{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T13:42:08Z","timestamp":1774878128969,"version":"3.50.1"},"reference-count":31,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2005,6,29]],"date-time":"2005-06-29T00:00:00Z","timestamp":1120003200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["obgyn.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["BJOG"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p><jats:bold>Objective\u2003<\/jats:bold> To evaluate levels of 24\u2010hour urine insulin excretion before the onset of pre\u2010eclampsia and gestational hypertension.<\/jats:p><jats:p><jats:bold>Design\u2003<\/jats:bold> Nested case\u2013control study within the Calcium for Preeclampsia Prevention (CPEP) study cohort.<\/jats:p><jats:p><jats:bold>Setting\u2003<\/jats:bold> Five university medical centres in the United States.<\/jats:p><jats:p><jats:bold>Sample\u2003<\/jats:bold> Cases had developed pre\u2010eclampsia (<jats:italic>n<\/jats:italic>= 70) or gestational hypertension (<jats:italic>n<\/jats:italic>= 142) in the absence of gestational diabetes. Controls (<jats:italic>n<\/jats:italic>= 429) had remained normotensive without gestational diabetes.<\/jats:p><jats:p><jats:bold>Methods\u2003<\/jats:bold> Subjects were required to have had an adequate baseline 24\u2010hour urine collection prior to CPEP enrolment at 13\u201321 weeks. Controls were matched to cases by enrolment site and specimen storage time, without regard to gestational age or CPEP treatment. Adjusted mean 24\u2010hour urine insulin excretion was, however, calculated using analysis of covariance, with adjustment models for pre\u2010eclampsia considering body mass index, race and smoking status; and for gestational hypertension, gestational age at specimen collection, height, body mass index and smoking. Urine insulin was measured by radio\u2010immunoassay.<\/jats:p><jats:p><jats:bold>Main outcome measures\u2003<\/jats:bold> Twenty\u2010four\u2010hour urine insulin excretion.<\/jats:p><jats:p><jats:bold>Results\u2003<\/jats:bold> Adjusted 24\u2010hour urine insulin excretion at baseline (mean 17 weeks of gestation) was greater in women who developed pre\u2010eclampsia than in normotensive controls (mean [SE]: 15.6 [1.5] <jats:italic>vs<\/jats:italic> 13.1 [1.2] \u00d7 10<jats:sup>3<\/jats:sup>\u03bcIU\/24 hour, <jats:italic>P<\/jats:italic>= 0.06), but not in women who developed gestational hypertension (14.7 [0.9] <jats:italic>vs<\/jats:italic> 15.0 [0.6] \u00d7 10<jats:sup>3<\/jats:sup>\u03bcIU\/24 hour, <jats:italic>P<\/jats:italic>= 0.79, in cases <jats:italic>vs<\/jats:italic> controls). Among women who developed pre\u2010eclampsia, adjusted urine insulin excretion was greater than controls only in women with mild pre\u2010eclampsia and not in severe pre\u2010eclampsia (mild pre\u2010eclampsia <jats:italic>vs<\/jats:italic> controls: 17.3 [2.0] <jats:italic>vs<\/jats:italic> 13.7 [1.6] \u00d7 10<jats:sup>3<\/jats:sup>\u03bcIU\/24 hour, <jats:italic>P<\/jats:italic>= 0.04; severe pre\u2010eclampsia <jats:italic>vs<\/jats:italic> controls: 12.3 [2.2] <jats:italic>vs<\/jats:italic> 11.5 [1.2], <jats:italic>P<\/jats:italic>= 0.69).<\/jats:p><jats:p><jats:bold>Conclusion\u2003<\/jats:bold> The data suggest that early hyperinsulinaemia, a marker of insulin resistance, may predispose to mild pre\u2010eclampsia.<\/jats:p>","DOI":"10.1111\/j.1471-0528.2005.00720.x","type":"journal-article","created":{"date-parts":[[2005,10,17]],"date-time":"2005-10-17T05:59:09Z","timestamp":1129528749000},"page":"1479-1485","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Twenty\u2010four\u2010hour urine insulin as a measure of hyperinsulinaemia\/insulin resistance before onset of pre\u2010eclampsia and gestational hypertension"],"prefix":"10.1111","volume":"112","author":[{"given":"Stephen P.","family":"Emery","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard J.","family":"Levine","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cong","family":"Qian","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marian G.","family":"Ewell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucinda J.","family":"England","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kai F.","family":"Yu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrick M.","family":"Catalano","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"name":"for the CPEP Study Group","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,9,22]]},"reference":[{"key":"e_1_2_6_2_2","first-page":"E15","article-title":"Insulin action and resistance in obesity and non\u2010insulin\u2010dependent type II diabetes mellitus","volume":"243","author":"Olefsky JM","year":"1982","journal-title":"Am J 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