{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T15:25:11Z","timestamp":1787239511157,"version":"build-2736575974"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2010,12,31]],"date-time":"2010-12-31T00:00:00Z","timestamp":1293753600000},"content-version":"vor","delay-in-days":943,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["obgyn.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Obstet Gynecol Scand"],"published-print":{"date-parts":[[2008,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Objective.<\/jats:italic>\n                    There is growing evidence that hypertensive pregnancy complications and other adverse pregnancy outcomes are associated with the presence of inherited or acquired thrombophilias. As hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome is one of the most severe forms of pre\u2010eclampsia we aimed to assess the prevalence of the factor V Leiden, the prothrombin 20210G &gt;A mutation and the methylenetetrahydrofolate reductase (MTHFR) 677C &gt;T polymorphism in women with HELLP syndrome and in their fetuses from the same index pregnancy.\n                    <jats:italic>Design.<\/jats:italic>\n                    The study was performed retrospectively in a case\u2013control design.\n                    <jats:italic>Sample.<\/jats:italic>\n                    Seventy\u2010one mother\u2013child pairs with HELLP syndrome and 79 control mother\u2013child pairs with uncomplicated pregnancies were included in the study.\n                    <jats:italic>Methods.<\/jats:italic>\n                    Genotyping of the three thrombophilic mutations was performed using the LightCycler technology. The chi\u2010squared test was used for statistical analysis. Main outcome measures were maternal and fetal genotypes and their correlation with clinical parameters.\n                    <jats:italic>Results.<\/jats:italic>\n                    Maternal heterozygosity for factor V Leiden was significantly more prevalent in the HELLP group than in controls (OR 4.45, 95% CI 1.31\u201315.31). No significant association was observed for maternal prothrombin mutation or MTHFR polymorphism (\n                    <jats:italic>p<\/jats:italic>\n                    = 0.894,\n                    <jats:italic>p<\/jats:italic>\n                    = 0.189, respectively). The fetal genotype was not associated with HELLP syndrome for any of the three mutations investigated. Analysis of gene\u2013gene interactions and genotype\u2013phenotype correlation with respect to clinical parameters and perinatal outcome revealed no further differences.\n                    <jats:italic>Conclusions.<\/jats:italic>\n                    Our study confirms that women heterozygous for factor V Leiden have an increased risk of developing HELLP syndrome, while the most frequent mutations of the prothrombin and MTHFR gene do not play a major role in the pathogenesis of HELLP syndrome.\n                  <\/jats:p>","DOI":"10.1080\/00016340802112740","type":"journal-article","created":{"date-parts":[[2008,5,12]],"date-time":"2008-05-12T13:04:54Z","timestamp":1210597494000},"page":"635-642","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Maternal factor V Leiden mutation is associated with HELLP syndrome in Caucasian women"],"prefix":"10.1111","volume":"87","author":[{"given":"SABINE","family":"MUETZE","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"BRIGITTE","family":"LEENERS","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"JAN R.","family":"ORTLEPP","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"SABINE","family":"KUSE","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"CARMEN G.","family":"TAG","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"RALF","family":"WEISKIRCHEN","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"AXEL M.","family":"GRESSNER","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"SABINE","family":"RUDNIK\u2010SCHOENEBORN","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"KLAUS","family":"ZERRES","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"WERNER","family":"RATH","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2010,12,31]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.1515\/JPM.2000.033"},{"key":"e_1_2_5_3_2","doi-asserted-by":"publisher","DOI":"10.1097\/00006254-200209000-00023"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1538-7836.2007.02501.x"},{"key":"e_1_2_5_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2141.2005.05847.x"},{"key":"e_1_2_5_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0049-3848(94)00138-4"},{"issue":"1","key":"e_1_2_5_7_2","doi-asserted-by":"crossref","first-page":"139","DOI":"10.1055\/s-0038-1642667","article-title":"New molecular insights into the genetics of thrombophilia. 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