Hematological Markers: Emerging Diagnostic and Therapeutic Targets in Preeclampsia

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Preeclampsia is a morbid hypertensive disease with an onset at &gt;20 weeks ofgestation. It has a global incidence of 2-10%, contributing to a large share of fetal andmaternal mortality. Pathophysiology of the disease is multifaceted with theinvolvement of immunological, genetic, and inflammatory factors. Faulty placentationwith abnormal angiogenesis and apoptosis is pivotal with subsequent hypoxia andoxidative stress leading to widespread systemic inflammation. For years placenta hasbeen the center of research to elucidate the pathogenesis and treatment strategies ofpreeclampsia. Recently numerous circulating immunological, genetic, andinflammatory markers have emerged as a focus of interest and intrigued the researchersto mark their contribution to the pathogenesis of the disease. Elevated levels of proinflammatoryfactors like Tumor Necrosis Factor-alpha (TNF-α), soluble Endoglin(sENG), soluble Flt-1 (sFlt-1), Nuclear factor kappa B (NFκB), Interleukin 6 (IL-6),Interleukin 8 (IL-8), and Angiotensin II, etc. have been labeled as contributors to thematernal endothelial dysfunction, a hallmark of preeclampsia. MicroRNAs (theemerging field of research) belong to the noncoding RNAs that can modulate theexpression of these inflammatory markers. Recent reports on the differential profile ofvarious microRNAs in preeclampsia have focused on using these as diagnostic andtherapeutic targets. Modifying the expression levels of different genes involved ininflammation, angiogenesis, and apoptosis can change the clinical picture andprognosis of the disease.