What is everyones take on the following:

How do you determine clinical significance of an anti-M? What I am consistently seeing and what we have all learned is that anti-M should be considered clinically significant when reactive at 37C and AHG phase to which I agree. Unfortunately with the introduction of automation (both gel and solid phase) the phase of testing is limited to a Coombs phase. The 17^th Edition Technical Manual still references 37C testing but if tube or LISS testing is not being used in the hospital setting, is it acceptable to rely only on the AHG result provided by automation?

e.g. Antibody screen is negative but immediate screen crossmatches are positive. Anti-M is identified in panel studies. I would select random units (not M antigen negative) and perform AHG crossmatches considering the anti-M is not significant since reactivity has not been detected at AHG.

Some individuals are questioning the necessity of repeating the antibody screen in tubes to include the 37C phase. Do anyone know of a reference that states clinical significance can be identified by reactivity at 37C or AHG? I just want to prevent the additional extra work for my staff to prove the clinical insignificance of an antibody.

Much frustration over anti-M so hopefully someone can help!

A very good reason to use the computer crossmatch instead of immediate spin.

It seems to me that you already know that you have an antibody that doesn't react at 37 degrees, because it doesn't react at AHG which is incubated at 37. I generally oppose "getting rid of" reactivity without knowing what it is, but short of an anti-Vel that uncharacteristically doesn't react also at AHG, I can't see that you would be risking much. Certainly no more than those of use doing computer crossmatches and never finding that incompatibility to start with.

AABB Technical Manual states clinically significant antibodies can be reactive "at 37C and/or AHG"

We use an automated system for our type and screen testing but all crosmatches are done in tube including extended crossmatch which is done at all phases. I can see that my blood bank suppervisor is concerned with Anti-M and like antibodies, and I appreciate her insight as well as this thread. Thank you SABarry.

I was also always under the impression that if an Anti-M reacted at IgG, you "honor it" by giving AHG crossmatch compatible units. We would only ask for Anti-M neg from our reference lab (we don't carry the antisera here, too expensive) if it was a high risk patient (mom, baby, etc) and that's probably even unnecessary.

What is your test of record for panels? Our automation/Gel is more sensitive than tube. So if we do type and screen by Gel we always use same methodology for the extended crossmatch. SOme time when we give same specimen to our students who uses tube method, the same specimen is non reactive with tube.

We use an automated system for our type and screen testing but all crosmatches are done in tube including extended crossmatch which is done at all phases. I can see that my blood bank suppervisor is concerned with Anti-M and like antibodies, and I appreciate her insight as well as this thread. Thank you SABarry.

Edited August 12, 201212 yr by aakupaku

everytime we have anti-M reactive with Gel we give gel crossmatch compatible units. For pregnant women, we perform tube method screening and if anti-M is reacting at 37 & AHG phase we do prewarm screen and if prewarm screen is negative(99.9%) we give gel crossmatch compatible units.

In my experience we often detect and identify Ant-M be the Gel technique automated or manual. However, my understanding is that the only way to determine the thermal reactivity range of the anti-M is by repeating the tests in tubes at 4°C, RT and 37°C. If the anti-M does not react at 37°C (in tubes) then cross-match compatible blood can be issued. If the anti-M reacts at 37°C then M antigen negative blood should be cross-matched and issued. Pre-warming cells, sera, gel cassette, reagents etc. does not work well, if at all with anti-M. The anti-M binds to the M antigen on the cells too strongly to disassociate during the incubation stage of the gel cassette. I have also been lead to believe that the gels are slightly acidic which increases the strength of the reaction between anti-M and M antigen.

In practice we refer all new anti-M samples to our local RCI laboratory for confirmation of the thermal range of the antibody.

Regards

Steve

:)

Issitt says that it is never necessary to screen units for M--XM compatible is fine. Of course, it is sometimes faster than doing all those AHG/gel crossmatches.

Unfortunately Mabel, the BCSH guideines in the UK say that antigen (M) negative blood should be given to patients with an anti-M reacting at 37°C.

Steve

We see many, many examples of anti-M per year.

The only ones that we would suggest require M- blood are those that react by pre-warmed, warm-washed LISS tube IAT at 37oC, otherwise our advice is always to give cross-match compatible blood.

No patient that has received cross-match compatible blood in these circumstances has had the slightest reaction in the past 12 years whilst I have been working at the Reference Laboratory.

The problem is that, when using CAT, the reactants are not mixed at strictly 37oC, and "cold-reacting" antibodies can sensitise red cells expressing the corrresponding antigen extremely quickly, but do not come back off anything like as quickly, so that, by CAT, they appear to react at 37oC. In addition, as Steve suggested, an anti-M - even those that are not clinically significant.the columns are slightly acidic, which is an ideal medium to detect

In addition, as Steve suggested, an anti-M - even those that are not clinically significant.the columns are slightly acidic, which is an ideal medium to detect

Guess who educated me about Anti-M and the slightly acidic gel!!!!

Steve

Yes I remembered that as well. The wording changed with the 16th Edition to only mention the 37C testing and stated that anti-M could be avoided with not performing immediate spin crossmatches and antibody screen testing. The wording was changed again with the 17th Edition and now only references 37C reactivity. The BBTS 28th Edition states that (paraphased) only a 37C incubation phase needs to be performed to determine clinical significance. I have written to AABB for clarification. Unfortunately the reply said I could expect an answer in about 4 weeks.

Thanks to everyone for their responses. I will keep you posted on the AABB reply.

Edited August 22, 201212 yr by SABarry