Эффективность применения препаратов кальция и витамина д в лечении остеопороза в раннем климактерического периоде

Аннотация

This study systematically investigates the etiopathogenesis, clinical course, and histostructural changes of respiratory distress syndrome (RDS) in neonates born to mothers infected with COVID-19 during pregnancy. Histopathological evaluation revealed alveolar structural disorganization, intra-alveolar fibrinoid exudation, surfactant deficiency, interstitial hemorrhages, and microvascular perfusion defects. These alterations suggest that SARS-CoV-2-mediated placental injury contributes to intrauterine hypoxia and subsequent pulmonary dysfunction. The results provide a foundation for early diagnosis and optimization of neonatal intensive care protocols. 114 https://universalpublishings.com МЕДИЦИНА, ПЕДАГОГИКА И ТЕХНОЛОГИЯ: ТЕОРИЯ И ПРАКТИКА Researchbib Impact factor: 13.14/2024 SJIF 2024 = 5.444 Том 3, Выпуск 04, Апрель Introduction.The COVID-19 pandemic has posed significant challenges to global healthcare systems, particularly concerning maternal and neonatal health outcomes. The vertical impact of SARS-CoV-2 infection during pregnancy is now recognized as a critical concern, as it may lead to direct and indirect fetal complications. In particular, the virus's influence on the fetal pulmonary system may predispose newborns to serious postnatal respiratory conditions[2,4]. Respiratory distress syndrome (RDS), a common neonatal disorder characterized by surfactant deficiency and alveolar collapse, has long been a major contributor to neonatal morbidity and mortality, particularly among preterm infants. The emergence of SARS-CoV-2 introduces a new variable in this equation, as the virus has shown potential to affect the placenta, fetal circulation, and organogenesis, especially during the critical stages of lung maturation[7,20]. Current data indicate that SARS-CoV-2 can cause placental vasculopathy, chronic villitis, and intervillous thrombi, all of which are capable of inducing chronic intrauterine hypoxia. Hypoxia, in turn, disrupts the structural and functional development of the lungs. Moreover, inflammatory mediators, such as IL-6, TNF- alpha, and interferons released during maternal infection, may interfere with fetal surfactant synthesis and immune regulation. Such systemic responses may accelerate or exacerbate lung immaturity, compounding the risk for RDS even in near-term neonates[5,16]. Despite increased awareness, detailed investigations into the pathophysiological mechanisms linking maternal COVID-19 to neonatal RDS remain limited. This study aims to expand our understanding by integrating clinical findings with detailed histomorphological examination of neonatal lung tissues, offering new perspectives on disease characterization, prognosis, and therapeutic strategies[9,13,19]. Literature Review Hecht et al. (2020) and Patberg et al. (2021) reported extensive placental damage in pregnant women with COVID-19, including thrombotic lesions and inflammatory infiltrates. These changes are associated with impaired fetal oxygenation. Studies also suggest alterations in surfactant production due to inflammatory cytokines, such as TNF-α and IL-6, impacting type II pneumocyte 115 https://universalpublishings.com МЕДИЦИНА, ПЕДАГОГИКА И ТЕХНОЛОГИЯ: ТЕОРИЯ И ПРАКТИКА Researchbib Impact factor: 13.14/2024 SJIF 2024 = 5.444 Том 3, Выпуск 04, Апрель function. However, few studies have correlated these findings with concrete histological patterns in neonatal lungs[8,18]. A study by Schwartz (2021) highlights that SARS-CoV-2 placentitis can lead to intervillous inflammatory responses, often culminating in villous infarction and impaired nutrient and gas exchange between mother and fetus. These conditions are directly linked to intrauterine growth restriction and fetal distress syndromes. Similarly, Hosier et al. (2020) demonstrated that maternal viremia can affect the expression of ACE2 receptors in the placenta and fetal lungs, disrupting normal angiogenesis and vasculogenesis, which are essential for alveolar development[6,11]. Animal models have also contributed to this field. Research using murine models of viral-induced maternal inflammation (Simonet et al., 2021) has shown that systemic maternal immune activation leads to upregulation of proinflammatory markers in fetal lung tissue, accompanied by reduced expression of SP-B and SP-C surfactant proteins. This suggests a mechanistic pathway through which maternal infection impairs neonatal respiratory function[10,15]. Furthermore, a meta-analysis by Kotlyar et al. (2021) reviewing over 400 cases concluded that while vertical transmission of SARS-CoV-2 is rare, the inflammatory sequelae of maternal infection are sufficient to cause placental dysfunction and fetal compromise. These findings stress the need for more robust histopathological correlation, which this current study attempts to provide through direct microscopic examination of lung tissues from neonates exposed to SARS-CoV-2 in utero[14,17]. Literature Review Hecht et al. (2020) and Patberg et al. (