Abstract
ObjectiveInflammatory 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 designA 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.ResultsHigher 5-α-pregnan-3β,20α-diol disulfate, and lower 1-linoleoylglycerophosphoethanolamine and octadecanedioate, predicted increased odds of preeclampsia.ConclusionsAmong 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.
Highlights
Preeclampsia is a gestation-specific syndrome, defined by the presence of hypertension combined with proteinuria or evidence of systemic disease that presents after 20 weeks gestational age (GA) [1]
Metabolomic analyses of blood and urine collected from women with preeclampsia versus healthy pregnancies have identified several potential metabolic pathways implicated in preeclampsia, including insulin resistance, mitochondrial dysfunction, energy metabolism disturbances, oxidative dysfunction and lipid dysfunction [3,4,5,6,7,8,9,10,11,12,13,14,15]
Women diagnosed with preeclampsia had marginally higher prepregnancy body mass index (BMI), t(127) = −1.92, p = 0.057 (27.6 ± 7.57 kg/m2 versus 25.3 ± 5.85 kg/m2)
Summary
Preeclampsia is a gestation-specific syndrome, defined by the presence of hypertension combined with proteinuria or evidence of systemic disease that presents after 20 weeks gestational age (GA) [1]. Affecting 2−8% of pregnancies, preeclampsia is a major cause of maternal mortality [2]. The etiology of preeclampsia is still poorly understood, it is considered to be a vascular disorder caused by distress signals released by an ischemic placenta [1]. Similar to nonpregnancy vascular and cardio-metabolic disorders, e.g. atherosclerosis and metabolic syndrome, preeclampsia is believed to have etiological roots in inflammatory and metabolic disturbances [1]. The evidence supports preeclampsia as a proinflammatory state [16,17,18,19,20,21,22,23]. Most studies of Second trimester inflammatory and metabolic markers in women delivering preterm with and without
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