Assessment of the level of neurotrophic factors VEGF, BDNF, β-NGF in newborns with transient tachypnea in comparison with healthy children
Authors:   Ural State Medical University, Yekaterinburg, Sverdlovsk Oblast, Russia, Shestak E.V. ,   Yekaterinburg Clinical Perinatal Center, Yekaterinburg, Sverdlovsk Oblast, Russia, Kovtun O.P. ,   Ural State Medical University, Yekaterinburg, Sverdlovsk Oblast, Russia, Bazarnyi V.V. ,   Ural State Medical University, Yekaterinburg, Sverdlovsk Oblast, Russia, Polushina L.G. ,   Ural State Medical University, Yekaterinburg, Sverdlovsk Oblast, Russia, Maximova A.Yu. ,   Ural State Medical University, Yekaterinburg, Sverdlovsk Oblast, Russia
Published: February 2024

Cerebral damage in a newborn can occur as due to various reasons that include respiratory disorders in transient tachypnea of newborns (TTN). Hypoxic-ischemic brain damage is characterized not only by the clinical picture and morphological changes during neuroimaging, but also by biochemical changes in the body. The purpose of the research was to evaluate the level of neurotrophic factors in patients with TTN. Materials and methods used: a single-center cohort prospective clinical study was conducted; patients in the study and control groups were recruited using a continuous method. The levels of three factors were analyzed: vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF) and nerve growth factor beta (β-NGF). For the study, Authors have used a Multiscan Go enzyme immunoassay device (photometer) by Thermo Scientific (USA) and commercial test systems: Chemikine BDNF ELISA Kit by Chemicon (USA), RayBio Human β-NGF ELISA Kit by RayBio® (USA) and Invitrogen Human beta-VEGF-A ELISA Kit by Invitrogen™ (Austria). The research duration was over 6 months in 2021. Blood sampling for the 1st study of neurotrophic factors was carried out 6-12 hours after birth in 85 patients with TTN and 20 healthy newborns in the control group. The 2nd study was conducted in 23 patients with TTN on days 5-10 of life who have been admitted at the neonatal pathology department. Results: in patients with TTN, as well as with TTN in combination with cerebral ischemia at birth, the level of β-NGF was statistically significantly lower compared to healthy newborns (3152 (27; 4680) and 4056 (2484; 5286) pg/ml versus 5230 (4373-5815) pg/ml, p˂0.001 and p=0.028, respectively). However, after 5-10 days of life, the levels of β-NGF in healthy and sick newborns had no statistically significant differences. The presence of TTN at birth was statistically significantly associated with the development of cerebral ischemia in newborns (p=0.004). The ROC analysis made it possible to determine the cut-off point for the β-NGF level to detect TTN (cut-off=12.2 pg/ml), with ROC-AUC=0.79±0.054 (95% CI 0.686-0.898, p˂0.001). Conclusion: despite rapid regression of respiratory impairment in patients with TTN, there is still a significant impact on CNS function as evidenced by decreased levels of nerve growth factor beta (β-NGF). The restoration of β-NGF levels in patients with TTN with cerebral ischemia and without this diagnosis to the levels of healthy newborns may indicate that, despite the significant effect of respiratory failure on the depression of nerve growth factor, the normalization of the activity of neurotrophic processes is ongoing.