I've posted a similar question regarding this on the AABB website but I'm hoping to cover all bases to get some feedback.

We recently encountered a high-titered anti-M and treated the serum with DTT. The saline control Coombs titer was 128 and the DTT-treated serum titer was zero. Now it seems to me that some time ago I saw a paper detailing a case in which an IgM anti-M had been implicated in HDN. Does anyone recall something like this?

Is anyone using DTT or 2ME in cases like this? We have recommended that the doc followup with DTT testing every 3-4 weeks. Thanks!

I don't recall anything like this. But we use DTT to treat the plasma/serum.

There was an article in Transfusion in the last year or two about this. As I recall it involved a fetal death and IgM anti-M. I cannot find it right now.

(This is the first time I have tried searching since Transfusion migrated from Blackwell to Wiley Scientific, and I don't think I know what I am doing.)

Linda Frederick

Ok, I figured it out:

Fetal hemolytic anemia and intrauterine death caused by anti-M immunization

Transfusion

Volume 47, Issue 5, Date: May 2007, Pages: 911-917

Agneta Wikman, Ann Edner, Gunilla Gryfelt, Baldvin Jonsson, Jan-Inge Henter

STUDY DESIGN AND METHODS:This study reports on three pregnancies in one family that all resulted in severe fetal anemia. The first fetus died in utero with hydrops fetalis during the 20th gestational week and the second child was delivered after 28 weeks of gestation with hydrops fetalis and a hemoglobin level of 16 g per L whereas the third affected child was treated with intrauterine red cell (RBC) transfusions before delivery at 28 weeks of gestation.

RESULTS:The direct antiglobulin test was negative but anti-M in a low titer was detected through the three pregnancies, and its clinical relevance, which initially was uncertain, was confirmed by pronounced in vivo hemolysis in maternal blood of chromate (51Cr)-labeled M+ RBCs and normal survival of 51Cr labeled M– RBCs.

CONCLUSION:It is concluded that anti-M immunization in a few cases may cause severe fetal hemolytic anemia and intrauterine death. It remains to be elucidated why a normally clinically insignificant antibody is this aggressive in a small proportion of cases. Because the condition is treatable, anti-M must be considered as a possible cause of fetal anemia and intrauterine death.

Ok, I figured it out:

Fetal hemolytic anemia and intrauterine death caused by anti-M immunization

Transfusion

Volume 47, Issue 5, Date: May 2007, Pages: 911-917

Agneta Wikman, Ann Edner, Gunilla Gryfelt, Baldvin Jonsson, Jan-Inge Henter

STUDY DESIGN AND METHODS:This study reports on three pregnancies in one family that all resulted in severe fetal anemia. The first fetus died in utero with hydrops fetalis during the 20th gestational week and the second child was delivered after 28 weeks of gestation with hydrops fetalis and a hemoglobin level of 16 g per L whereas the third affected child was treated with intrauterine red cell (RBC) transfusions before delivery at 28 weeks of gestation.

RESULTS:The direct antiglobulin test was negative but anti-M in a low titer was detected through the three pregnancies, and its clinical relevance, which initially was uncertain, was confirmed by pronounced in vivo hemolysis in maternal blood of chromate (51Cr)-labeled M+ RBCs and normal survival of 51Cr labeled M– RBCs.

CONCLUSION:It is concluded that anti-M immunization in a few cases may cause severe fetal hemolytic anemia and intrauterine death. It remains to be elucidated why a normally clinically insignificant antibody is this aggressive in a small proportion of cases. Because the condition is treatable, anti-M must be considered as a possible cause of fetal anemia and intrauterine death.

Thanks for the followup Linda. Somehow I definitely missed this article.

I'm not sure whether an isolated case like this this should change the way we look at an IgM anti-M. For several years our reference lab has run into a few of these on a daily basis and we have never had a response from a client indicating a problem at delivery. Was wondering if anyone on the board has experienced or become aware of a similar problem.

My quandry is....do I do a titer for pregnant patients if the antibody is non-reactive in AHG at 37C? The old wisdom says no titer, but this article makes me uneasy. On the one hand, I hate to rack up big bills for these patients. On the other hand, maybe the (ultra) conservative course of doing the titer is best.

My quandry is....do I do a titer for pregnant patients if the antibody is non-reactive in AHG at 37C? The old wisdom says no titer, but this article makes me uneasy. On the one hand, I hate to rack up big bills for these patients. On the other hand, maybe the (ultra) conservative course of doing the titer is best.

I'm not sure what good a Coombs titer would do if the antibody is not active at 37C; unless of course you are referring to a room temp titer. In that case I think you would be creating a lot of patient/physician anxiety for no reason.

This whole situation reminds me of the days of using enzyme-treated screening cells to

detect anti-JkA/B. Might you miss a Kidd antibody without using these cells? Sure! But is it worth the time, expense and frustration dealing with treated cells to pick up the rare enzyme-only antibody? I think most of us would say, "No!"!

Ok, I figured it out:

Fetal hemolytic anemia and intrauterine death caused by anti-M immunization

Transfusion

Volume 47, Issue 5, Date: May 2007, Pages: 911-917

Agneta Wikman, Ann Edner, Gunilla Gryfelt, Baldvin Jonsson, Jan-Inge Henter

STUDY DESIGN AND METHODS:This study reports on three pregnancies in one family that all resulted in severe fetal anemia. The first fetus died in utero with hydrops fetalis during the 20th gestational week and the second child was delivered after 28 weeks of gestation with hydrops fetalis and a hemoglobin level of 16 g per L whereas the third affected child was treated with intrauterine red cell (RBC) transfusions before delivery at 28 weeks of gestation.

RESULTS:The direct antiglobulin test was negative but anti-M in a low titer was detected through the three pregnancies, and its clinical relevance, which initially was uncertain, was confirmed by pronounced in vivo hemolysis in maternal blood of chromate (51Cr)-labeled M+ RBCs and normal survival of 51Cr labeled M– RBCs.

CONCLUSION:It is concluded that anti-M immunization in a few cases may cause severe fetal hemolytic anemia and intrauterine death. It remains to be elucidated why a normally clinically insignificant antibody is this aggressive in a small proportion of cases. Because the condition is treatable, anti-M must be considered as a possible cause of fetal anemia and intrauterine death.

I have not opportunity to read this article,what a pity! I have some questions, need some help, thanks advance: Is it IgM antibodies caused HDFN? Had the mother experience any invaded treatment, like intrauterine

injection or trauma?

Consistency is a problem in regards to anti-M titers. The major OB/Gyn practice in my area has most of their prenatal work done here, but some of their patients go to a neighboring facility for their prenatal workups for deliveries that will happen here. We aren't currently doing titers for anti-Ms that are AHG nonreactive but the other lab does. Makes for some interesting discussions with the doctors. So far I have managed to persuade them to skip the titer.

I wouldn't get too concerned with IgM anti-M. The aforementioned article does not state the Ig classification, I would assume the Anti-M causing the HDN was IgG. That's why it is important to determine if anti-M detected in OB patient's is IgG or IgM and the IgG portion titered.

In Chinese there have IgG anti-M caused HDFN and transfusion reaction.