OBJECTIVE: Our purpose was to test the hypothesis that maternal anti-Kell alloimmunization produces fetal anemia by erythroid suppression. STUDY DESIGN: Erythropoiesis in 11 anemic fetuses from maternal anti-Kell alloimmunization was compared with that in 11 fetuses where the mother was alloimmunized to RhD; each was matched for hematocrit, gestational age, hydrops, and perinatal outcome. Comparisons of the difference were performed by either paired t or Wilcoxon tests. RESULTS: The anti-Kell group had reduced reticulocytosis (p = 0.007) and erythroblastosis (p = 0.045) and lower amniotic fluid bilirubin concentrations (p = 0.02) in comparison with the anti-D group. No correlation was found between hematocrit and reticulocytosis in the anti-Kell group, whereas the anti-D group had a significant linear relationship (r = 0.63, p < 0.05), indicating a progressive reticulocytosis in response to the degree of anemia. CONCLUSION: These findings suggest that erythroid suppression, rather than hemolysis, is the predominant mechanism in producing fetal anemia related to maternal Kell alloimmunization. Fetal blood sampling is the investigation of choice in the evaluation of anemia related to maternal Kell alloimmunization, because reduced hemolysis means amniotic fluid bilirubin concentrations correlate poorly with anemia.
OBJECTIVE: Our purpose was to test the hypothesis that maternal anti-Kell alloimmunization produces fetal anemia by erythroid suppression. STUDY DESIGN: Erythropoiesis in 11 anemic fetuses from maternal anti-Kell alloimmunization was compared with that in 11 fetuses where the mother was alloimmunized to RhD; each was matched for hematocrit, gestational age, hydrops, and perinatal outcome. Comparisons of the difference were performed by either paired t or Wilcoxon tests. RESULTS: The anti-Kell group had reduced reticulocytosis (p = 0.007) and erythroblastosis (p = 0.045) and lower amniotic fluid bilirubin concentrations (p = 0.02) in comparison with the anti-D group. No correlation was found between hematocrit and reticulocytosis in the anti-Kell group, whereas the anti-D group had a significant linear relationship (r = 0.63, p < 0.05), indicating a progressive reticulocytosis in response to the degree of anemia. CONCLUSION: These findings suggest that erythroid suppression, rather than hemolysis, is the predominant mechanism in producing fetal anemia related to maternal Kell alloimmunization. Fetal blood sampling is the investigation of choice in the evaluation of anemia related to maternal Kell alloimmunization, because reduced hemolysis means amniotic fluid bilirubin concentrations correlate poorly with anemia.
Authors: H Howard; V Martlew; I McFadyen; C Clarke; J Duguid; I Bromilow; J Eggington Journal: Arch Dis Child Fetal Neonatal Ed Date: 1998-01 Impact factor: 5.747
Authors: Sean R Stowell; Kate L Henry; Nicole H Smith; Krystalyn E Hudson; Greg R Halverson; Jaekeun C Park; Ashley M Bennett; Kathryn R Girard-Pierce; C Maridith Arthur; Silvia T Bunting; James C Zimring; Jeanne E Hendrickson Journal: Blood Date: 2013-06-25 Impact factor: 22.113
Authors: Lisa Lee Pate; Jessica C Myers; Jonathan P Palma; Maurene Viele; Susan A Galel; Zenaida Ferrer; Christopher L Gonzalez; William E Benitz; George Garratty; Magali J Fontaine Journal: Transfusion Date: 2012-12-12 Impact factor: 3.157
Authors: Arwa Z Al-Riyami; Mouza Al-Salmani; Sabria N Al-Hashami; Sabah Al-Mahrooqi; Ali Al-Marhoobi; Sumaiya Al-Hinai; Saif Al-Hosni; Sathiya M Panchatcharam; Zainab A Al-Arimi Journal: Sultan Qaboos Univ Med J Date: 2018-04-04