Transfusion reaction about anti-Mia

[Yanxia]

I have read a post on line, which suspect anti-Mia caused intra circulation hemolysis(I don't sure how to call it, it is the reaction can have hemoglobin urine)

but it is delayed hemolysis reaction.

The poster said the pre transfusion screening test is neg and crossmatch is neg, but after transfusion ( the second day the reaction happen) the cross match is postive, but screening is negtive too. The serum is pink after transfusion but normal before transfusion, the pathent have purpura, and faster heart beat. And reduced hemogoglobin. Pre 141g/l and after 56g/l.

I cann't remember the anti-Mia caused so strong reaction, and disappear and occur so quickly.

Am I wrong?

Any suggestion is appreciated, and thanks in advance!

Edited November 30, 2010 by shily

[Malcolm Needs ☆]

I have read a post on line, which suspect anti-Mia caused intra circulation hemolysis(I don't sure how to call it, it is the reaction can have hemoglobin urine)

but it is delayed hemolysis reaction.

The poster said the pre transfusion screening test is neg and crossmatch is neg, but after transfusion ( the second day the reaction happen) the cross match is postive, but screening is negtive too. The serum is pink after transfusion but normal before transfusion, the pathent have purpura, and faster heart beat. And reduced hemogoglobin. Pre 141g/l and after 56g/l.

I cann't remember the anti-Mia caused so strong reaction, and disappear and occur so quickly.

Am I wrong?

Any suggestion is appreciated, and thanks in advance!

I don't know this case, and so I don't know if this answer is correct or incorrect, but I will have a go.

It could well be that the anti-Mia was at a level too low for detection when the original cross-match was performed. The apparently compatible blood was transfused, although one or more of the units was Mi(a+).

This unit could then have caused an anamnestic response, leading to a rapid increase in the level of anti-Mia. This anti-Mia could possibly have initiated the classical complement pathway, leading to intravascular cell haemolysis which, in turn, could have caused "innocent bystander" haemolysis of autologous red cells and, hence, the dramatic fall in haemoglobin post-transfusion.

The fact that the unit was incompatible when re-cross-matched, whilst the screen was negative could be simply that the screening cells did not express the Mi(a) antigen. Although using red cells that express such antigens may be common in the Far East, it certainly is not throughout the world.

The dramatic drop in haemoglobin could also be explained by a concurrent bout of hyperhaemolysis, at the same time as a mild delayed haemolytic transfusion reaction.

Reactions are very rare with anti-Mia, But Broadberry et al published some data in 1994 (Transfusion; 34: 349-352) about reactions and HDN in Tiawan.

I could well be talking nonsense (again!), but at least these thoughts may give others some ideas, ready to shoot me down!!!!!!!!!!!!!!!

:surrender:surrender:surrender:surrender:surrender

[Yanxia]

Thank you very much, Malcolm. Your reply is so helpful to me!

[Liz]

thanks Malcolm for, once more, awakening my neurons.

[dheathco]

Whether or not the screening cells will detect antibodies to hybrid glycophorin antibodies depends on what particular screening cells are being employed. The use of screening cells that include putative GP.Mur cells occurs in some parts of Asia but not in others. When they are included they have not usually been genotypically identified so there is no absolute guarantee on their identity. Remember that at best they will almost certainly be heterozygous for the mutation. What we do know is that examples of these antibodies have been implicated in severe transfusion reactions and severe HDFN. My colleagues and I have reviewed all the known cases in the literature and our review article is scheduled for publication in the April edition of Transfusion Medicine Reviews.

Regards

Damien Heathcote

Technical Services Manager

CSL Biotherapies IH

Melbourne, Australia

[Malcolm Needs ☆]

I look forward to reading your article.

Thanks Damien.

[TimOz]

Hi All,

I have been away for a while.

The article Damien mentioned is in print. the reference is:

Heathcote D, Carroll T, Flower R. Sixty years of antibodies to MNS system hybrid glycophorins: What have we learned?. Transfusion Medicine Reviews (Volume 25 #2); April 2011

Shily,

We have seen an HTR case similar to your in Australia. Negative antibody screen (no MNS system hybrid glycophorin phenotypes on the screening cells used). No IAT crossmatch performed as blood was issued on a "Group, Screen Electronic Blood Release" protocol. 2 unit crossmatch. Reaction to second unit with haemolysis. Patient was female and incompatible with her husband's red cells in an IAT crossmatch.

[Yanxia]

Hi All,

I have been away for a while.

The article Damien mentioned is in print. the reference is:

Heathcote D, Carroll T, Flower R. Sixty years of antibodies to MNS system hybrid glycophorins: What have we learned?. Transfusion Medicine Reviews (Volume 25 #2); April 2011

Shily,

We have seen an HTR case similar to your in Australia. Negative antibody screen (no MNS system hybrid glycophorin phenotypes on the screening cells used). No IAT crossmatch performed as blood was issued on a "Group, Screen Electronic Blood Release" protocol. 2 unit crossmatch. Reaction to second unit with haemolysis. Patient was female and incompatible with her husband's red cells in an IAT crossmatch.

Thank you, TimOz. Is the case you countered acute or delayed hemolysis, intra or extra circulation hemolysis?

[TimOz]

Hi Yanxia,

This was not my case but one I know of. The notes I have are this:

60 year old female with endometrial and ovarian Carcinoma. Had been transfused with 26 units of blood uneventfully

Case notes:

1200 hrs Transfusion commenced

1230 hrs C/O back, neck and chest pain, dyspnoea and very distressed, Transfusion stopped

Temp 36.7 – 36.7, Pulse 94 – 102, BP 90/60 – 120/60

1245 hrs Feeling better so transfusion recommenced

1300 hrs Rigors started, Temp 37.5, Pulse 112, BP 140/80, TRANSFUSION STOPPED AND CEASED!

Follow up: Antibody screen negative, DAT negative, Unit gave 12 reaction in DiaMed AHG crossmatch, Crossmatch repeated with same result.

Reference lab reproduced findings + Antibody detected in Saline 22 and 37 when tested against the donor cells. Antibody did not react by enzyme technique

Plasma positive with: Plasma negative with:

Vw Mi VII

Mi III Hil and MINY-

Mi IV

Mi VI

Mi X

At the time (2005) this was interpreted as an Anti-Vw reacting with Mi III cells but the pattern (if the reference cell phenotypes are correct) looks like an anti-Mia.

Donor cells were typed as M POS, N NEG, S NEG, AND s POS. Typing with antibodies to various Miltenberger classes showed the donor is almost certainly Mi III (GP.Mur).

This was a first time donor of unknown ethnicity.

Shily, If you can get your hands on the clinical case review publication mentioned above you can see quite a bit of data that you should find useful.

In summary, there is likely to be a very significant underreporting of these cases. There are a total of 35 clinical cases attributed to antibodies to MNS system hybrid glycophorins reported in the literature, 8 (23%) detailed HTRs, one of which was associated with a fatality.

In all 8 reported HTR cases there has been IgG present, and in 1 case, only IgG was present. IgG titers in reported cases range from 8 to 512, although in only 3 cases were titers reported.

Unsurprisingly, to date, there have been no cases of HTR reported in which only IgM alloantibodies were present.