scholarly journals 432 To determine the rate of decline of fetal hemoglobin following an intrauterine blood transfusion

2021 ◽  
Vol 224 (2) ◽  
pp. S275-S276
Author(s):  
Sarah L. O'Riordan ◽  
Gillian Ryan ◽  
Peter McParland
Keyword(s):  
Blood Transfusion ◽  
Fetal Hemoglobin ◽  
Rate Of Decline ◽  
Intrauterine Blood Transfusion

Twin anemia polycythemia sequence – modern approaches to diagnosis and antenatal correction

2021 ◽  
Vol 20 (2) ◽  
pp. 134-140
Author(s):  
A.V. Mikhailov ◽  
◽  
A.N. Romanovsky ◽  
T.A. Kashtanova ◽  
A.A. Kuznetsov ◽  
...  
Keyword(s):  
Blood Transfusion ◽  
Fetal Hemoglobin ◽  
Laser Coagulation ◽  
Multiple Birth ◽  
Monochorionic Twins ◽  
Specific Complication ◽  
Intrauterine Transfusion ◽  
Fetoscopic Laser Coagulation ◽  
Real Value ◽  
Intrauterine Blood Transfusion

Twin anemia polycythemia sequence (TAPS) is a specific complication of the monochorionic multiple birth, which is based on chronic feto-fetal blood transfusion over placental vascular anastomoses, and the main clinical symptom is discordant fetal hemoglobin level in the absence amniotic fluid imbalance. Currently, there is no generally recognized consensus on the optimal treatment tactics. Dynamic observation, labor, intrauterine blood transfusion, selective fetocide, fetoscopic laser coagulation of placental vascular anastomoses are applied, although the latter is recognized by the majority of researchers as the most promising method for treating TAPS. There are disagreements in estimating the frequency of perinatal morbidity and mortality during pregnancy, complicated by the development of TAPS, and their real value has not yet been completely defined. Key words: intrauterine transfusion, Solomon method, monochorionic twins, twin anemia polycythemia sequence, fetoscopic laser coagulation

A rare case of intra-uterine blood transfusion for fetal anemia caused by a giant placental chorioangioma

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Shira Raviv ◽  
Alon Shrim ◽  
Julia Eidel ◽  
Yoav Yinon ◽  
Boaz Weiz ◽  
...  
Keyword(s):  
Blood Transfusion ◽  
Peak Systolic Velocity ◽  
Fetal Hemoglobin ◽  
Vascular Lesion ◽  
Hemoglobin Level ◽  
Fetal Anemia ◽  
Fetal Heart Rate Monitoring ◽  
Fetal Complications ◽  
Tumor Like Lesions ◽  
Fetal Hemoglobin Level

Abstract Objectives Chorioangiomas (CAs) are the most frequent tumor-like-lesions of the placenta. Giant CAs (more than 4–5 cm in diameter) is rare and may result in severe maternal fetal complications. Case presentation A 38-year-old multigravida presented at 31 weeks’ gestation with contractions. Upon evaluation, contractions were spontaneously ceased, and the cervix was closed. Ultrasound examination revealed a single viable fetus, polyhydramnios and a 75 x 48 x 82 mm vascular lesion located on the placental surface near the cord insertion. Doppler assessment was suggestive of fetal anemia with middle cerebral artery-peak systolic velocity (MCA-PSV) 1.8 MoM’s. Fetal heart rate monitoring and biophysical scores were reassuring. Following betamethasone fetal cord sampling that revealed fetal hemoglobin level of 8.8 g/dL, 57 cc of blood was transfused resulting in final hemoglobin level of 14.3 g/dL measured prior to needle extraction. MCA-PSV was normalized immediately after the procedure, however aggravated at the following day with MCA-PSV 65 cm/s (1.46 MoM’s). No other intervention was taken and MCA-PSV continued to fluctuate from slight to severe anemia spontaneously over a period of two weeks. At 34 gestational weeks, the women delivered a healthy baby. Fetal hemoglobin level at delivery was 21 g/dL. Conclusions Fetal blood transfusion is a reasonable treatment for fetal anemia in cases of giant chorioangiomas. Following transfusion, MCA-PSV may act unexpectedly reflecting various mechanisms affecting the flow.

Management of Twin Anemia-Polycythemia Sequence Using Intrauterine Blood Transfusion for the Donor and Partial Exchange Transfusion for the Recipient

2013 ◽  
Vol 34 (2) ◽  
pp. 121-126 ◽  
Author(s):  
L. Genova ◽  
F. Slaghekke ◽  
F.J. Klumper ◽  
J.M. Middeldorp ◽  
S.J. Steggerda ◽  
...  
Keyword(s):  
Blood Transfusion ◽  
Exchange Transfusion ◽  
Intrauterine Blood Transfusion

scholarly journals Infusion of Autologous Retrodifferentiated Stem Cells into Patients with Beta-Thalassemia

2006 ◽  
Vol 6 ◽  
pp. 1278-1297 ◽  
Author(s):  
Ilham Saleh Abuljadayel ◽  
Tasnim Ahsan ◽  
Huma Quereshi ◽  
Shakil Rizvi ◽  
Tamseela Ahmed ◽  
...  
Keyword(s):  
Blood Transfusion ◽  
Blood Cell ◽  
Red Blood Cell ◽  
White Blood Cells ◽  
Fetal Hemoglobin ◽  
Beta Thalassemia ◽  
Mean Corpuscular Hemoglobin ◽  
Beta Globin ◽  
Globin Chain ◽  
Adult Hemoglobin

Beta-thalassemia is a genetic, red blood cell disorder affecting the beta-globin chain of the adult hemoglobin gene. This results in excess accumulation of unpaired alpha-chain gene products leading to reduced red blood cell life span and the development of severe anemia. Current treatment of this disease involves regular blood transfusion and adjunct chelation therapy to lower blood transfusion–induced iron overload. Fetal hemoglobin switching agents have been proposed to treat genetic blood disorders, such as sickle cell anemia and beta-thalassemia, in an effort to compensate for the dysfunctional form of the beta-globin chain in adult hemoglobin. The rationale behind this approach is to pair the excess normal alpha-globin chain with the alternative fetal gamma-chain to promote red blood cell survival and ameliorate the anemia. Reprogramming of differentiation in intact, mature, adult white blood cells in response to inclusion of monoclonal antibody CR3/43 has been described. This form of retrograde development has been termed “retrodifferentiation”, with the ability to re-express a variety of stem cell markers in a heterogeneous population of white blood cells. This form of reprogramming, or reontogeny, to a more pluripotent stem cell state ought to recapitulate early hematopoiesis and facilitate expression of a fetal and/or adult program of hemoglobin synthesis or regeneration on infusion and subsequent redifferentiation. Herein, the outcome of infusion of autologous retrodifferentiated stem cells (RSC) into 21 patients with beta-thalassemia is described. Over 6 months, Infusion of 3-h autologous RSC subjected to hematopoietic-conducive conditions into patients with beta-thalassemia reduced mean blood transfusion requirement, increased mean fetal hemoglobin synthesis, and significantly lowered mean serum ferritin. This was always accompanied by an increase in mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC) in such patients. No adverse side effects in response to the infusion of autologous RSC were noted.This novel clinical procedure may profoundly modify the devastating course of many genetic disorders in an autologous setting, thus paving the way to harnessing pluripotency from differentiated cells to regenerate transiently an otherwise genetically degenerate tissue such as thalassemic blood.

A Humanized Cooley’s Anemia Mouse Model.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1784-1784
Author(s):  
Yongliang Huo ◽  
Sean C. McConnell ◽  
Clayton L. Ulrey ◽  
Ting-Ting Zhang ◽  
Rui Yang ◽  
...  
Keyword(s):  
Blood Transfusion ◽  
Mouse Model ◽  
Adult Mouse ◽  
Globin Gene ◽  
Embryonic Stem ◽  
Fetal Hemoglobin ◽  
Globin Genes ◽  
Inherited Disorders ◽  
Nucleotide Mutation ◽  
Cooley's Anemia

Abstract Cooley’s Anemia (CA) is a heterogeneous group of inherited disorders all marked by the complete absence of adult β-globin chains in red blood cells (RBCs). Newborns with CA are healthy because of the high level of fetal hemoglobin (HbF) present at birth. As HbF levels decline during the first year of life, the absence of functional adult β-globin genes results in a severe anemia that necessitates the initiation of regular blood transfusions for the remainder of life. CA has been difficult to study in murine models due to the lack of a human fetal hemoglobin equivalent in the mouse. This study reports a novel preclinical animal model of CA that survives solely on human fetal hemoglobin at birth and is blood transfusion dependent for life upon completion of the hemoglobin switch after birth. These humanized CA mice were generated by targeted gene replacement in embryonic stem cells of the adult mouse α-globin genes with human α-globin and the adult mouse β-globin genes with a delayed switching γδβ0-globin gene cassette. The nonfunctional human β0-globin knock-in allele contains a single G to A nucleotide mutation in the first base of intervening sequence 1. Both wild-type and hereditary persistence of fetal hemoglobin (HPFH) promoter mutations were tested in the human γ-globin knock-in allele. Heterozygous knock-in mice exhibit β thalassemia intermedia. Newborn homozygous knock-in mice express 100% human hemoglobin in their RBCs, suffer from ineffective erythropoiesis, survive from one to ten days after birth, and are blood transfusion dependent for adult life. This is the first CA mouse model that recapitulates the temporal onset of the disease in human patients. This CA disease model is useful for the study of the regulation of globin gene expression, synthesis, and switching; development of transfusion and iron chelation therapies; induction of fetal hemoglobin synthesis; and the testing of novel genetic and cell-based therapies for the correction of thalassemia.

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