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.
CONCLUSION: 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.
LEVEL OF EVIDENCE: III
Amniotic fluid eicosanoids vary in preterm and term births, and oxidative stress is associated with cigarette smoking and term parturition.
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.
Supported in part by PHS grant UL1 RR025008 from the Clinical and Translational Science Award program, National Institutes of Health, National Center for Research Resources, and University Research Committee award (2009163) to Ramkumar Menon.
Corresponding author: Ramkumar Menon, PhD, Departments of Epidemiology and Gynecology and Obstetrics, Emory University, Room 4053, 1518 Clifton Road NE, Atlanta, GA 30322; e-mail: email@example.com.
Financial Disclosure The authors did not report any potential conflicts of interest.