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1.
Front Pediatr ; 12: 1385726, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38606368

RESUMO

Objective: Aim was to investigate whether acid-base and metabolic parameters obtained from arterial umbilical cord blood affect cerebral oxygenation after birth in preterm neonates with respiratory support and in term neonates without respiratory support. Study design: This was a post-hoc analysis of secondary outcome parameters of a prospective observational study including preterm neonates with and term neonates without respiratory support. Non-asphyxiated neonates with cerebral oxygenation measured with near-infrared spectroscopy during the first 15 min and with blood gas analyses from arterial umbilical cord blood were included. Arterial oxygen saturation (SpO2) and heart rate (HR) were monitored with pulse oximetry. Potential correlations were investigated between acid-base and metabolic parameters (pH-value, bicarbonate, base-excess, and lactate) and crSO2/cFTOE 5 min after birth. Results: Seventy-seven neonates were included: 14 preterm neonates with respiratory support (mean gestational age [GA] 31.4 ± 4.1 weeks; mean birth weight [BW] 1,690 ± 640 g) and 63 term neonates without respiratory support (GA 38.7 ± 0.8 weeks; BW 3,258 ± 443 g). Mean crSO2 5 min after birth was 44.0% ± 24.2% in preterm and 62.2% ± 20.01% in term neonates. Mean cFTOE 5 min after birth was 0.46 ± 0.06 in preterm and 0.27 ± 0.19 in term neonates. In preterm neonates with respiratory support higher lactate was significantly associated with lower crSO2 and SpO2 and tended to be associated with higher cFTOE. In term neonates without respiratory support no significant correlations were found. Conclusion: In non-asphyxiated preterm neonates with respiratory support, lactate levels were negatively associated with crSO2 and SpO2, whereas in term neonates without respiratory support no associations were observed.

2.
J Clin Med ; 12(3)2023 Feb 03.
Artigo em Inglês | MEDLINE | ID: mdl-36769887

RESUMO

Background: Hemodynamic alterations in Fontan patients (FP) are associated with hemostatic dysbalance and Fontan-associated liver disease. Studies of other hepatopathologies indicate an interplay between cholestasis, tissue factor (TF), and von Willebrand factor (VWF). Hence, we hypothesized a relationship between the accumulation of bile acids (BA) and these hemostatic factors in FP. Methods: We included 34 FP (Phenprocoumon n = 15, acetylsalicylic acid (ASA) n = 16). BA were assessed by mass spectrometry. TF activity and VWF antigen (VWF:Ag) were determined by chromogenic assays. VWF collagen-binding activity (VWF:CB) was assessed via ELISA. Results: Cholestasis was observed in 6/34 FP (total BA ≥ 10 µM). BA levels and TF activity did not correlate (p = 0.724). Cholestatic FP had lower platelet counts (p = 0.013) from which 5/6 FP were not treated with ASA. VWF:Ag levels were increased in 9/34 FP and significantly lower in FP receiving ASA (p = 0.044). Acquired von Willebrand syndrome (AVWS) was observed in 10/34-FP, with a higher incidence in cholestatic FP (4/6) (p = 0.048). Conclusions: Cholestasis is unexpectedly infrequent in FP and seems to be less frequent under ASA therapy. Therefore, ASA may reduce the risk of advanced liver fibrosis. FP should be screened for AVWS to avoid bleeding events, especially in cholestatic states.

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