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Panagglutination due to Alloantibody(ies)                                                           

A Blog from Eric Ching:

There seemed to be lots of interests among blood bankers at the antibody club meeting on a case report of antibody to a high-incidence antigen a few months earlier in Edmonton. I just want to put in my two cents worth on the subject in this blog entry under the heading:                                                    
 
                                                          Do you want to….                                                     
                      know Eric’s strategy to manage panagglutinaton due to alloantibody(ies)

 

Tech, “OMG, every panel cell is positive!”
Eric,” Is the auto positive?”
Tech, ”Yeah.”
Eric, “ Yes, I can show you how to handle this.”

If the technologist says no, we have a bigger problem at hand. By this time, your colleagues must have done 2 or more panels and noted the antibody preference of reactive temperature.

Let’s deal with the more problematic warm reactive alloantibody(ies) in this entry:

There are several possibilities:
  1. A single alloantibody to a high-incidence antigen. For example, anti-Jk3
  2. 2 or more alloantibodies reactive at the same strength. For example, anti-e, anti-Fyb and Jka
  3. Multiple alloantibodies including those so-called high titred low avidity HTLA antibody
  4. A combination of any two or three of the above!
Step 1

Notify attending physician and blood bank medical director that there is a delay or even no compatible blood for transfusion. Clinical assessment determines the timeliness of transfusion so that alternative measures can be considered.

ASK THE PATIENT IF HE/SHE HAS A HISTORY OF DIFFICULTY OF GETTING BLOOD OR HAS BEEN GIVEN AN ANTIBODY CARD!
I recall a patient from out of town with pure red cell aplasia had an antibody card from Vancouver CBS stating that he had 7 alloantibodies, or patients with anti-Vel or anti Gya.
 
Step 2

If red cell genotyping is not available on site, samples should be collected and sent to a molecular immunohematology laboratory at CBS. Be aware of the turnaround time in regard to patient’s need of blood transfusion.

Step 3
 
I firmly believe that “many roads lead to Rome”. My approach to this problem is personal, and it is not written in any SOP at the hospital where I worked. You may set up your own investigative algorithm.

Initial observations:

Are reactions uniform?

  • Most: “single allo to hi”
  • Sometimes: multiple alloantibodies reactive at the same strength. For example, anti-e and anti-Fyb at 2+, anti-K at 1+ and anti-Jka showing dosage at 1-2+
  • Rare: combination of the above

Reactivity varied?

  • Slightly and weak to 1+: most probable HTLA, multiple alloantibodies with some showing dosage
  • Highly varied: most likely multiple alloantibodies
Step 4

Investigation:

My first gambit is to titrate patient’s sample with the strongest reactive panel cell. Use the end point titre to set up a panel to:
  • see if there is a “HTLA” component eg, anti-e + anti-Cha
  • reveal a single allo or multiple allo antibodies. For example, anti-Kpb titre32 and anti-e titre 256
Step 5
  1. Panel red cell membrane modification to provide clues to the nature of antigen or specificity.

Proteolytic enzymes

  • Enhance: ABO, Hh, Rh, Lewis, Kidd, Ii, P, Colton and Dombrock
  • Inhibits or depresses: M,N,S,Fya,Fyb,Ena,Pr,Cha, Rg, JMH,Yta,T,Tn,Mg,Mia/Vw,Cla,Jea,Nya, Lu8,Lu14, In, Inb and Xga. (High Incidence antigens are in bold letters)

ZZAP (WARMTM)

  • Destroys enzyme-sensitive antigens PLUS Lwa,Yta,Ge2,3,4, Yka.McCa/Kna, and high incidence antigens  in the Dombrock, Lutheran and Kell blood group system

6% AET 2-aminoethylisothiouronium bromide (not commercially available)

  • Depresses or destroys JMH, Yta, Gy, Hy, Kna, McCa, Yka, LWa and high incidence antigens in the Kell, Lutheran and Cromer Blood Group Systems

EGA EDTA, glycine, acid

  • All Kell Blood Group System Antigens including those high incidence antigens. Era and Bg
  1. Use of cord red cells

Cord red cells have depressed expression of: A1,I,Sda, Lea,Leb,Lua,Lub,Vel, Yta, Gy,Hy,McCa, Csa,Ch,Rg and JMH.

  1. Use of collector rare cells of null phenotype if available. 
  1. Use of rare antisera to phenotype for high incidence antigen if available.

  2. Use neutralization where appropriate (mostly for cold reactive antibody, except pooled plasma for Chido and Roger)  
Personal note: Marilyn Moulds gave me a plasma sample taken from the late John Case, who was Roger negative.

Step 6

Antibody Identified:

Don’t be overwhelmed by the joy of identifying a rare antibody; there could be additional alloantibodies hidden underneath! Ruling out additional antibodies are often difficult in a hospital transfusion service laboratory, therefore, CBS reference laboratories are essential.

Do a literature search to see if the antibody is clinically significant, insignificant or may be significant occasionally.

Ask blood bank director to discuss with attending physician to determine transfusion and/or alternative management.

Patient’s race, family (siblings), medical and donation information are helpful to find compatible donors. Look up AABB’s Technical Manual (Table 16-1 on page 394-5 in the 18th ed) for listing of race and the lack of high incidence antigens.

Pre-deposit of patient’s own blood should be considered as well.   

I encountered a patient who produced an antibody card showing he had an anti-Vel and had autologous units frozen in several cities! His sister was O Rh negative, Vel- came and donated a unit for his surgery!

Antibody unidentified:

Transfusion decision should be based on risk vs benefit under patient’s clinical conditions. If time allows AND one or more of the following tests are available, they may offer clues to predict survival of transfused red cells. One must understand the limitation of each of the following tests

  • 51Cr labelled red cell survival study
  • Monocyte Monolayer Assay
  • Antibody Dependent Cellular Cytotoxicity
  • Biological Crossmatch
Cheers,

Eric

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