A study of the protective factors in heterospecific blood group pregnancy and their role in the prevention of hæmolytic disease of the newborn

1945 ◽  
Vol 57 (3) ◽  
pp. 295-305 ◽  
Author(s):  
Geoffrey H. Tovey
Keyword(s):  
Protective Factors ◽  
Blood Group ◽  
Haemolytic Disease

‘Heibel’ a New Rare Human Blood Group Antigen, Revealed by a Haemolytic Disease of a Newborn

Vox Sanguinis ◽  
1968 ◽  
Vol 14 (4) ◽  
pp. 307-309 ◽  
Author(s):  
L. Ballowitz ◽  
H. Fiedler ◽  
Ch. Hoffmann ◽  
H. Pettenkofer
Keyword(s):  
Blood Group ◽  
Human Blood ◽  
Blood Group Antigen ◽  
Haemolytic Disease ◽  
Human Blood Group

scholarly journals Haemolytic Disease of Newborn due to Minor Blood Group C IncompatibilityA Case Report

2019 ◽  
Vol 8 (36) ◽  
pp. 2826-2827
Author(s):  
Kelawala Pooja M. ◽  
Mangal Dhananjay ◽  
Singh Sourabh ◽  
Singhal Chanchal
Keyword(s):  
Case Report ◽  
Blood Group ◽  
Haemolytic Disease

scholarly journals Severe hemolytic disease of the premature newborn due to RH1 incompatibility: a case report

2016 ◽  
Vol 89 (4) ◽  
pp. 565-568 ◽  
Author(s):  
Jean Uwingabiye ◽  
Hafid Zahid ◽  
Fayçal Labrini ◽  
Abdelhak El Khazraji ◽  
Anass Yahyaoui ◽  
...  
Keyword(s):  
Blood Group ◽  
Serum Bilirubin ◽  
Serum Bilirubin Level ◽  
Total Serum ◽  
Hemolytic Disease ◽  
Close Collaboration ◽  
Haemolytic Disease ◽  
Total Serum Bilirubin Level ◽  
Antiglobulin Test ◽  
History Of

We report a case of dramatic outcome of severe haemolytic disease in a newborn due to RH1 incompatibility. A newborn with A RH1 blood group was admitted in the Mohammed V Military Teaching Hospital for the problem of hydrops fetalis associated with RH1 incompatibility. The blood group of his mother, aged 31, was AB RH1-negative and that of his 37 year old father was A RH1.The mother had a history of 4 term deliveries, 3 abortions, and 1 living child. There was no prevention by anti-D immunoglobulin postpartum. The mother‘s irregular agglutinin test was positive and the pregnancy was poorly monitored. The laboratory tests of the newborn showed a high total serum bilirubin level (30 mg/L) and macrocytic regenerative anemia (Hemoglobin=4 g/dL, mean corpuscular volume = 183 fL, reticulocytes count =176600/m3). The blood smear showed 1256 erythroblasts per 100 leukocytes, Howell–Jolly bodies and many macrocytes. The direct antiglobulin test was positive. He was transfused with red blood cell concentrates and treated with conventional phototherapy. The evolution was unfavourable; he died three days after the death of his mother. The monitoring of these high-risk pregnancies requires specialized centers and a close collaboration between the gynaecologist and the blood transfusion specialist to strengthen the prevention, as well as clinico-biological monitoring in patients with a history of RH1 fetomaternal alloimunization.

scholarly journals Haemolytic disease of the newborn due to anti-Jkb antibody of the Kidd blood group system

Research ◽  
2014 ◽  
Vol 1 ◽  
Author(s):  
Doris Lau Sie Chong ◽  
Rabeya Yousuf ◽  
Chooi-Fun Leong ◽  
Fook-Choe Cheah
Keyword(s):  
Blood Group ◽  
Blood Group System ◽  
Haemolytic Disease ◽  
Group System

Toxoplasmaand reaction time: role of toxoplasmosis in the origin, preservation and geographical distribution of Rh blood group polymorphism

Parasitology ◽  
2008 ◽  
Vol 135 (11) ◽  
pp. 1253-1261 ◽  
Author(s):  
M. NOVOTNÁ ◽  
J. HAVLÍČEK ◽  
A. P. SMITH ◽  
P. KOLBEKOVÁ ◽  
A. SKALLOVÁ ◽  
...  
Keyword(s):  
Blood Group ◽  
Balancing Selection ◽  
Reaction Times ◽  
Protozoan Parasite ◽  
Modern Medicine ◽  
Blood Group System ◽  
Haemolytic Disease ◽  
Health Impairment ◽  
D Antigen ◽  
Rh Blood Group

SUMMARYThe RhD protein which is theRHDgene product and a major component of the Rh blood group system carries the strongest blood group immunogen, the D-antigen. This antigen is absent in a significant minority of the human population (RhD-negatives) due toRHDdeletion or alternation. The origin and persistence of this RhD polymorphism is an old evolutionary enigma. Before the advent of modern medicine, the carriers of the rarer allele (e.g. RhD-negative women in the population of RhD-positives or RhD-positive men in the population of RhD-negatives) were at a disadvantage as some of their children (RhD-positive children born to pre-immunized RhD-negative mothers) were at a higher risk of foetal or newborn death or health impairment from haemolytic disease. Therefore, the RhD-polymorphism should be unstable, unless the disadvantage of carriers of the locally less abundant allele is counterbalanced by, for example, higher viability of the heterozygotes. Here we demonstrated for the first time that amongToxoplasma-free subjects the RhD-negative men had faster reaction times than Rh-positive subjects and showed that heterozygous men with both the RhD plus and RhD minus alleles were protected against prolongation of reaction times caused by infection with the common protozoan parasiteToxoplasma gondii. Our results suggest that the balancing selection favouring heterozygotes could explain the origin and stability of the RhD polymorphism. Moreover, an unequal prevalence of toxoplasmosis in different countries could explain pronounced differences in frequencies of RhD-negative phenotype in geographically distinct populations.

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