title: Amniotic fluid eicosanoids in preterm and term births: effects of risk factors for spontaneous preterm labor.
abstract: OBJECTIVE
  To evaluate amniotic fluid arachidonic acid metabolites using enzymatic and nonenzymatic (lipid peroxidation) pathways in spontaneous preterm birth and term births, and to estimate whether prostanoid concentrations correlate with risk factors (race, cigarette smoking, and microbial invasion of amniotic cavity) associated with preterm birth.
  
  
  METHODS
  In a case-control study, amniotic fluid was collected at the time of labor or during cesarean delivery. Amniotic fluid samples were subjected to gas chromatography, negative ion chemical ionization, and mass spectrometry for prostaglandin (PG) E2, PGF2α, and PGD2 and for 6-keto-PGF1α (thromboxane 2 and F2-isoprostane). Primary analysis examined differences between prostanoid concentrations in preterm birth (n=133) compared with term births (n=189). Secondary stratified analyses (by race, cigarette smoking, and microbial invasion of amniotic cavity) compared eicosanoid concentrations in three epidemiological risk factors.
  
  
  RESULTS
  Amniotic fluid F2-isoprostane, PGE2, and PGD2 were significantly higher at term than in preterm birth, whereas PGF2α was higher in preterm birth 6-keto-PGF1α and thromboxane 2 concentrations were not different. Data stratified by race (African American or white) showed no significant disparity among prostanoid concentrations. Regardless of gestational age status, F2-isoprostane was threefold higher in smokers, and other eicosanoids were also higher in smokers compared with nonsmokers. Preterm birth with microbial invasion of amniotic cavity had significantly higher F2-isoprostane compared with preterm birth without microbial invasion of amniotic cavity.
  
  
  CONCLUSIONS
  Most amniotic fluid eicosanoid concentrations (F2-isoprostane, PGE2, and PGD2), are higher at term than in preterm births. The only amniotic fluid eicosanoid that is not higher at term is PGF2α.
authors.affiliation: From the Departments of Epidemiology and Biostatistics, Rollins School of Public Health, and the Department of Gynecology and Obstetrics, Emory University, Atlanta, Georgia; The Perinatal Research Center, Nashville, Tennessee; the Division of Clinical Pharmacology, Eicosanoid Core Laboratory, Vanderbilt University, Nashville, Tennessee; and the Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia.
authors.forename: Ramkumar
authors.initials: R
authors.lastname: Menon
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Fortunato
authors.forename: Ginger L
authors.initials: GL
authors.lastname: Milne
authors.forename: Lina
authors.initials: L
authors.lastname: Brou
authors.forename: Claudine
authors.initials: C
authors.lastname: Carnevale
authors.forename: Stephanie C
authors.initials: SC
authors.lastname: Sanchez
authors.forename: Leah
authors.initials: L
authors.lastname: Hubbard
authors.forename: Martha
authors.initials: M
authors.lastname: Lappas
authors.forename: Cayce Owens
authors.initials: CO
authors.lastname: Drobek
authors.forename: Robert N
authors.initials: RN
authors.lastname: Taylor
mesh_terms: D000653:Amniotic Fluid / Q000378:metabolism*; D001034:Apgar Score; D016718:Arachidonic Acid / Q000378:metabolism*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D015237:Dinoprost / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D028441:F2-Isoprostanes / Q000378:metabolism; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation; D013058:Mass Spectrometry; D007752:Obstetric Labor, Premature / Q000453:epidemiology* / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology; D011247:Pregnancy; D015230:Prostaglandin D2 / Q000378:metabolism; D012907:Smoking / Q000503:physiopathology; D047929:Term Birth / Q000378:metabolism*
chemical_list: D028441:F2-Isoprostanes; D016718:Arachidonic Acid; D015237:Dinoprost; D015232:Dinoprostone; D015230:Prostaglandin D2