4.3 Article

Second trimester inflammatory and metabolic markers in women delivering preterm with and without preeclampsia

期刊

JOURNAL OF PERINATOLOGY
卷 39, 期 2, 页码 314-320

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NATURE PUBLISHING GROUP
DOI: 10.1038/s41372-018-0275-8

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资金

  1. NIH/NHLBI grants [RC2 HL101748, RO1 HD-57192, R01 HD-52953]
  2. March of Dimes Prematurity Center at Stanford University School of Medicine
  3. Stanford Child Health Research Institute at Stanford University School of Medicine
  4. Stanford Clinical and Translational Science Award CTSA [UL1 TR001085]
  5. Bill and Melinda Gates Millennium grants [OPP52256, RSDP 5K12 HD-00849-23]
  6. March of Dimes grants [6-FY11-261, FY10-180]
  7. California Preterm Birth Initiative (PTBi-CA) at the University of California San Francisco
  8. National Institute for Health [R01 HD073491]
  9. Eunice Kennedy Shriver National Institute of Child Health and Human Development [R01 HD072021-01A1]

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Objective Inflammatory and metabolic pathways are implicated in preterm birth and preeclampsia. However, studies rarely compare second trimester inflammatory and metabolic markers between women who deliver preterm with and without preeclampsia. Study design A sample of 129 women (43 with preeclampsia) with preterm delivery was obtained from an existing population-based birth cohort. Banked second trimester serum samples were assayed for 267 inflammatory and metabolic markers. Backwards-stepwise logistic regression models were used to calculate odds ratios. Results Higher 5-alpha-pregnan-3 beta,20 alpha-diol disulfate, and lower 1-linoleoylglycerophosphoethanolamine and octadecanedioate, predicted increased odds of preeclampsia. Conclusions Among women with preterm births, those who developed preeclampsia differed with respect metabolic markers. These findings point to potential etiologic underpinnings for preeclampsia as a precursor to preterm birth.

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