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dc.contributor.authorLynch, Caoimhe M
dc.contributor.authorO'Kelly, Ruth
dc.contributor.authorStuart, Bernard
dc.contributor.authorTreumann, Achim
dc.contributor.authorConroy, Ronan
dc.contributor.authorRegan, Carmen L
dc.date.accessioned2012-02-01T10:57:10Z
dc.date.available2012-02-01T10:57:10Z
dc.date.issued2012-02-01T10:57:10Z
dc.identifier.citationProstaglandins Other Lipid Mediat. 2011 Aug;95(1-4):63-7. doi:, 10.1016/j.prostaglandins.2011.06.007. Epub 2011 Jun 23.en_GB
dc.identifier.issn1098-8823 (Print)en_GB
dc.identifier.issn1098-8823 (Linking)en_GB
dc.identifier.pmid21723954en_GB
dc.identifier.doi10.1016/j.prostaglandins.2011.06.007en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207996
dc.description.abstractBACKGROUND: To examine the effect of maternal smoking in pregnancy on the production of two eicosanoids, thromboxane A(2) and prostacyclin I2, and their role in the pathogenesis of intrauterine growth restriction. METHODS: Prospective case control study enrolled smoking and non-smoking women at
dc.language.isoengen_GB
dc.subject.mesh6-Ketoprostaglandin F1 alpha/analogs & derivatives/urineen_GB
dc.subject.meshAdulten_GB
dc.subject.meshCase-Control Studiesen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshFetal Growth Retardation/*etiology/metabolismen_GB
dc.subject.meshHumansen_GB
dc.subject.meshPregnancyen_GB
dc.subject.meshSmoking/*adverse effectsen_GB
dc.subject.meshThromboxane A2/*metabolismen_GB
dc.subject.meshThromboxane B2/analogs & derivatives/urineen_GB
dc.subject.meshYoung Adulten_GB
dc.titleThe role of thromboxane A(2) in the pathogenesis of intrauterine growth restriction associated with maternal smoking in pregnancy.en_GB
dc.contributor.departmentCoombe Women and Infants University Hospital, Dublin, Ireland., caoimhemlynch@eircom.neten_GB
dc.identifier.journalProstaglandins & other lipid mediatorsen_GB
dc.description.provinceLeinster
html.description.abstractBACKGROUND: To examine the effect of maternal smoking in pregnancy on the production of two eicosanoids, thromboxane A(2) and prostacyclin I2, and their role in the pathogenesis of intrauterine growth restriction. METHODS: Prospective case control study enrolled smoking and non-smoking women at </=14 weeks gestation. Maternal urine samples were obtained at </=14, 28 and 36 weeks. High performance liquid chromatography tandem mass spectrometry (LC-MS-MS) was used to quantify 11-dehydrothromboxane B(2) (TX-M) and 2,3 dinor-6-ketoprostaglandin F1alpha (PG-M), stable urinary metabolites of thromboxane A(2) and prostacyclin I2. Confirmation of the smoking status was performed by quantitation of urinary nicotine metabolites. Data was analysed using SPSS and Stata((R)). RESULTS: Thirty five were enrolled in the smoking group and 32 in the non-smoking group. Smoking resulted higher levels of TX-M at </=14, 28 and 36 weeks gestation. There was no difference in PG-M at any gestational time point between the two groups. The median customised birthweight centile in the smoking group was 17.0 (0-78) compared to 55.5 (4-100) in the non-smoking group (P<0.001). A causal relationship between elevated TX-M and IUGR could not be established. CONCLUSIONS: Maternal smoking in pregnancy is associated with altered eicosanoid production in favour of the vasoconstrictor thromboxane A(2) which occurs early in the first trimester.


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