Fetal growth and the etiology of preterm delivery
To confirm that preterm delivery is associated with fetal growth restriction (FGR), and to determine if the various etiologies of preterm delivery are associated with the same degree and type of FGR. Two hundred ninety young, primarily minority gravidas who had routine initial ultrasound examination...
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Veröffentlicht in: | Obstetrics and gynecology (New York. 1953) 1995-02, Vol.85 (2), p.175-182 |
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creator | Hediger, Mary L. Scholl, Theresa O. Schall, Joan I. Miller, Laurie W. Fischer, Richard L. |
description | To confirm that preterm delivery is associated with fetal growth restriction (FGR), and to determine if the various etiologies of preterm delivery are associated with the same degree and type of FGR.
Two hundred ninety young, primarily minority gravidas who had routine initial ultrasound examinations also had subsequent ultrasound examinations at 32 weeks' gestation. Fetal growth characteristics were compared between preterm (less than 37 weeks' gestation) and term deliveries, and among preterm deliveries with medical or obstetric indications, premature rupture of membranes (PROM), and spontaneous preterm labor.
Forty-six infants (15.9%) were born preterm. At 32 weeks' gestation, all fetuses later delivered preterm were already smaller than fetuses later delivered at term (
P < .05) for all dimensions: head circumference (HC), abdominal circumference (AC), biparietal diameter (BPD), and femur length (FL). However, after stratifying by cause of preterm delivery for those fetuses later delivered for medical or obstetric indications, we found that only AC was decreased (
P < .01) and that the HC-AC ratio was elevated (asymmetric FGR). Neonates delivered after unsuccessfully treated PROM or preterm labor were symmetrically smaller in all characteristics (HC, AC, BPD, and FL).
By 32 weeks' gestation, fetuses later delivered preterm are already significantly smaller than fetuses later delivered at term. However, when stratified by the etiology of preterm delivery, infants delivered preterm for medical or obstetric indications had asymmetric growth patterns, which suggests a growth failure late in pregnancy. Infants delivered preterm after PROM or after failed or no tocolysis for spontaneous preterm labor were proportionately smaller, implying an overall slowing of growth that may originate early in pregnancy and possibly demonstrate a more chronic stress. |
doi_str_mv | 10.1016/0029-7844(94)00365-K |
format | Article |
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Two hundred ninety young, primarily minority gravidas who had routine initial ultrasound examinations also had subsequent ultrasound examinations at 32 weeks' gestation. Fetal growth characteristics were compared between preterm (less than 37 weeks' gestation) and term deliveries, and among preterm deliveries with medical or obstetric indications, premature rupture of membranes (PROM), and spontaneous preterm labor.
Forty-six infants (15.9%) were born preterm. At 32 weeks' gestation, all fetuses later delivered preterm were already smaller than fetuses later delivered at term (
P < .05) for all dimensions: head circumference (HC), abdominal circumference (AC), biparietal diameter (BPD), and femur length (FL). However, after stratifying by cause of preterm delivery for those fetuses later delivered for medical or obstetric indications, we found that only AC was decreased (
P < .01) and that the HC-AC ratio was elevated (asymmetric FGR). Neonates delivered after unsuccessfully treated PROM or preterm labor were symmetrically smaller in all characteristics (HC, AC, BPD, and FL).
By 32 weeks' gestation, fetuses later delivered preterm are already significantly smaller than fetuses later delivered at term. However, when stratified by the etiology of preterm delivery, infants delivered preterm for medical or obstetric indications had asymmetric growth patterns, which suggests a growth failure late in pregnancy. Infants delivered preterm after PROM or after failed or no tocolysis for spontaneous preterm labor were proportionately smaller, implying an overall slowing of growth that may originate early in pregnancy and possibly demonstrate a more chronic stress.</description><identifier>ISSN: 0029-7844</identifier><identifier>EISSN: 1873-233X</identifier><identifier>DOI: 10.1016/0029-7844(94)00365-K</identifier><identifier>PMID: 7824227</identifier><identifier>CODEN: OBGNAS</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Biological and medical sciences ; Birth Weight ; Cohort Studies ; Delivery. Postpartum. Lactation ; Disorders ; Embryonic and Fetal Development ; Female ; Gestational Age ; Gynecology. Andrology. Obstetrics ; Humans ; Male ; Medical sciences ; Obstetric Labor, Premature - physiopathology ; Pregnancy ; Pregnancy Outcome ; Prospective Studies ; Ultrasonography, Prenatal</subject><ispartof>Obstetrics and gynecology (New York. 1953), 1995-02, Vol.85 (2), p.175-182</ispartof><rights>1995 The American College of Obstetricians and Gynecologists</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4313-3ad456bf7808475471f0d930cedaec63c3493a0dc8bdd7b60d015ab499cd88bb3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3405525$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7824227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hediger, Mary L.</creatorcontrib><creatorcontrib>Scholl, Theresa O.</creatorcontrib><creatorcontrib>Schall, Joan I.</creatorcontrib><creatorcontrib>Miller, Laurie W.</creatorcontrib><creatorcontrib>Fischer, Richard L.</creatorcontrib><title>Fetal growth and the etiology of preterm delivery</title><title>Obstetrics and gynecology (New York. 1953)</title><addtitle>Obstet Gynecol</addtitle><description>To confirm that preterm delivery is associated with fetal growth restriction (FGR), and to determine if the various etiologies of preterm delivery are associated with the same degree and type of FGR.
Two hundred ninety young, primarily minority gravidas who had routine initial ultrasound examinations also had subsequent ultrasound examinations at 32 weeks' gestation. Fetal growth characteristics were compared between preterm (less than 37 weeks' gestation) and term deliveries, and among preterm deliveries with medical or obstetric indications, premature rupture of membranes (PROM), and spontaneous preterm labor.
Forty-six infants (15.9%) were born preterm. At 32 weeks' gestation, all fetuses later delivered preterm were already smaller than fetuses later delivered at term (
P < .05) for all dimensions: head circumference (HC), abdominal circumference (AC), biparietal diameter (BPD), and femur length (FL). However, after stratifying by cause of preterm delivery for those fetuses later delivered for medical or obstetric indications, we found that only AC was decreased (
P < .01) and that the HC-AC ratio was elevated (asymmetric FGR). Neonates delivered after unsuccessfully treated PROM or preterm labor were symmetrically smaller in all characteristics (HC, AC, BPD, and FL).
By 32 weeks' gestation, fetuses later delivered preterm are already significantly smaller than fetuses later delivered at term. However, when stratified by the etiology of preterm delivery, infants delivered preterm for medical or obstetric indications had asymmetric growth patterns, which suggests a growth failure late in pregnancy. Infants delivered preterm after PROM or after failed or no tocolysis for spontaneous preterm labor were proportionately smaller, implying an overall slowing of growth that may originate early in pregnancy and possibly demonstrate a more chronic stress.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Birth Weight</subject><subject>Cohort Studies</subject><subject>Delivery. Postpartum. Lactation</subject><subject>Disorders</subject><subject>Embryonic and Fetal Development</subject><subject>Female</subject><subject>Gestational Age</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Obstetric Labor, Premature - physiopathology</subject><subject>Pregnancy</subject><subject>Pregnancy Outcome</subject><subject>Prospective Studies</subject><subject>Ultrasonography, Prenatal</subject><issn>0029-7844</issn><issn>1873-233X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1vEzEQhi1EVULLPwBpDwjBYcv4a72-IKGK0qqVuFCJm-W1ZxuDEwd70yj_HodE6a2nkWfeZ8Z6CHlL4YIC7T4DMN2qXoiPWnwC4J1sb1-QGe0Vbxnnv16S2THyirwu5TdA5TQ_JaeqZ4IxNSP0Cicbm4ecNtO8sUvfTHNscAoppodtk8ZmlXHCvGg8xvCIeXtOTkYbC7451DNyf_Xt5-V1e_fj-83l17vWCU55y60XshtG1UMvlBSKjuA1B4feouu440JzC971g_dq6MADlXYQWjvf98PAz8iH_d5VTn_XWCazCMVhjHaJaV2MUpRT1kENin3Q5VRKxtGscljYvDUUzM6U2WkwOw1GC_PflLmt2LvD_vWwQH-EDmrq_P1hbouzccx26UI5xrgAKZl8ur5JsXoqf-J6g9nM0cZpXo8BdExCS7WWwOqr3bV4xb7sMawKH0Mligu4rHZCRjcZn8Lz3_8Hp3aTLg</recordid><startdate>199502</startdate><enddate>199502</enddate><creator>Hediger, Mary L.</creator><creator>Scholl, Theresa O.</creator><creator>Schall, Joan I.</creator><creator>Miller, Laurie W.</creator><creator>Fischer, Richard L.</creator><general>Elsevier Inc</general><general>The American College of Obstetricians and Gynecologists</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199502</creationdate><title>Fetal growth and the etiology of preterm delivery</title><author>Hediger, Mary L. ; Scholl, Theresa O. ; Schall, Joan I. ; Miller, Laurie W. ; Fischer, Richard L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4313-3ad456bf7808475471f0d930cedaec63c3493a0dc8bdd7b60d015ab499cd88bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Birth Weight</topic><topic>Cohort Studies</topic><topic>Delivery. Postpartum. Lactation</topic><topic>Disorders</topic><topic>Embryonic and Fetal Development</topic><topic>Female</topic><topic>Gestational Age</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Obstetric Labor, Premature - physiopathology</topic><topic>Pregnancy</topic><topic>Pregnancy Outcome</topic><topic>Prospective Studies</topic><topic>Ultrasonography, Prenatal</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hediger, Mary L.</creatorcontrib><creatorcontrib>Scholl, Theresa O.</creatorcontrib><creatorcontrib>Schall, Joan I.</creatorcontrib><creatorcontrib>Miller, Laurie W.</creatorcontrib><creatorcontrib>Fischer, Richard L.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Obstetrics and gynecology (New York. 1953)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hediger, Mary L.</au><au>Scholl, Theresa O.</au><au>Schall, Joan I.</au><au>Miller, Laurie W.</au><au>Fischer, Richard L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fetal growth and the etiology of preterm delivery</atitle><jtitle>Obstetrics and gynecology (New York. 1953)</jtitle><addtitle>Obstet Gynecol</addtitle><date>1995-02</date><risdate>1995</risdate><volume>85</volume><issue>2</issue><spage>175</spage><epage>182</epage><pages>175-182</pages><issn>0029-7844</issn><eissn>1873-233X</eissn><coden>OBGNAS</coden><abstract>To confirm that preterm delivery is associated with fetal growth restriction (FGR), and to determine if the various etiologies of preterm delivery are associated with the same degree and type of FGR.
Two hundred ninety young, primarily minority gravidas who had routine initial ultrasound examinations also had subsequent ultrasound examinations at 32 weeks' gestation. Fetal growth characteristics were compared between preterm (less than 37 weeks' gestation) and term deliveries, and among preterm deliveries with medical or obstetric indications, premature rupture of membranes (PROM), and spontaneous preterm labor.
Forty-six infants (15.9%) were born preterm. At 32 weeks' gestation, all fetuses later delivered preterm were already smaller than fetuses later delivered at term (
P < .05) for all dimensions: head circumference (HC), abdominal circumference (AC), biparietal diameter (BPD), and femur length (FL). However, after stratifying by cause of preterm delivery for those fetuses later delivered for medical or obstetric indications, we found that only AC was decreased (
P < .01) and that the HC-AC ratio was elevated (asymmetric FGR). Neonates delivered after unsuccessfully treated PROM or preterm labor were symmetrically smaller in all characteristics (HC, AC, BPD, and FL).
By 32 weeks' gestation, fetuses later delivered preterm are already significantly smaller than fetuses later delivered at term. However, when stratified by the etiology of preterm delivery, infants delivered preterm for medical or obstetric indications had asymmetric growth patterns, which suggests a growth failure late in pregnancy. Infants delivered preterm after PROM or after failed or no tocolysis for spontaneous preterm labor were proportionately smaller, implying an overall slowing of growth that may originate early in pregnancy and possibly demonstrate a more chronic stress.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>7824227</pmid><doi>10.1016/0029-7844(94)00365-K</doi><tpages>8</tpages></addata></record> |
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subjects | Adult Biological and medical sciences Birth Weight Cohort Studies Delivery. Postpartum. Lactation Disorders Embryonic and Fetal Development Female Gestational Age Gynecology. Andrology. Obstetrics Humans Male Medical sciences Obstetric Labor, Premature - physiopathology Pregnancy Pregnancy Outcome Prospective Studies Ultrasonography, Prenatal |
title | Fetal growth and the etiology of preterm delivery |
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