Abstract
Hypertensive disorders of pregnancy (HDP) are the most common cardiometabolic complications of pregnancy, affecting nearly 10% of US pregnancies and contributing substantially to maternal and infant morbidity and mortality. In the US, women of African American race are at increased risk for HDP. Early biomarkers that reliably identify women at risk for HDP remain elusive, yet are essential for the early identification and targeting of interventions to improve maternal and infant outcomes. We employed high-resolution metabolomics (HRM) to identify metabolites and metabolic pathways that were altered in early (8-14 weeks) gestation serum samples of pregnant African American women who developed HDP after 20 weeks' gestation (n = 20)—either preeclampsia (PE; n = 11) or gestational hypertension (gHTN; n = 9)—compared to those who delivered full term without complications (n = 80). We found four metabolic pathways that were significantly (p < 0.05) altered in women who developed PE and five pathways that were significantly (p < 0.05) altered in women who developed gHTN compared to women who delivered full term without complications. We also found that four specific metabolites (p < 0.05) were distinctly upregulated (retinoate, kynurenine) or downregulated (SN-glycero-3-phosphocholine, 2′4′-dihydroxyacetophenone) in women who developed PE compared to gHTN. These findings support that there are systemic metabolic disruptions that are detectable in early pregnancy (8-14 weeks of gestation) among pregnant African American women who develop PE and gHTN. Furthermore, the early pregnancy metabolic disruptions associated with PE and gHTN are distinct, implying they are unique entities rather than conditions along a spectrum of the same disease process despite the common clinical feature of high blood pressure.
Highlights
Hypertensive disorders of pregnancy (HDP) include gestational hypertension, preeclampsia (PE) that is de novo or superimposed on preexisting chronic hypertension, and preexisting chronic hypertension [1]
In the US, women of African American race are at the highest risk for developing HDP, and their overall pregnancy-related mortality ratio is 3.4 times higher relative to white women [4]
The purpose of the current study was to expand this body of inquiry and employ high-resolution metabolomics (HRM) on early (8-14 weeks) gestation serum samples to identify metabolites and metabolic pathways that were altered among AA women who developed HDP (PE and/or gestational hypertension (gHTN)) compared to those who delivered full term without complications
Summary
Hypertensive disorders of pregnancy (HDP) include gestational hypertension (gHTN), preeclampsia (PE) that is de novo or superimposed on preexisting chronic hypertension, and preexisting chronic hypertension [1]. HDP are responsible for 76,000 maternal and 500,000 infant deaths globally each year. Together they are the most common cardiometabolic complications of pregnancy, affecting nearly 10% of US pregnancies [2] and have been increasing in recent years [3]. Risk factors for gHTN include obesity, maternal age less than 20 or more than 40 years, and family history. Risk factors for PE are less understood but include both nulliparity and grand multiparity, history of PE or chronic hypertension, diabetes, renal disease, and obesity [5, 6]. Despite the tremendous morbidity and mortality burden of HDP, the etiology and pathogenesis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
