Author(s)

Stephen Walker

Affiliation(s)

Mercy Hospital for Women, Heidelberg, Australia.

Corresponding Author

Stephen Walker

ABSTRACT

Preeclampsia (PE) is one of the common serious complications during pregnancy, with an incidence rate of about 5% to 8%. It is the main cause of maternal death and poor fetal prognosis. The main manifestations of PE are systolic blood pressure = 140 mmHg or diastolic blood pressure = 90 mmHg after 20 weeks of pregnancy, accompanied by proteinuria, or involvement of organs or systems such as the heart, lungs, liver, kidneys, and coagulation system. Clinical practice shows that PE not only endangers maternal health, but is also closely related to fetal intrauterine growth restriction, premature birth, and low birth weight infants. It is estimated that 76,000 pregnant women and 500,000 fetuses die from this disease every year worldwide [1]. In addition, pregnant women who develop PE are at increased risk of future cardiovascular disease and end-stage renal disease. Children born to mothers with preeclampsia are also more likely to develop hypertension, stroke, cognitive decline and depression as adults [2]. Therefore, early prediction, diagnosis and timely intervention of PE are crucial to improving patient prognosis and pregnancy outcomes. Relying solely on high-risk factors such as patient race, age, previous history of eclampsia, and obesity to predict PE is limited, so more research has focused on the identification of high-risk predictors. Current relevant biological research is mainly based on the pathophysiological changes of PE. The basic pathophysiological changes of PE are systemic small vessel spasm, endothelial damage and local ischemia. Its pathogenesis is related to many factors such as genetics, immunity, placental ischemia and hypoxia, endothelial dysfunction and so on. It is currently believed that the disease progression of PE includes two stages: (1) During the formation of the placenta, the invasion of the extravillous trophoblast into the muscular layer of the uterine spiral artery is insufficient, the remodeling of the uterine spiral artery is obstructed, and the fetal blood flow supply is limited; oxidative stress The stimulation reaction further aggravates placental ischemia, causing hypoperfusion, inflammation, cell apoptosis and structural damage. (2) The stage of organ damage, leading to the occurrence of various clinical signs. In recent years, with the widespread application of genomics, proteomics, and metabolomics in clinical research on PE, a series of PE-related markers for vascular endothelial cells, metabolism, oxidative stress, placenta, hemolysis, and inflammation have been discovered. It can be used as a candidate biomarker for predicting and diagnosing PE. There are currently more than a hundred types of biological markers used to predict or elucidate the pathological mechanisms of PE. The author briefly reviews the latest markers with clinical application potential in research in the past 10 years.

KEYWORDS

Preeclampsia; Pregnancy; Complications; Biomarkers

CITE THIS PAPER

Stephen Walker. Thorough investigation of biomarkers for the prediction of preeclampsia. World Journal of Biomedical Sciences. 2024, 2(2): 1-5. DOI: 10.61784/wjbsv2n229.

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