Date of Award
Preeclampsia (PE) is responsible for about 20% of the 13 million preterm births each year worldwide, including 100,000 cases annually in the United States. Despite being a leading cause of maternal and perinatal morbidity, the mechanisms of pathogenesis are still largely unknown. PE is progesterone deficient state characterized by hypertension, chronic immune activation, endothelial dysfunction and severe forms can lead to seizures. Treatment of seizures includes the administration of magnesium sulfate (MgSO4) though not all PE patients are responsive, and it does not decrease PE-associated hypertension. To resolve these conditions, PE patients are delivered early thereby making PE the leading cause for fetal mortality and morbidity worldwide. Hypothesizing that the reduced progesterone levels accounted for the onset of hypertension in PE, the effects of both 17-hydroxyprogesterone caproate (17-OHPC) and Progesterone Induced Blocking Factor (PIBF) were studied in hypertensive pregnant rat models of PE. Following the intervention, blood pressure and endothelin-1 were reduced while nitric oxide was elevated.
Comley, Kyleigh M., "The Effects of Progesterone Induced Blocking Factor and 17-Hydroxyprogesterone Caproate on the Pathophysiology of Preeclampsia" (2021). Honors Theses. 1676.
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