. Maternal and fetal clinical outcomes and placental pathology in stillborn and live-born infants. Reduced fetal movements were reported (77%) and time from onset of maternal COVID-19 symptoms to signs of fetal distress among live-born infants was 6 (3-12) days and to diagnosis of stillbirth 11 (2-25) days. Two of the live-born infants died during the postnatal period. Signs of fetal distress led to emergency caesarean section in all live-born infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one live-born neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillositis and trophoblast necrosis were associated with SARS-CoV-2 placental infection and congenital transmission. SARS-CoV-2 can cause rapid placental dysfunction with subsequent acute fetal hypoxia leading to intrauterine fetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillositis and trophoblast degeneration. Objective To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and live-born infants presenting with fetal distress. Design Retrospective, observational. Setting Nationwide. Population Five stillborn and nine live-born infants from 13 pregnant women infected with SARS-CoV-2 seeking care at seven different maternity units in Sweden. Methods Clinical outcomes and placental pathology were studied in 14 cases (one twin pregnancy) of maternal SARS-CoV-2 infection with impaired fetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus-related pathology on the villous capillary endothelium, trophoblast and other cells. Main outcome measures Maternal and fetal clinical outcomes and placental pathology in stillborn and live-born infants. Results Reduced fetal movements were reported (77%) and time from onset of maternal COVID-19 symptoms to signs of fetal distress among live-born infants was 6 (3-12) days and to diagnosis of stillbirth 11 (2-25) days. Two of the live-born infants died during the postnatal period. Signs of fetal distress led to emergency caesarean section in all live-born infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one live-born neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillositis and trophoblast necrosis were associated with SARS-CoV-2 placental infection and congenital transmission. Conclusions SARS-CoV-2 can cause rapid placental dysfunction with subsequent acute fetal hypoxia leading to intrauterine fetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillositis and trophoblast degeneration. ObjectiveTo correlate clinical outcomes to pathology in SARS‐CoV‐2 infected placentas in stillborn and live‐born infants presenting with fetal distress.DesignRetrospective, observational.SettingNationwide.PopulationFive stillborn and nine live‐born infants from 13 pregnant women infected with SARS‐CoV‐2 seeking care at seven different maternity units in Sweden.MethodsClinical outcomes and placental pathology were studied in 14 cases (one twin pregnancy) of maternal SARS‐CoV‐2 infection with impaired fetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus‐related pathology on the villous capillary endothelium, trophoblast and other cells.Main outcome measuresMaternal and fetal clinical outcomes and placental pathology in stillborn and live‐born infants.ResultsReduced fetal movements were reported (77%) and time from onset of maternal COVID‐19 symptoms to signs of fetal distress among live‐born infants was 6 (3–12) days and to diagnosis of stillbirth 11 (2–25) days. Two of the live‐born infants died during the postnatal period. Signs of fetal distress led to emergency caesarean section in all live‐born infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one live‐born neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillositis and trophoblast necrosis were associated with SARS‐CoV‐2 placental infection and congenital transmission.ConclusionsSARS‐CoV‐2 can cause rapid placental dysfunction with subsequent acute fetal hypoxia leading to intrauterine fetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillositis and trophoblast degeneration. Objective To correlate clinical outcomes to pathology in SARS‐CoV‐2 infected placentas in stillborn and live‐born infants presenting with fetal distress. Design Retrospective, observational. Setting Nationwide. Population Five stillborn and nine live‐born infants from 13 pregnant women infected with SARS‐CoV‐2 seeking care at seven different maternity units in Sweden. Methods Clinical outcomes and placental pathology were studied in 14 cases (one twin pregnancy) of maternal SARS‐CoV‐2 infection with impaired fetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus‐related pathology on the villous capillary endothelium, trophoblast and other cells. Main outcome measures Maternal and fetal clinical outcomes and placental pathology in stillborn and live‐born infants. Results Reduced fetal movements were reported (77%) and time from onset of maternal COVID‐19 symptoms to signs of fetal distress among live‐born infants was 6 (3–12) days and to diagnosis of stillbirth 11 (2–25) days. Two of the live‐born infants died during the postnatal period. Signs of fetal distress led to emergency caesarean section in all live‐born infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one live‐born neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillositis and trophoblast necrosis were associated with SARS‐CoV‐2 placental infection and congenital transmission. Conclusions SARS‐CoV‐2 can cause rapid placental dysfunction with subsequent acute fetal hypoxia leading to intrauterine fetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillositis and trophoblast degeneration. Tweetable SARS‐CoV‐2 can cause rapid placental dysfunction and intrauterine fetal compromise. Linked article: This article is commented on by Yves Ville, pp. 1375 in this issue. To view this minicommentary visit https://doi.org/10.1111/1471-0528.17162. This article includes Author Insights, a video available at: https://vimeo.com/bjog/authorinsights17132 SARS‐CoV‐2 can cause rapid placental dysfunction and intrauterine fetal compromise. Linked article: This article is commented on by Yves Ville, pp. 1375 in this issue. To view this minicommentary visit https://doi.org/10.1111/1471-0528.17162 . This article includes Author Insights, a video abstract available at: https://vimeo.com/bjogabstracts/authorinsights17132 Objective: To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and liveborn infants presenting with foetal distress. Design: Retrospective, observational. Setting: Nationwide. Population or sample: Five stillborn and 9 liveborn infants from 13 pregnant women infected with SARS-CoV-2 seeking care at 7 different maternity units in Sweden. Methods: Clinical outcomes and placental pathology were studied in 14 cases (1 twin pregnancy) of maternal SARS-CoV-2 infection with impaired foetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus-related pathology on the villous capillary endothelium, trophoblast and other cells. Main outcome measures: Maternal and foetal clinical outcomes and placental pathology in stillborn and liveborn infants. Results: Reduced foetal movements were reported (77%) and time from onset of maternal COVID-19 symptoms to signs of foetal distress among liveborn infants was 6 (3-12) days and to diagnosis of stillbirth 11 (2-25) days. Two of the liveborn infants died during the postnatal period. Signs of foetal distress led to emergency Caesarean section in all liveborn infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one liveborn neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillousitis and trophoblast necrosis was associated with SARS-CoV-2 placental infection and congenital transmission. Conclusions: SARS-CoV-2 can cause rapid placental dysfunction with subsequent acute foetal hypoxia leading to intrauterine foetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillousitis and trophoblast degeneration. SARS‐CoV‐2 can cause rapid placental dysfunction and intrauterine fetal compromise. Linked article: This article is commented on by Yves Ville, pp. 1375 in this issue. To view this minicommentary visit https://doi.org/10.1111/1471-0528.17162. This article includes Author Insights, a video abstract available at: https://vimeo.com/bjogabstracts/authorinsights17132 To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and live-born infants presenting with fetal distress.OBJECTIVETo correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and live-born infants presenting with fetal distress.Retrospective, observational.DESIGNRetrospective, observational.Nationwide.SETTINGNationwide.Five stillborn and nine live-born infants from 13 pregnant women infected with SARS-CoV-2 seeking care at seven different maternity units in Sweden.POPULATIONFive stillborn and nine live-born infants from 13 pregnant women infected with SARS-CoV-2 seeking care at seven different maternity units in Sweden.Clinical outcomes and placental pathology were studied in 14 cases (one twin pregnancy) of maternal SARS-CoV-2 infection with impaired fetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus-related pathology on the villous capillary endothelium, trophoblast and other cells.METHODSClinical outcomes and placental pathology were studied in 14 cases (one twin pregnancy) of maternal SARS-CoV-2 infection with impaired fetal outcome. Outcomes were correlated to placental pathology in order to investigate the impact of virus-related pathology on the villous capillary endothelium, trophoblast and other cells.Maternal and fetal clinical outcomes and placental pathology in stillborn and live-born infants.MAIN OUTCOME MEASURESMaternal and fetal clinical outcomes and placental pathology in stillborn and live-born infants.Reduced fetal movements were reported (77%) and time from onset of maternal COVID-19 symptoms to signs of fetal distress among live-born infants was 6 (3-12) days and to diagnosis of stillbirth 11 (2-25) days. Two of the live-born infants died during the postnatal period. Signs of fetal distress led to emergency caesarean section in all live-born infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one live-born neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillositis and trophoblast necrosis were associated with SARS-CoV-2 placental infection and congenital transmission.RESULTSReduced fetal movements were reported (77%) and time from onset of maternal COVID-19 symptoms to signs of fetal distress among live-born infants was 6 (3-12) days and to diagnosis of stillbirth 11 (2-25) days. Two of the live-born infants died during the postnatal period. Signs of fetal distress led to emergency caesarean section in all live-born infants with umbilical cord blood gases and low Apgar scores confirming intrauterine hypoxia. Five stillborn and one live-born neonate had confirmed congenital transmission. Massive perivillous fibrinoid deposition, intervillositis and trophoblast necrosis were associated with SARS-CoV-2 placental infection and congenital transmission.SARS-CoV-2 can cause rapid placental dysfunction with subsequent acute fetal hypoxia leading to intrauterine fetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillositis and trophoblast degeneration.CONCLUSIONSSARS-CoV-2 can cause rapid placental dysfunction with subsequent acute fetal hypoxia leading to intrauterine fetal compromise. Associated placental pathology included massive perivillous fibrinoid deposition, intervillositis and trophoblast degeneration. |
| Author | Blomberg, Marie Schwartz, David A. Zaigham, Mehreen Wowern, Emma Sengpiel, Verena Iorizzo, Linda Papadogiannakis, Nikos Wikström, Anna‐Karin Holmström, Sandra Leijonhfvud, Åsa Nelander, Maria Sand, Anna Gisselsson, David |
| AuthorAffiliation | 7 Department of Women's and Children's Health Uppsala University Uppsala Sweden 9 Department of Pathology Medical College of Georgia, Augusta University Augusta Georgia USA 10 Department of Obstetrics and Gynaecology, Helsingborg Hospital, Department of Clinical Science Helsingborg Lund University Lund Sweden 8 Perinatal and Cardiovascular Epidemiology Institution of Clinical Sciences Malmö, Lund University Lund Sweden 1 Obstetrics & Gynaecology, Institution of Clinical Sciences Lund Lund University Lund Sweden 14 Department of Obstetrics and Gynaecology Sahlgrenska Academy, University of Gothenburg Gothenburg Sweden 11 Department of Obstetrics and Gynaecology and Department of Biomedical and Clinical Sciences Linköping University Linköping Sweden 12 Department of Laboratory Medicine, Division of Pathology, Karolinska Institute and Department of Pathology Karolinska University Hospital Stockholm Sweden 15 Region Västra Götaland, Sahlgrenska University Hospital Department of Obstetrics and Gyna |
| AuthorAffiliation_xml | – name: 5 Department of Women's and Children's Health Karolinska Institute Stockholm Sweden – name: 6 Department of Obstetrics and Gynaecology Karolinska University Hospital Stockholm Sweden – name: 4 Division of Clinical Genetics, Department of Laboratory Medicine Lund University Lund Sweden – name: 8 Perinatal and Cardiovascular Epidemiology Institution of Clinical Sciences Malmö, Lund University Lund Sweden – name: 15 Region Västra Götaland, Sahlgrenska University Hospital Department of Obstetrics and Gynaecology Gothenburg Sweden – name: 1 Obstetrics & Gynaecology, Institution of Clinical Sciences Lund Lund University Lund Sweden – name: 12 Department of Laboratory Medicine, Division of Pathology, Karolinska Institute and Department of Pathology Karolinska University Hospital Stockholm Sweden – name: 10 Department of Obstetrics and Gynaecology, Helsingborg Hospital, Department of Clinical Science Helsingborg Lund University Lund Sweden – name: 3 Clinical Genetics and Pathology, Laboratory Medicine Skåne University Hospital Lund Sweden – name: 14 Department of Obstetrics and Gynaecology Sahlgrenska Academy, University of Gothenburg Gothenburg Sweden – name: 9 Department of Pathology Medical College of Georgia, Augusta University Augusta Georgia USA – name: 11 Department of Obstetrics and Gynaecology and Department of Biomedical and Clinical Sciences Linköping University Linköping Sweden – name: 7 Department of Women's and Children's Health Uppsala University Uppsala Sweden – name: 2 Department of Obstetrics and Gynaecology Skåne University Hospital Lund Sweden – name: 13 Department of Obstetrics and Gynaecology Halland Hospital Varberg Sweden |
| Author_xml | – sequence: 1 givenname: Mehreen orcidid: 0000-0003-0129-1578 surname: Zaigham fullname: Zaigham, Mehreen email: mehreen.zaigham@med.lu.se organization: Skåne University Hospital – sequence: 2 givenname: David surname: Gisselsson fullname: Gisselsson, David organization: Lund University – sequence: 3 givenname: Anna surname: Sand fullname: Sand, Anna organization: Karolinska University Hospital – sequence: 4 givenname: Anna‐Karin surname: Wikström fullname: Wikström, Anna‐Karin organization: Uppsala University – sequence: 5 givenname: Emma surname: Wowern fullname: Wowern, Emma organization: Institution of Clinical Sciences Malmö, Lund University – sequence: 6 givenname: David A. surname: Schwartz fullname: Schwartz, David A. organization: Medical College of Georgia, Augusta University – sequence: 7 givenname: Linda orcidid: 0000-0002-5840-4062 surname: Iorizzo fullname: Iorizzo, Linda organization: Lund University – sequence: 8 givenname: Maria surname: Nelander fullname: Nelander, Maria organization: Uppsala University – sequence: 9 givenname: Marie surname: Blomberg fullname: Blomberg, Marie organization: Linköping University – sequence: 10 givenname: Nikos surname: Papadogiannakis fullname: Papadogiannakis, Nikos organization: Karolinska University Hospital – sequence: 11 givenname: Sandra surname: Holmström fullname: Holmström, Sandra organization: Halland Hospital – sequence: 12 givenname: Åsa surname: Leijonhfvud fullname: Leijonhfvud, Åsa organization: Lund University – sequence: 13 givenname: Verena surname: Sengpiel fullname: Sengpiel, Verena organization: Department of Obstetrics and Gynaecology |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35243759$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-184733$$DView record from Swedish Publication Index (Linköpings universitet) https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-485881$$DView record from Swedish Publication Index (Uppsala universitet) https://gup.ub.gu.se/publication/317889$$DView record from Swedish Publication Index (Göteborgs universitet) http://kipublications.ki.se/Default.aspx?queryparsed=id:149364089$$DView record from Swedish Publication Index (Karolinska Institutet) |
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| ContentType | Journal Article |
| Copyright | 2022 The Authors. BJOG: An International Journal of Obstetrics and Gynaecology published by John Wiley & Sons Ltd. 2022. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| CorporateAuthor | Pathways of cancer cell evolution Section V Institutionen för kliniska vetenskaper, Lund Lunds universitet Department of Laboratory Medicine Department of Clinical Sciences, Malmö Lund University Sektion V Obstetrics and Gynaecology (Lund) Division of Clinical Genetics Institutionen för laboratoriemedicin Department of Clinical Sciences, Lund Cancercellers evolution Obstetrik och gynekologi, Lund Faculty of Medicine Perinatal and cardiovascular epidemiology Medicinska fakulteten Avdelningen för klinisk genetik Perinatal och kardiovaskulär epidemiologi Institutionen för kliniska vetenskaper, Malmö |
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| Keywords | COVID-19 COVID-19 maternal-fetal transmission fetal distress SARS-CoV-2 SARS-CoV-2 placental infection placental endothelial cells maternal floor infarction vertical SARS-CoV-2 transmission coronavirus placental pathology chronic histiocytic intervillositis villous macrophages |
| Language | English |
| License | Attribution-NonCommercial 2022 The Authors. BJOG: An International Journal of Obstetrics and Gynaecology published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
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| Notes | Funding information This article is commented on by Yves Ville, pp. 1375 in this issue. To view this minicommentary visit https://doi.org/10.1111/1471-0528.17162 https://vimeo.com/bjog/authorinsights17132 MZ was financed by grants from the Swedish state under an agreement between the Swedish government and the county councils, the ALF‐agreement YF0054; and the South Hospital Region Project Grant (2021‐2020‐0689). The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. Linked article . This article includes Author Insights, a video abstract available at ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Undefined-3 Funding informationMZ was financed by grants from the Swedish state under an agreement between the Swedish government and the county councils, the ALF‐agreement YF0054; and the South Hospital Region Project Grant (2021‐2020‐0689). The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. Linked article: This article is commented on by Yves Ville, pp. 1375 in this issue. To view this minicommentary visit https://doi.org/10.1111/1471-0528.17162. This article includes Author Insights, a video abstract available at: https://vimeo.com/bjogabstracts/authorinsights17132 |
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| References | 2021; 9 2021; 27 2021; 21 2021; 4 2021; 45 2021; 145 2021; 225 2019; 98 2020; 60 2002; 5 2009 2020; 127 2020; 324 2020; 59 2013; 146 2005 2020; 144 2020; 56 2020; 12 2020; 99 2020; 11 2020; 323 2020; 98 2020; 223 2021; 30 1990; 163 2020; 8 2010; 89 2021; 57 1987; 69 2021; 1321 2021; 10 2021; 11 2021; 112 2022 2021 2020; 370 2022; 13 1996; 85 2016; 594 2021; 175 2007; 21 2022; 128 2022; 129 e_1_2_11_32_1 e_1_2_11_55_1 e_1_2_11_30_1 e_1_2_11_36_1 e_1_2_11_51_1 e_1_2_11_13_1 e_1_2_11_34_1 e_1_2_11_53_1 e_1_2_11_11_1 e_1_2_11_29_1 e_1_2_11_6_1 e_1_2_11_4_1 e_1_2_11_48_1 e_1_2_11_2_1 e_1_2_11_20_1 e_1_2_11_45_1 e_1_2_11_47_1 e_1_2_11_24_1 e_1_2_11_41_1 e_1_2_11_8_1 e_1_2_11_43_1 e_1_2_11_17_1 e_1_2_11_15_1 e_1_2_11_38_1 e_1_2_11_19_1 Poisson TM (e_1_2_11_27_1) 2021; 30 e_1_2_11_50_1 e_1_2_11_10_1 e_1_2_11_31_1 e_1_2_11_14_1 e_1_2_11_35_1 e_1_2_11_52_1 e_1_2_11_12_1 e_1_2_11_33_1 e_1_2_11_54_1 e_1_2_11_7_1 e_1_2_11_28_1 e_1_2_11_5_1 e_1_2_11_26_1 e_1_2_11_3_1 e_1_2_11_49_1 e_1_2_11_21_1 e_1_2_11_44_1 Naidu SAG (e_1_2_11_22_1) 2020; 8 e_1_2_11_46_1 e_1_2_11_25_1 e_1_2_11_9_1 e_1_2_11_23_1 e_1_2_11_42_1 e_1_2_11_18_1 e_1_2_11_16_1 e_1_2_11_37_1 e_1_2_11_39_1 Laurin J (e_1_2_11_40_1) 1987; 69 35352874 - BJOG. 2022 Jul;129(8):1375. doi: 10.1111/1471-0528.17162 |
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reference: 35352874 - BJOG. 2022 Jul;129(8):1375. doi: 10.1111/1471-0528.17162 |
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| Snippet | Objective
To correlate clinical outcomes to pathology in SARS‐CoV‐2 infected placentas in stillborn and live‐born infants presenting with fetal distress.... SARS‐CoV‐2 can cause rapid placental dysfunction and intrauterine fetal compromise. Linked article: This article is commented on by Yves Ville, pp. 1375 in... To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and live-born infants presenting with fetal distress. Retrospective,... ObjectiveTo correlate clinical outcomes to pathology in SARS‐CoV‐2 infected placentas in stillborn and live‐born infants presenting with fetal... To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and live-born infants presenting with fetal distress.OBJECTIVETo... SARS‐CoV‐2 can cause rapid placental dysfunction and intrauterine fetal compromise. Linked article: This article is commented on by Yves Ville, pp. 1375 in... Objective To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and live-born infants presenting with fetal distress.... Objective: To correlate clinical outcomes to pathology in SARS-CoV-2 infected placentas in stillborn and liveborn infants presenting with foetal distress.... |
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| SubjectTerms | Apgar score association Cesarean Section chronic histiocytic intervillositis Clinical Medicine Clinical outcomes Congenital diseases Cord blood coronavirus COVID-19 COVID-19 maternal-fetal transmission Degeneration Endothelium Female fetal Fetal Distress Fetuses Gynaecology, Obstetrics and Reproductive Medicine Gynekologi, obstetrik och reproduktionsmedicin Humans Hypoxia Infant, Newborn Infants Infections Infectious Disease Transmission, Vertical Infectious Medicine Infektionsmedicin Klinisk medicin macrophages maternal floor infarction maternal-fetal transmission Medical and Health Sciences Medicin och hälsovetenskap Obstetrics & Gynecology Pathology Pathophysiology Placenta Placenta - blood supply placental endothelial cells placental infection placental pathology Pregnancy Pregnancy Complications, Infectious - diagnosis Prenatal development Retrospective Studies SARS-CoV-2 SARS-CoV-2 placental infection Severe acute respiratory syndrome coronavirus 2 Stillbirth - epidemiology Umbilical cord vertical SARS-CoV-2 transmission villous villous macrophages |
| Title | Clinical‐pathological features in placentas of pregnancies with SARS‐CoV‐2 infection and adverse outcome: case series with and without congenital transmission |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2F1471-0528.17132 https://www.ncbi.nlm.nih.gov/pubmed/35243759 https://www.proquest.com/docview/2678266149 https://www.proquest.com/docview/2636140545 https://pubmed.ncbi.nlm.nih.gov/PMC9111112 https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-184733 https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-485881 https://gup.ub.gu.se/publication/317889 http://kipublications.ki.se/Default.aspx?queryparsed=id:149364089 |
| Volume | 129 |
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