Hormonal status and cardiorespiratory adaptation of late premature newborns in the early neonatal period

The growth of late preterm labor in recent years and the increased frequency of neonatal complications in 34–36-week gestation newborns explain the interest of researchers in the problem of late prematurity. The loss of the last weeks of pregnancy by late prematurity interruptsthe formation of hierarchical connections between regulatory links and target organs, but the questionsremain open, how significant is the effect of late prematurity on the hormonal status of the newborn and what are the immediate and long-term consequences of hormonal disorders that occurred in the early neonatal period.

Purpose. This study analyzes the effect of hormonal status on cardio-respiratory adaptation of late premature newborns in the early neonatal period.

Materials and methods. The study included 105 newborns with a gestation period of 34–36 weeks. A comprehensive assessment of the early adaptation period was carried out, the levels of TSH, T3, T4 total, T4 free, cortisol were determined. Blood sampling was carried out immediately after birth from the umbilical cord vein and on the 4th day after birth from the subcutaneous veins. The concentration of hormones was determined by solid-phase enzyme immunoassay using standard sets (Alkor Bio, Russia).

Results. The  results of  the work established a relationship between the thyroostatic state, cortisol concentration and the course of cardio-respiratory adaptation in late premature newborns. Newborns in need of respiratory and cardiotonic therapy had reduced concentrations of T3, T4 free and cord blood cortisol. On the 4th day of life, newborns in  need of  respiratory therapy showed a decrease in free T4 and an increase in cortisol, children receiving cardiotonic support had a reduced concentration of free T4.

Conclusion. Hormonal maladaptation can be considered as an additional factor in the pathogenesis of respiratory disorders in late premature newborns along with a reduced gas exchange area in the lungs, immaturity of sodium pumpsin alveolocytes and surfactant deficiency. 

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