Read the paper in Lab Medicine or listen to the podcast to learn more about one institution’s ficin protocol.
Tag: blood bank
Acquired B Phenotype
Students learning about the ABO blood group system commonly get confused about two unique situations: The Acquired B phenotype and the Bombay phenotype.
These two entities are VERY different, but they are similar in this way: people are asked about both on exams all the time, but hardly anyone every actually SEES either one in real life! It is essential for students of blood banking to understand Acquired B clearly, as it remains a real possibility in everyday practice. I’ll cover Acquired B in this month’s blog, and next month I will discuss Bombay.
Routine ABO testing is performed in two distinct (but usually simultaneous) stages, known as “red cell grouping” (forward grouping or “front type”) and “serum grouping” (reverse grouping or “back type”). Here’s an example of how it works: If a person’s red blood cells (RBCs) react strongly with reagent anti-A but not anti-B, we would interpret their red cell grouping as blood group A. If there is no ABO discrepancy, that same person’s serum should have no reaction with reagent group A1 RBCs and strong reaction with reagent group B RBCs (demonstrating the expected presence of anti-B in the serum). Thus, the serum grouping interpretation would also be blood group A, and no ABO discrepancy would exist (see this illustrated in the figure below).
ABO discrepancies occur any time the interpretations of a person’s red cell and serum grouping do not agree. ABO discrepancy takes on many forms, and acquired B is a great, if not terribly common, example.
Students learning about the ABO blood group system commonly get confused about two unique situations: The Acquired B phenotype and the Bombay phenotype.
Usually, Acquired B occurs when the RBCs from a blood group A patient come in contact with bacterial enzymes known as “deacetylases.” These enzymes, commonly carried by bacteria that live in the colon, catalyze the removal of the acetyl group from the residue that gives the A antigen its specificity, N-acetylgalactosamine (GalNAc). This modification leaves the A-specific sugar as galactosamine (N-acetylgalactosamine with the acetyl group removed = galactosamine). Recall that normally, the group B-specific sugar is galactose.
As a result of this modification, anti-B in both human group A serum and especially certain monoclonal reagents will weakly agglutinate the group A RBCs carrying the acquired B antigen. This means that the patient’s RBCs may have a weakly positive reaction with anti-B in serum grouping tests instead of the expected negative (see image below). The serum grouping for these patients is no different from that expected for a group A individual (negative with group A reagent RBCs, strong positive with group B RBCs).
So, what does this actually mean? How do these patients actually get transfused? This is where the recognition of the entity in a transfusion service or reference laboratory is essential. Several simple strategies can be employed to prove that this patient is really NOT group AB. First, I always advise people to check the patient history! The rare cases of acquired B that are still seen will often be associated with colorectal malignancy, gastrointestinal obstruction, or gram-negative sepsis (where those bacteria can contact the RBCs). Second, adding the patient’s own serum to his RBCs (autoincubation) reveals no incompatibility. In other words, this patient’s own very strong anti-B does not recognize the acquired B antigen (which is really just a partially modified group A antigen) as being an actual group B antigen. We already know that this patient has anti-B in his serum from his serum grouping results (see above), but the patient’s own anti-B completely ignores the acquired B antigen on his RBCs (even though human anti-B from other people will react). Third, the technologist can use a different form of monoclonal anti-B in the patient’s red cell grouping test. Certain clones are known to react with acquired B, while others are not (normally specified in the package insert), and choosing a different clone (often easier in reference lab settings) will render the forward grouping consistent with that of a group A person. Also, incubating the Acquired B RBCs with acetic anhydride will lead to “re-acetylation” of the modified A antigen and loss of the B-like activity. Finally, acidifying the reaction mixture of the patient’s RBCs with human anti-B (non-self) can eliminate the incompatibility with that source of anti-B.
In the end, Acquired B is a serologic problem that is fairly easy to recognize, especially on examinations (I always tell my students that when they see a problem that starts with words like, “A 73 year old male with colon cancer…”, check the answer for Acquired B!). In real life, experienced blood bankers can diagnose and confirm Acquired B fairly easily in the rare times that it is seen. These patients can receive group A blood without a problem, and the ABO discrepancy will disappear as the infection or other situation causing causing contact with bacterial enzymes clears. Thanks for your time and attention. See you next month when I will discuss the Bombay Phenotype!
-Joe Chaffin, MD, is the new Vice President and Chief Medical Officer for LifeStream, a Southern California blood center headquartered in San Bernardino, CA. He has a long history of innovative educational efforts and is most widely known as the founder and chief author of “The Blood Bank Guy” website (www.bbguy.org).
Stocking Shelves
My struggle in the community hospital setting is having the appropriate inventory for the patient population I need to serve. When I stocked the refrigerator during my golf club days the oldest inventory went up front and the new product went to the back. Later in graduate school I learned that was the FIFO method of inventory management. Blood Bankers have a unique twist thrown our way in that as blood sits on our shelves certain things happen that make an older unit less desirable than one collected a few days prior. The life span of a red cell is around 100-120 days depending on which literature you cite. Our job as blood bankers is to get the freshest blood to each patient we serve, so inventory management becomes more of an art than science.
Let’s take first the type specific debate. Some will say always transfuse type specific blood; if the patient is type A then the patient receives type A blood. Some will say to give whatever is most fresh; if we have fresh O cells an A person will get O. What I found when I first came to be the supervisor in my blood bank is that we were outdating a lot of type A blood. So instead of just decreasing the amount of type A, I also increased the number of type O I had on my shelf. This allowed me to be more flexible; I would give out more O when my inventory of A was low. Also, the blood I was giving out was always fresher than before I changed the inventory.
Let’s take this another direction. My policy states that any patient with an antibody has to have two red cell units set up so there is no delay if a transfusion is necessary. I would rather have two type O units typed for some antigens, because if the patient with the antibody doesn’t need it, the units are readily available to anyone else. I use the flexibility of type O blood to be more versatile and to make sure that my patients are getting the freshest possible unit. I have searched for literature that says giving type specific blood is better for patient outcomes but I haven’t found it. If anyone has literature on the topic please send it my way.
This really comes down to what type of setting your blood bank serves. If you are in a medium size community hospital you will need to make these type of decisions to be flexible with your inventory. If you are a large medical center and are going through blood as soon as it gets delivered then you may not have to worry as much. The majority of us do not work for large centers, however, so we must look and analyze how we can best use this precious resource.
–Tommy Transfusion is the pseudonym of a blood bank supervisor in the midwest.
Lablogatory 