Lewis glycolipids are passively adsorbed onto the surface of red cells which we can detect as the Lewis antigens. During pregnancy the amount of Lewis antigens changes and patients may be mis-typed.
The physiological increase in plasma volume during pregnancy dilutes the concentration of circulating Lewis glycolipids. There is also a fourfold increase in plasma lipoprotein, which ‘competes’ with the Lewis glycolipids to adsorb onto the red cells. These two changes lead to a reduced Lewis antigen dosage on red cells and this may fall below the level of detection of conventional anti-sera. As a result, a pregnant patient may falsely type as Le(a-b-), and may even be at risk of developing a transient anti-Lea or anti-Leb.
When you find a pregnant patient with a Lewis antibody, you may not be able to rely on your phenotyping tests. To find that person’s true Lewis phenotype you will need to repeat their phenotype after delivery. Lewis antigen expression returns to normal on erythrocytes postpartum and the transient Lewis antibodies generally become undetectable.
Did you know? The expression of Lewis antigens on the surface of red cells may also be lost during infectious mononucleosis that is complicated with haemolytic anaemia, severe alcoholic cirrhosis and pancreatitis.
Want to know more?
Have a read of this case report from the USA.
Have a read of these recent reviews (part I and part II) on the biologic roles of the Lewis and ABH blood group antigens.
Check out “Beyond ABO: a guided tour of the other 35 blood group systems” webinar for an overview of the clinically significant non-ABO red cell blood group systems.