Preeclampsia, eclampsia, and HELLP syndrome, are a continuum of a dangerous disease process that can occur in pregnancy. Preeclampsia is defined by new onset hypertension and proteinuria. In more severe cases, preeclampsia can be associated with pulmonary edema, oliguria, persistent headaches, and impaired liver function. These symptoms reveal maternal end organ damage which may result in danger to the fetus such as oligohydramnios, decreased fetal growth, and placental abruption. The defining difference between preeclampsia and eclampsia is the presence of new onset seizure activity. HELLP syndrome occurs when the mother experiences hemolysis, elevated liver enzymes, and low platelets. This syndrome is seen in about 0.6% of pregnancies. Each of these conditions (preeclampsia, eclampsia, and HELLP) increase both the fetal and maternal morbidity and mortality rates with the most definitive cure being delivery of child and placenta.A 28 year-old Caucasian, G1P0 female at 26w4d presented to OB triage on the recommendation of her physician due to elevated uric acid levels and a recorded blood pressure of 180/110. The patient reported rapid onset of weight gain, facial edema, diminished fetal movements, and frequent headaches. Although the patient denied labor symptoms, she complained of back pain and was admitted to the hospital at 26w4d for observation due to elevated blood pressures. The patient was diagnosed with preeclampsia with severe features. As her presentation progressed, the patient developed massive ascites and pulmonary edema along with decreasing platelet counts and increasing liver enzyme values. Due to decreasing biophysical profile (BPP) scores of the fetus and decompensating lab values of the mother, an emergency cesarean was performed for the safety of mother and baby.This case presentation demonstrates the progression of hypertensive disorders of pregnancy with a rare and severe presentation of early-onset preeclampsia with severe features, pulmonary edema, and massive ascites that ultimately led to class III HELLP syndrome and extreme prematurity of the infant.
MALAT1 sponges miR-26a and miR-26b to regulate endothelial cell angiogenesis via PFKFB3-driven glycolysis in early-onset preeclampsia