Abstract
Aim.
To analyze current scientific data on the mechanisms of impaired blood oxygen transport function in pregnant women with COVID-19.
Materials and methods.
A systematic search and pathophysiological analysis of relevant literature in the PubMed, Google Scholar, and eLibrary databases for the period 2015–2026 was conducted using the keywords: pregnancy, COVID-19, SARS-CoV-2, hemic hypoxia, erythron, hemoglobin, cytokine storm, hepcidin, hypoxia-inducible factor (HIF). Based on the inclusion criteria, 47 publications were selected and reviewed in detail.
Results.
It was substantiated that gestational remodeling (physiological hemodilution and increased tissue oxygen demand) initially reduces the adaptive reserve of the oxygenation system. The key factor in the development of hemic hypoxia in COVID-19 was established to be complex, mediated damage to the erythron: cytokine-induced hepcidin-ferroportin blockade (anemia of inflammation), viral infection of erythroid precursor cells in the bone marrow, as well as membranopathy and hemolysis of mature erythrocytes driven by oxidative stress. The role of HIF-1α as a trigger of the vicious cycle of hypoxia and inflammation is described. These disturbances were shown to form a three-phase cascade (hyperinflammation → hemic hypoxia → thromboembolic complications), which manifests predominantly during infection in the third trimester of gestation, critically increasing the risk of severe obstetric and fetal complications.
Conclusion. I
mpairment of blood oxygen transport function in pregnant women with COVID-19 is multifactorial, with the leading role belonging to functional and structural dysfunction of the erythron. Understanding the molecular mechanisms of this process substantiates the ineffectiveness of standard isolated iron therapy in anemia of inflammation. This necessitates the development of fundamentally new, comprehensive approaches to early diagnosis, pathogenetic therapy, and prevention of hemic hypoxia to reduce maternal and perinatal losses.