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  • Clinical Research Article
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Preterm newborns exposed to early-onset preeclampsia have altered postnatal Tumor Necrosis Factor-related apoptosis-inducing ligand trends versus controls

Abstract

Background

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a protein with anti-atherogenic and vasoprotective effects that has never been studied in newborns exposed to preeclampsia. Our aim was to examine TRAIL serum concentrations in such neonates after birth and during the transitional period.

Methods

Serum TRAIL levels were measured on the first and fifth day of life (DOL1 and DOL5, respectively) in 38 newborns exposed to early-onset preeclampsia and 38 controls born of normotensive mothers.

Results

TRAIL values on DOL1 and DOL5 did not differ between cases and controls. However, from DOL1 to DOL5 TRAIL levels increased in controls (from 20.54 ± 7.35 to 23.93 ± 11.02 pg/ml, p = 0.044) but decreased in those exposed to preeclampsia (from 25.58 ± 15.74 to 20.53 ± 10.72 pg/ml, p = 0.035). Overall, the relative change of TRAIL values from DOL1 to DOL5 was positively related to birth weight (beta coefficient 0.234, p = 0.042) and inversely related to preeclampsia (beta coefficient –0.241, p = 0.036).

Conclusion

Newborns exposed to early-onset preeclampsia present a decrease in serum TRAIL levels during the transitional period. This pattern is exactly the opposite from what is observed in neonates born to normotensive mothers, and most likely points towards a defective mechanism of extrauterine adaptation related to preeclampsia exposure in utero.

Impact

  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) levels during the transitional period do not differ between infants exposed to early-onset preeclampsia and controls

  • The pattern of change of TRAIL levels after birth is different; TRAIL decreases in newborns exposed to preeclampsia but increases in controls

  • The decrease of TRAIL levels during the transitional period points towards a defective mechanism of extrauterine adaptation and an altered cardiometabolic profile in newborns exposed to early-onset preeclampsia.

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Fig. 1: TRAIL values on DOL 1 and DOL 5 in the two study groups.
Fig. 2: TRAIL values on DOL 1 and DOL 5 in the two study groups.

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Data availability

The data that support the findings of this study are available from the corresponding author (Dr. Karatza) but restrictions apply to the availability of these data, which were used under license for the current study, and so are not publicly available. Data are however available from the authors upon reasonable request and with permission of the corresponding author (Dr. Karatza).

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Acknowledgements

This research is co-financed by Greece and the European Union (European Social Fund- ESF) through the Operational Programme «Human Resources Development, Education and Lifelong Learning» in the context of the project “Strengthening Human Resources Research Potential via Doctorate Research” (MIS-5000432), implemented by the State Scholarships Foundation (ΙΚΥ). The publication of the article has been financed by the research committee of the university of Patras.

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Contributions

N.K., S.F., D.K., G.D., D.C., A.A.K. have made substantial contributions to conception and design, acquisition of data, analysis and interpretation of data, A.A.K. and has performed the drafting the article, S.F. and G.D. have revised it critically for important intellectual content, N.K., S.F., D.K., G.D., D.C., A.A.K. give final approval of the version to be published.

Corresponding author

Correspondence to Ageliki A. Karatza.

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The authors declare no competing interests.

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The study was approved by the local Ethics Committee of the University hospital of Patras, Greece and a written informed consent was obtained from the parents.

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Oikonomou, N., Fouzas, S., Kritikou, D. et al. Preterm newborns exposed to early-onset preeclampsia have altered postnatal Tumor Necrosis Factor-related apoptosis-inducing ligand trends versus controls. Pediatr Res 93, 1955–1958 (2023). https://doi.org/10.1038/s41390-022-02301-7

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