Jolly, a 16 year old girl, met with an accident resulting in huge blood loss. She was admitted to a hospital where the doctors advised immediate blood transfusion. Before proceeding with blood transfusion, she was subjected to blood grouping tests. What do you understand about blood grouping?
- Understand the molecular basis of blood groups and the reasons for transfusion reactions.
- Explain Landsteiner’s Law on blood grouping.
- Describe the various hemolytic diseases associated with blood group incompatibility.
- Explain the hazards associated with blood transfusion.
The membranes of human RBCs contain a variety of blood group antigens, which are also called as agglutinogens. The most important and best known of these are the A&B antigens, but there are many more.
Group specific substances A & B are not limited to the RBCs but are also found in many organs like pancreas, lungs, kidney, liver, testes, salivary gland, urine, semen and amniotic fluid.
The ABO system
The A and B antigens (agglutinogens) are inherited as mendelian dominants. Type A individuals have the A antigen, type B have the B, type AB have both, and type O have neither.
How do we differentiate the blood group antigens?
An antigen called H antigen, which is coded by an H gene is present in all individuals.
Individuals with A blood group have a terminal N- acetylgalactosamine attached to the H antigen.
Individuals with B blood group have a terminal galactose on the H antigen.
Individuals with AB blood group will have both N-acetylgalactosamine and galactose on the H antigen.
Individual with O blood group will have H antigen as such, without any additional molecule attached terminally.
Integrate the structure of blood group antigens with the Biochemistry session on carbohydrates (in the context of an example under functions of carbohydrates).
Antibodies against red cell agglutinogens are called agglutinins (antibodies). The agglutinins are globulins of IgM type and cannot cross the placenta.
How do these agglutinins develop in our plasma?
Antigens very similar to A and B are common in intestinal bacteria and possibly in foods to which new born individuals are exposed. Therefore infants rapidly develop antibodies against the antigens not present in their own cells.
Thus type A individuals develop anti-B antibodies, type B individuals develop anti-A antibodies, type O individuals develop both, and type AB individuals develop neither.
It was framed by Karl Landsteiner. It has two major components:
- If an agglutinogen is present in the RBCs of an individual, the corresponding agglutinin must be absent from the plasma.
- It the agglutinogen is absent in the individual RBCs, the corresponding agglutinin must be present in the plasma.
Inheritance of A & B antigens
As mentioned earlier, the A and B antigens are inherited as mendelian allelomorphs, A and B being dominant.
In AB blood group, A and B are codominant, giving the AB phenotype.
When the blood types of parents are known, the possible genotypes of their children can be stated.
When the blood types of a mother and her child are known, blood grouping can prove that a man cannot be the father, although it cannot prove that he is the father.
In addition to the ABO system of antigens in human RBCs, there are systems such as the Rh, MNSs, Lutheran, Kell, Kidd, and many others.
The Rh group
Discovered by Landsteiner and Weiner in 1940.
The Rh factor, named for the rhesus monkey because it was studied using the blood of this animal, is a system composed of C, D, and E antigens. D is by far the most antigenic component, and the term Rh positive means that the individual has agglutinogen D.
Unlike the ABO system, the Rh system has not been detected in tissues other than RBCs.The Rh- negative individual has no D antigen and forms the anti-D agglutinin when injected with D-positive cells and thus may develop transfusion reactions when transfused again with D-positive blood.
The Rh antibodies are of the IgG type and can cross the placenta.
Hemolytic disease of the newborn
This complication due to Rh incompatibility arises when an Rh-negative mother carries an Rh-positive fetus. Small amounts of fetal blood leak into the maternal circulation at the time of delivery, and some mothers develop significant amounts of anti-D antibodies during the postpartum period. Sensitization of the mothers can also occur during pregnancy during fetal-maternal hemorrhage in pregnancy.
In any case, when anti Rh-agglutinins cross the placenta to an Rh-positive fetus during the next pregnancy, they can cause hemolysis and various forms of hemolytic disease of the newborn.
We have seen that when IgG antibodies can cross the placenta, the IgM antibodies are restricted from crossing the placental barrier. Integrate the concept with Embryology (Anatomy) for more details.
The various forms of hemolytic disease of the newborn are:
- Hydrops fetalis : The fetus is grossly edematous, it either dies in utero or if born prematurely or at term, it dies within a few hours.
- Icterus gravis neonatorum :
- The infant born at term is jaundiced or becomes so in 24 hours, due to excessive destruction of RBCs (hemolytic jaundice).
- Excessive destruction of RBCs is compensated by an intense normoblastic response of the marrow, associated with high reticulocyte count and presence of many nucleated RBCs in the circulation (erythroblastosis fetalis).
In cases of hemolytic disease of the newborn, the first child is usually normal. Why does this condition mainly affect the second Rh positive child?
This is because sensitisation of Rh negative mothers by carrying an Rh positive child generally occurs at birth, sparing the first child.
Is it possible to prevent the sensitisation from occurring the first time?
Yes, it is. It is done by administering a single dose of anti-Rh antibodies to the mother in the form of Rh immune globulin during the postpartum period. Such immunisation prevents active antibody formation by the mother.
Usually done in conditions like:
- Blood loss- accidents, surgery
- Blood disorders- haemophilia, purpura
- Blood diseases- leukemia, severe anemia
- Poisoning- CO poisoning
- Acute infections or fever, when γ-globulins are needed
What are the basic rules to be observed during blood transfusion?
- The plasma of the donor which contains the agglutinins can be ignored, but account need to be taken of the effect of the serum agglutinins of the recipient on the cells (agglutinogens) of the donor.
- No Rh female at any age before menopause should ever be given a Rh positive blood transfusion, since that can cause the building up of anti-Rh antibodies in her blood.
- The blood groups of the recipient and donor must be compatible.
Individuals with type O Rh D negative blood are often called universal donors, and those with type AB Rh D positive blood are called universal recipients.
Hazards associated with blood transfusion
- Effects of incompatible blood transfusion:
- Inapparenthemolysis due to destruction of donor RBCs
- Post-transfusion jaundice- Hemoglobin from the destroyed RBCs gets metabolised to bilirubin causing hemolytic jaundice.
- Hemoglobinuria and renal failure
Karl Landsteiner will always be honoured for his outstanding work on the blood groups, for which he was given the Nobel Prize for Physiology or Medicine in 1930.
Read more for the detailed biography of Karl Landsteiner and his contributions towards medicine Source link
"Karl Landsteiner - Biographical".Nobelprize.org. Nobel Media AB 2014.Web. 16 Mar 2017.
|Bombay blood group||Description on a rare blood type called hh (Bombay)blood group||hh blood group. Wikipedia, the free encyclopedia, 22 February 2017; accessed through the link on 14 Mar 2017. Source link|
|Cross matching||Explains the principle behind cross matching||Cross-Matching : Types, Purpose, Principle, Procedure and Interpretation. DhurbaGiri in Hematology, Immunology; June 21, 2015; accessed through the link on 14 Mar 2017. Source link|
- Landsteiner’s law
- Hemolytic disease of the newborn
- Erythroblastosis fetalis
- Hazards of blood transfusion
- Define ABO and Rh blood group systems. Describe the physiological basis of blood grouping. What is erythroblastosis fetalis?