THE EFFECT OF THE INFLAMMATORY RESPONSE ON THE DEVELOPMENT OF PREGNANCY COMPLICATED BY PREECLAMPSIA

Preeclampsia remains one of the main causes of obstetric and perinatal complications. The frequency of preeclampsia in the structure of pregnancy complications varies from 6 % to 12 % in healthy pregnant women and from 20 % to 40 % in pregnant women with extragenital pathology. There is growing interest in investigating the exact pathophysiological mechanism of the preeclampsia process as this may identify new potential screening biomarkers. There is evidence that inflammatory mechanisms are a key link between placental ischemia and endothelial dysfunction. It has been hypothesized that impaired regulatory systems are unable to regulate the resolution of inflammatory pathways, contributing to an exaggerated immune response. It is appropriate to call pregnancy a unique immune state that is modulated, but not suppressed. Modulation of the immune system leads to differentiated reactions depending on the stage of pregnancy. Each stage of pregnancy is characterized by a unique inflammatory state. The first and third trimesters are pro-inflammatory, while the second trimester is an anti-inflammatory phase. Proinflammatory mediators, such as IL-6, directly and indirectly through TNF-α, bradykinin, thrombin cause degradation of the endothelial glycocalyx, which leads to an increase in the permeability of the vascular wall with the progression of capillary leakage into the interstitial space. Inflammatory damage to the glycocalyx that occurs during preeclampsia increases intercellular permeability associated with leakage of fluid and albumin into the interstitial space. As a result of damage to the endothelium, there is an increase in the volume of extracellular fluid, which is manifested in women with severe preeclampsia in the form of edema with pathological fluid retention. Further studies are needed to clarify the role of inflammatory mediators in predicting the risk of developing preeclampsia. Further study of the problem will reveal potential targets for treatment, primarily related to inhibition of inflammatory processes and prevention of damage to the endothelial glycocalyx.