There are 2 clusters of term preeclampsia, supporting evidence of the disease’s heterogeneity, according to a recent study published in the American Journal of Obstetrics & Gynecology.
Takeaways
- Preeclampsia, affecting 3% to 7% of pregnancies, remains a significant cause of maternal and perinatal morbidity and mortality, with its prevalence rising in the United States, potentially linked to increasing obesity rates.
- The heterogeneity of preeclampsia is highlighted by the recommendation to categorize it based on onset and pathophysiological factors, such as "early- or late-onset" and "placental or maternal preeclampsia."
- Intravascular inflammation plays a crucial role in preeclampsia's pathogenesis, alongside the antiangiogenic state, yet understanding how these factors interact remains a challenge.
- A nested case-control study revealed distinct profiles among women with preeclampsia at term, with variations in angiogenic profiles, cytokine concentrations, and adverse maternal outcomes.
- Accurate subclassification of preeclampsia patients is essential for both research and clinical practice, offering insights into tailored management approaches and improved outcomes.
Preeclampsia has been reported in 3% to 7% of pregnancies, making it one of the leading causes of maternal and perinatal morbidity and mortality. A significant increase in disease onset has been observed in the United States in the previous 10 years, linked to rising obesity rates.
Data has indicated heterogeneity of preeclampsia, with experts recommending categorizing the disease as “early- or late-onset” and “placental or maternal preeclampsia.” However, challenges have persisted for prediction and prevention of preeclampsia at term.
Preeclampsia pathophysiology may be influenced by intravascular inflammation, but there is little data about how exaggerated intravascular inflammation coexists with an antiangiogenic state, which is central to the disease’s pathogenesis. To further evaluate the pathophysiology of preeclampsia at term, investigators conducted a nested case–control study.
Participants included women with preeclampsia at term and an available blood sample collected within 1 week before delivery. Study cohorts included women with preeclampsia at term and a normal angiogenic profile, those with preeclampsia and an abnormal angiogenic profile, and those with an uncomplicated pregnancy.
Exclusion criteria included multiple gestation, major obstetric complication, severe medical illness, chronic hypertension, asthma requiring steroids, active hepatitis, fetal anomalies, and needing antiplatelet or nonsteroidal anti-inflammatory drugs.
Preeclampsia was determined by hypertension onset after 20 weeks’ gestation and proteinuria, with hypertension defined as systolic 140 mm Hg or higher or diastolic 90 mm Hg or higher blood pressure. Blood pressure was measured twice, with a duration between 4 hours and 1 week separating measurements.
A urine protein level over 300 mg indicated proteinuria. Composite adverse maternal outcomes included stroke, blindness, eclampsia, elevated liver enzymes, myocardial ischemia, pulmonary edema, thrombocytopenia, acute kidney injury, hepatic hematoma, disseminated intravascular coagulopathy, placental abruption, and maternal death.
