Sophia Ali

 Introduction. Preeclampsia is a pregnancy complication defined as hypertension with either proteinuria, thrombocytopenia, impaired liver function, renal insufficiency, pulmonary edema, or new-onset cerebral or visual disturbances¹. The incidence of preeclampsia is between 3-5% of all pregnancies complications of preeclampsia result in one-third of all pregnancy-related deaths¹. Additionally, women who develop preeclampsia are at an increased risk for end-stage renal disease, chronic hypertension, heart failure, stroke, and death² Development of preeclampsia is due to the failure of embryonic trophoblasts to adequately invade the uterus and spiral arteries causing deficient spiral artery remodeling and inadequate utero-placental perfusion^1,3. Although much research has been conducted to better understand this condition, very little is known about the specific etiology, prevention, or treatment of preeclampsia. Several risk factors have been identified in developing preeclampsia which include previous preeclampsia, 40 years of age or older, family history, chronic autoimmune disease, type 1 diabetes mellitus, multiple gestation, nulliparity, obesity, preexisting hypertension, and preexisting renal disease¹. Studies have shown that toll-like receptors (TLRs) as well as inflammatory markers such as TNF-α, IL-6, and C-reactive protein are increased in women with preeclampsia as compared to normotensive women^4,5. Many bacterial and viral infections have been associated with preeclampsia⁶. These developments suggest potential treatment and prevention options for preeclampsia. Methods. Rat models were used in all studies. Preeclampsia was induced by injecting pregnant mice with lipopolysaccharide (LPS) or TLRs. Preeclamptic rats were then treated with a nitric-oxide (NO) mimetic, an immunosuppressant (Cyclosporin A), and placental expanded cells (PLX-PAD) to determine if there was an improvement in the clinical characteristics of preeclampsia and suppression of inflammation. All studies compared their results with controls. Results. Rats treated with a NO-mimetic showed prevention of altered uteroplacental perfusion, LPS-induced inflammation, renal structural and functional alterations, and increase in mean arterial pressure³. Rats treated with the immunosuppressant saw a significant reduction in systolic blood pressure, mean 24 hour urinary albumin excretion, pro-inflammatory cytokines and an increase in the anti-inflammatory cytokine IL-4⁷. PLX-PAD cells normalized systolic blood pressure, prevented increase in the urinary protein:creatinine ratio, reduced endothelial dysfunction, and restored placental health⁴. Conclusions. Studies have found several promising alternatives to decrease inflammation, systolic blood pressure, and preeclampsia like characteristics in rat models. NO-mimetics, immunosuppressants, and PLX-PAD cells may be treatment and prevention options for women with preeclampsia.

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7. Hu, B., Yang, J., Huang, Q., Bao, J., Brennecke, S. P., & Liu, H. (2016). Cyclosporin A significantly improves preeclampsia signs and suppresses inflammation in a rat model. Cytokine, 81, 77-81.