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Prospective Evaluation of Fetal Hemoglobin Expression in Maternal Erythrocytes: An Analysis of a Cohort of 345 Parturients.

Authors :
Blain, Laurence
Watier, Christian
Weng, Xiaoduan
Masse, Andre
Bédard, Marie-Josée
Bettache, Nazila
Weber, Florence
Mahone, Michele
Forté, Stéphanie
Lavallée, Vincent-Philippe
Gaudreau, Pierre-Olivier
Newmarch, Michael J.
Soulières, Denis
Source :
Diagnostics (2075-4418). Jun2023, Vol. 13 Issue 11, p1873. 12p.
Publication Year :
2023

Abstract

It is believed that fetal hemoglobin (HbF) expression in adults is largely genetically regulated. The increased expression of HbF in pregnancy has been reported in a small number of articles. Different mechanisms have been proposed, but the description of HbF expression during pregnancy remains unclear. The objectives of this study were to document HbF expression during peri and postpartum periods, confirm its maternal origin, and assess clinical and biochemical parameters potentially associated with HbF modulation. In this observational prospective study, 345 pregnant women were followed. At baseline, 169 had HbF expression (≥1% of total hemoglobin) and 176 did not have HbF expression. Women were followed at the obstetric clinic during their pregnancy. Clinical and biochemical parameters were measured at each visit. Analyses were made to determine which parameters had a significant correlation to HbF expression. Results show that HbF expression of ≥1% during peri and postpartum periods in pregnant women without influencing comorbidities is at its highest peak during the first trimester. In all women, it was proven that HbF was of maternal origin. A significant positive correlation between HbF expression, βeta-human chorionic gonadotropin (β-HCG), and glycosylated hemoglobin (HbA1c) was present. A significant negative association between HbF expression and total hemoglobin was found. HbF expression induction during pregnancy is probably associated with an increase in β-HCG and HbA1C, and a decrease in total hemoglobin, which could temporarily reactivate the fetal erythropoietic system. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
20754418
Volume :
13
Issue :
11
Database :
Academic Search Index
Journal :
Diagnostics (2075-4418)
Publication Type :
Academic Journal
Accession number :
164214299
Full Text :
https://doi.org/10.3390/diagnostics13111873