{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T05:27:24Z","timestamp":1783488444622,"version":"3.55.0"},"reference-count":26,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2015,1,2]],"date-time":"2015-01-02T00:00:00Z","timestamp":1420156800000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["obgyn.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Ultrasound in Obstet &amp;amp; Gyne"],"published-print":{"date-parts":[[2015,1]]},"abstract":"<jats:title><jats:styled-content style=\"fixed-case\">ABSTRACT<\/jats:styled-content><\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>To characterize the types of genetic abnormalities and their prevalence in early pregnancy loss at different developmental stages. We hypothesized that the prevalence of genetic abnormalities in pregnancy loss would differ across developmental stages.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Women with a pregnancy loss at &lt;\u200920\u2009weeks' gestation (<jats:italic>n<\/jats:italic>\u2009=\u200986) were enrolled at the time of diagnosis. Maternal tissue without a fetal component was found in 13 samples. Chromosomal microarray analysis (<jats:styled-content style=\"fixed-case\">CMA<\/jats:styled-content>) was performed on 74 samples (including two samples from a twin pregnancy); 15 were pre\u2010embryonic (no visible embryo on ultrasound examination), 31 were embryonic (embryo; 6\u2009+\u20090 to 9\u2009+\u20096\u2009weeks' gestation) and 28 were fetal (fetus; 10\u2009+\u20090 to 19\u2009+\u20096\u2009weeks' gestation) losses. The twin pregnancy was found to be monochorionic diamniotic  and was subsequently treated as a single sample in our analysis. Nine samples that underwent <jats:styled-content style=\"fixed-case\">CMA<\/jats:styled-content> were excluded from analysis because of 100% maternal\u2010cell contamination.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The overall prevalence of genetic abnormalities differed across developmental stages (9.1% pre\u2010embryonic, 69.2% embryonic and 33.3% fetal; <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.01). This difference persisted when comparing pre\u2010embryonic with embryonic samples (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.01) and embryonic with fetal samples (<jats:italic>P<\/jats:italic>\u2009=\u20090.02) but not pre\u2010embryonic with fetal samples (<jats:italic>P<\/jats:italic>\u2009=\u20090.12). Additionally, the prevalence of aneuploidy differed significantly across developmental stages (0.0% in pre\u2010embryonic samples <jats:italic>vs<\/jats:italic> 65.4% in embryonic samples <jats:italic>vs<\/jats:italic> 25.9% in fetal samples, <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001). Abnormalities were most common in embryonic cases, followed by fetal and then pre\u2010embryonic. Maternal cell contamination (<jats:styled-content style=\"fixed-case\">MCC<\/jats:styled-content>) was noted in 47.4% of 46,<jats:styled-content style=\"fixed-case\">XX<\/jats:styled-content> cases assessed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Genetic abnormalities detected by <jats:styled-content style=\"fixed-case\">CMA<\/jats:styled-content> are more likely to occur in the embryonic period than in pre\u2010embryonic or fetal stages. <jats:styled-content style=\"fixed-case\">MCC<\/jats:styled-content> is common in early pregnancy loss and should be excluded when results demonstrate a 46,<jats:styled-content style=\"fixed-case\">XX<\/jats:styled-content> karyotype. Copyright \u00a9 2014 ISUOG. Published by John Wiley &amp; Sons Ltd.<\/jats:p><\/jats:sec>","DOI":"10.1002\/uog.14713","type":"journal-article","created":{"date-parts":[[2014,10,31]],"date-time":"2014-10-31T08:09:11Z","timestamp":1414742951000},"page":"89-94","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":49,"title":["Differentiation\u2009of\u2009genetic\u2009abnormalities\u2009in\u2009early\u2009pregnancy loss"],"prefix":"10.1002","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2133-382X","authenticated-orcid":false,"given":"S. T.","family":"Romero","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology University of Utah School of Medicine  Salt Lake City UT USA"},{"name":"Division of Maternal Fetal Medicine Intermountain Medical Center  Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K. B.","family":"Geiersbach","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Utah School of Medicine  Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. N.","family":"Paxton","sequence":"additional","affiliation":[{"name":"ARUP Institute for Clinical and Experimental Pathology\u00ae University of Utah School of Medicine  Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N. C.","family":"Rose","sequence":"additional","affiliation":[{"name":"Division of Maternal Fetal Medicine Intermountain Medical Center  Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. F.","family":"Schisterman","sequence":"additional","affiliation":[{"name":"Epidemiology Branch Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health  Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. W.","family":"Branch","sequence":"additional","affiliation":[{"name":"Division of Maternal Fetal Medicine Intermountain Medical Center  Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. M.","family":"Silver","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology University of Utah School of Medicine  Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,1,2]]},"reference":[{"key":"e_1_2_6_2_1","first-page":"1","article-title":"Cytogenetics of pregnancy wastage","volume":"14","author":"Boue A","year":"1985","journal-title":"Adv Hum Genet"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-1809.1980.tb00955.x"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1097\/GRF.0b013e318161719c"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4419-1688-4"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1097\/AOG.0b013e3181bc6ab0"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/1471-0528.12382"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1086\/302878"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1203382"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1201569"},{"key":"e_1_2_6_11_1","unstructured":"Database of Genomic Variants.dgv.tcag.ca[Accessed 7 August 2013]."},{"key":"e_1_2_6_12_1","unstructured":"The International Standards for Cytogenomic Arrays Consortium.http:\/\/www.iscaconsortium.org[Accessed 7 August 2013]."},{"key":"e_1_2_6_13_1","unstructured":"Online Mendelian Inheritance in Man.http:\/\/www.ncbi.nlm.nih.gov\/omim[Accessed 7 August 2013]."},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-1809.1978.tb00930.x"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1097\/AOG.0b013e3182392977"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(14)60157-4"},{"key":"e_1_2_6_17_1","unstructured":"Associating Copy Number and SNP Variation with Human Disease. 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