La Preeclàmpsia : etiologia, evolució i tractament

Abstract

Preeclampsia is a significant maternal health problem with the presence of hypertension

and proteinuria or other end-organ damage after twenty weeks of gestation, increasing

the risk of several serious complications. Its etiology is unclear, as it is a heterogeneous

syndrome with various clinical and pathophysiological presentations. The leading cause

is believed to be placental malperfusion resulting from the abnormal remodelling of the

spiral arteries, leading to a hypoxic environment and impaired nutrient and oxygen

transfer. Cytokines released due to hypoxia alter the maternal vascular response,

affecting immune homeostasis. Genetic events, particularly the FLT-1 gene, play an

essential role in developing preeclampsia, as do multiple cardiometabolic factors.

Preeclampsia develops in two stages: placental development in early pregnancy, and

systemic maternal endothelial dysregulation and inflammation. Preeclampsia has two

subtypes: early-onset, before the thirty-seventh week; and late-onset, from the thirtyfourth week of gestation. The risks are greater in early-onset preeclampsia.

For prevention, the use of aspirin at low doses (50-150 mg daily) before 16 weeks of

gestation reduces the risk of preeclampsia. Regarding detection, the Bayes theorem

developed by the Fetal Medicine Foundation makes it possible to estimate the specific

individual risks of preeclampsia, showing a high detection rate. The most significant

biomarkers in preeclampsia include serum placental growth factor (PIGF) and soluble

fms-like tyrosine kinase-1 ratio (sFLT-1). High levels of sFLT-1 and low levels of PIGF

are associated with a greater risk of preeclampsia. Endocan-1 is also a proposed

biomarker, as its levels increase in preeclampsia maternal plasma.

At the moment, the only definitive treatment for preeclampsia is delivery, but early

detection allows better intervention. Low-dose aspirin and curcumin have been proposed

as therapeutic options, as they reduce the risk of development. Finally, treatment with

magnesium sulfate reduces the occurrence of convulsions in eclampsia. Despite all

these advances, more research is still needed to understand the molecular mechanisms

better, discover new biomarkers, and contribute to improving diagnosis and treatment