Erythrokinetic mechanism(s) causing the "late anemia" of hemolytic disease of the fetus and newborn.
Journal
Journal of perinatology : official journal of the California Perinatal Association
ISSN: 1476-5543
Titre abrégé: J Perinatol
Pays: United States
ID NLM: 8501884
Informations de publication
Date de publication:
12 Jan 2024
12 Jan 2024
Historique:
received:
26
10
2023
accepted:
04
01
2024
revised:
19
12
2023
medline:
13
1
2024
pubmed:
13
1
2024
entrez:
12
1
2024
Statut:
aheadofprint
Résumé
A transfusion-requiring "late anemia" can complicate the management of neonates convalescing from hemolytic disease of the fetus and newborn (HDFN). This anemia can occur in any neonate after HDFN but is particularly prominent in those who received intrauterine transfusions and/or double-volume exchange transfusions. Various reports describe this condition as occurring based on ongoing hemolysis, either due to passive transfer of alloantibody through breast milk or persistence of antibody not removed by exchange transfusion. However, other reports describe this condition as the result of inadequate erythrocyte production. Both hypotheses might have merit, because perhaps; (1) some cases are primarily due to continued hemolysis, (2) others are primarily hypoproductive, and (3) yet others result from a mixture of these two mechanisms. We propose prospective collaborative studies that will resolve this issue by serially quantifying end-tidal carbon monoxide. Doing this will better inform the assessment and treatment of neonates recovering from HDFN.
Identifiants
pubmed: 38216678
doi: 10.1038/s41372-024-01872-z
pii: 10.1038/s41372-024-01872-z
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2024. The Author(s), under exclusive licence to Springer Nature America, Inc.
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